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1
Pignoni, F., and S. L. Zipursky. "Induction of Drosophila eye development by decapentaplegic." Development 124, no. 2 (January 15, 1997): 271–78. http://dx.doi.org/10.1242/dev.124.2.271.
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The Drosophila decapentaplegic (dpp) gene, encoding a secreted protein of the transforming growth factor-beta (TGF-beta) superfamily, controls proliferation and patterning in diverse tissues, including the eye imaginal disc. Pattern formation in this tissue is initiated at the posterior edge and moves anteriorly as a wave; the front of this wave is called the morphogenetic furrow (MF). Dpp is required for proliferation and initiation of pattern formation at the posterior edge of the eye disc. It has also been suggested that Dpp is the principal mediator of Hedgehog function in driving progression of the MF across the disc. In this paper, ectopic Dpp expression is shown to be sufficient to induce a duplicated eye disc with normal shape, MF progression, neuronal cluster formation and direction of axon outgrowth. Induction of ectopic eye development occurs preferentially along the anterior margin of the eye disc. Ectopic Dpp clones situated away from the margins induce neither proliferation nor patterning. The Dpp signalling pathway is shown to be under tight transcriptional and post-transcriptional control within different spatial domains in the developing eye disc. In addition, Dpp positively controls its own expression and suppresses wingless transcription. In contrast to the wing disc, Dpp does not appear to be the principal mediator of Hedgehog function in the eye.
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Lecuit, T. "Histoire d'un morphogène nommé decapentaplegic (dpp)." médecine/sciences 15, no. 11 (1999): 1279. http://dx.doi.org/10.4267/10608/1257.
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Newfeld, Stuart J., Richard W. Padgett, Seth D. Findley, Brent G. Richter, Michele Sanicola, Margaret de Cuevas, and William M. Gelbart. "Molecular Evolution at the decapentaplegic Locus in Drosophila." Genetics 145, no. 2 (February 1, 1997): 297–309. http://dx.doi.org/10.1093/genetics/145.2.297.
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Using an elaborate set of cis-regulatory sequences, the decapentaplegic (dpp) gene displays a dynamic pattern of gene expression during development. The C-terminal portion of the DPP protein is processed to generate a secreted signaling molecule belonging to the transforming growth factor-β (TGF-β) family. This signal, the DPP ligand, is able to influence the developmental fates of responsive cells in a concentration-dependent fashion. Here we examine the sequence level organization of a significant portion of the dpp locus in Drosophila melanogaster and use interspecific comparisons with D. simulans, D. pseudoobscura and D.virilis to explore the molecular evolution of the gene. Our interspecific analysis identified significant selective constraint on both the nucleotide and amino acid sequences. As expected, interspecific comparison of protein coding sequences shows that the C-terminal ligand region is highly conserved. However, the central portion of the protein is also conserved, while the N-terminal third is quite variable. Comparison of noncoding regions reveals significant stretches of nucleotide identity in the 3′ untranslated portion of exon 3 and in the intron between exons 2 and 3. An examination of cDNA sequences representing five classes of dpp transcripts indicates that these transcripts encode the same polypeptide.
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Mullor, J. L., M. Calleja, J. Capdevila, and I. Guerrero. "Hedgehog activity, independent of decapentaplegic, participates in wing disc patterning." Development 124, no. 6 (March 15, 1997): 1227–37. http://dx.doi.org/10.1242/dev.124.6.1227.
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In the Drosophila wing imaginal disc, the Hedgehog (Hh) signal molecule induces the expression of decapentaplegic (dpp) in a band of cells abutting the anteroposterior (A/P) compartment border. It has been proposed that Dpp organizes the patterning of the entire wing disc. We have tested this proposal by studying the response to distinct levels of ectopic expression of Hh and Dpp, using the sensory organ precursors (SOPs) of the wing and notum and the presumptive wing veins as positional markers. Here, we show that Dpp specifies the position of most SOPs in the notum and of some of them in the wing. Close to the A/P compartment border, however, SOPs are specified by Hh rather than by Dpp alone. We also show that late signaling by Hh, after setting up dpp expression, is responsible for the formation of vein 3 and the scutellar region, and also for the determination of the distance between veins 3 and 4. One of the genes that mediates the Hh signal is the zinc-finger protein Cubitus interruptus (Ci). These results indicate that Hh has a Dpp-independent morphogenetic effect in the region of the wing disc near the A/P border.
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Nicholls, Russell E., and William M. Gelbart. "Identification of Chromosomal Regions Involved in decapentaplegic Function in Drosophila." Genetics 149, no. 1 (May 1, 1998): 203–15. http://dx.doi.org/10.1093/genetics/149.1.203.
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Abstract Signaling molecules of the transforming growth factor β (TGF-β) family contribute to numerous developmental processes in a variety of organisms. However, our understanding of the mechanisms which regulate the activity of and mediate the response to TGF-β family members remains incomplete. The product of the Drosophila decapentaplegic (dpp) locus is a well-characterized member of this family. We have taken a genetic approach to identify factors required for TGF-β function in Drosophila by testing for genetic interactions between mutant alleles of dpp and a collection of chromosomal deficiencies. Our survey identified two deficiencies that act as maternal enhancers of recessive embryonic lethal alleles of dpp. The enhanced individuals die with weakly ventralized phenotypes. These phenotypes are consistent with a mechanism whereby the deficiencies deplete two maternally provided factors required for dpp's role in embryonic dorsal-ventral pattern formation. One of these deficiencies also appears to delete a factor required for dpp function in wing vein formation. These deficiencies remove material from the 54F-55A and 66B-66C polytene chromosomal regions, respectively. As neither of these regions has been previously implicated in dpp function, we propose that each of the deficiencies removes a novel factor or factors required for dpp function.
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Segal, Daniel, and William M. Gelbart. "SHORTVEIN, A NEW COMPONENT OF THE DECAPENTAPLEGIC GENE COMPLEX IN DROSOPHILA MELANOGASTER." Genetics 109, no. 1 (January 1, 1985): 119–43. http://dx.doi.org/10.1093/genetics/109.1.119.
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ABSTRACT Our laboratory has been concerned with the structure and function of the decapentaplegic gene complex (DPP-C) in Drosophila melanogaster . To define the boundaries of the complex, we have studied the genetics of mutations allelic to a previously discovered mutation shortvein (shv), known to reside near decapentaplegic. We found that shortvein resides distal to Hin-d and dpp within the same polytene chromosome doublet, 22F1-2. Lesions in shv can affect not only the formation of the wing veins but also can interfere with normal development of parts of the adult and/or be lethal. Like those of dpp mutants, the shv-associated adult abnormalities affect distal epidermal structures. Some shv lesions cause a larval lethal syndrome which is associated with an unusually long larval stage (ca. five to six times its normal duration). Lesions in shv exhibit an involved pattern of complementation with dpp mutations, indicating that both shv and dpp are parts of a single gene complex. A subset of the array of mutant phenotypes displayed by shv/dpp trans-heterozygotes appear to be dpp-specific phenotypes; we interpret these as reflecting an inactivation effect of certain shv alleles on dpp functions. The other abnormalities displayed by these trans-heterozygotes appear to be shv-specific defects; we view these as indicating an inactivation effect of certain dpp mutations on shv functions. Furthermore, embryonic lethal (EL) mutations within the DPP-C exhibit allelic interactions with all shv mutations. We conclude that the shortvein region represents a newly identified integrated portion of the DPP-C.
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Raftery, L. A., V. Twombly, K. Wharton, and W. M. Gelbart. "Genetic screens to identify elements of the decapentaplegic signaling pathway in Drosophila." Genetics 139, no. 1 (January 1, 1995): 241–54. http://dx.doi.org/10.1093/genetics/139.1.241.
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Abstract Pathways for regulation of signaling by transforming growth factor-beta family members are poorly understood at present. The best genetically characterized member of this family is encoded by the Drosophila gene decapentaplegic (dpp), which is required for multiple events during fly development. We describe here the results of screens for genes required to maximize dpp signaling during embryonic dorsal-ventral patterning. Screens for genetic interactions in the zygote have identified an allele of tolloid, as well as two novel alleles of screw, a gene recently shown to encode another bone morphogenetic protein-like polypeptide. Both genes are required for patterning the dorsalmost tissues of the embryo. Screens for dpp interactions with maternally expressed genes have identified loss of function mutations in Mothers against dpp and Medea. These mutations are homozygous pupal lethal, engendering gut defects and severely reduced imaginal disks, reminiscent of dpp mutant phenotypes arising during other dpp-dependent developmental events. Genetic interaction phenotypes are consistent with reduction of dpp activity in the early embryo and in the imaginal disks. We propose that the novel screw mutations identified here titrate out some component(s) of the dpp signaling pathway. We propose that Mad and Medea encode rate-limiting components integral to dpp pathways throughout development.
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Theisen, H., T. E. Haerry, M. B. O'Connor, and J. L. Marsh. "Developmental territories created by mutual antagonism between Wingless and Decapentaplegic." Development 122, no. 12 (December 1, 1996): 3939–48. http://dx.doi.org/10.1242/dev.122.12.3939.
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Drosophila appendages develop from imaginal discs which become subdivided into distinct regions during normal patterning. At least 3 axes of asymmetry are required to produce a chiral appendage such as a leg. The A/P compartments provide one axis of asymmetry in all discs. In leg and antennal discs, the anterior compartment becomes asymmetric in the D/V axis with decapentaplegic (dpp) expression defining dorsal anterior leg, and wingless (wg) expression defining ventral anterior leg. However, unlike wing discs, no D/V compartment has been demonstrated in legs or antennae. How are the dorsal anterior and ventral anterior territories defined and maintained? Here we show that wg inhibits dpp expression and dpp inhibits wg expression in leg and eye/antennal discs. This mutual repression provides a mechanism for maintaining separate regions of wg and dpp expression in a developing field. We propose the term ‘territory’ to describe regions of cells that are under the domineering influence of a particular morphogen. Territories differ from compartments in that they are not defined by lineage but are dynamically maintained by continuous morphogen signaling. We propose that the anterior compartment of the leg disc is divided into dorsal and ventral territories by the mutual antagonism between WG and DPP signaling.
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Horsfield, J., A. Penton, J. Secombe, F. M. Hoffman, and H. Richardson. "decapentaplegic is required for arrest in G1 phase during Drosophila eye development." Development 125, no. 24 (December 15, 1998): 5069–78. http://dx.doi.org/10.1242/dev.125.24.5069.
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During eye development in Drosophila, cell cycle progression is coordinated with differentiation. Prior to differentiation, cells arrest in G1 phase anterior to and within the morphogenetic furrow. We show that Decapentaplegic (Dpp), a TGF-β family member, is required to establish this G1 arrest, since Dpp-unresponsive cells located in the anterior half of the morphogenetic furrow show ectopic S phases and ectopic expression of the cell cycle regulators Cyclins A, E and B. Conversely, ubiquitous over-expression of Dpp in the eye imaginal disc transiently inhibits S phase without affecting Cyclin E or Cyclin A abundance. This Dpp-mediated inhibition of S phase occurs independently of the Cyclin A inhibitor Roughex and of the expression of Dacapo, a Cyclin E-Cdk2 inhibitor. Furthermore, Dpp-signaling genes interact genetically with a hypomorphic cyclin E allele. Taken together our results suggest that Dpp acts to induce G1 arrest in the anterior part of the morphogenetic furrow by a novel inhibitory mechanism. In addition, our results provide evidence for a Dpp-independent mechanism that acts in the posterior part of the morphogenetic furrow to maintain G1 arrest.
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Zecca, M., K. Basler, and G. Struhl. "Sequential organizing activities of engrailed, hedgehog and decapentaplegic in the Drosophila wing." Development 121, no. 8 (August 1, 1995): 2265–78. http://dx.doi.org/10.1242/dev.121.8.2265.
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The Drosophila wing is formed by two cell populations, the anterior and posterior compartments, which are distinguished by the activity of the selector gene engrailed (en) in posterior cells. Here, we show that en governs growth and patterning in both compartments by controlling the expression of the secreted proteins hedgehog (hh) and decapentaplegic (dpp) as well as the response of cells to these signaling molecules. First, we demonstrate that en activity programs wing cells to express hh whereas the absence of en activity programs them to respond to hh by expressing dpp. As a consequence, posterior cells secrete hh and induce a stripe of neighboring anterior cells across the compartment boundary to secrete dpp. Second, we demonstrate that dpp can exert a long-range organizing influence on surrounding wing tissue, specifying anterior or posterior pattern depending on the compartmental provenance, and hence the state of en activity, of the responding cells. Thus, dpp secreted by anterior cells along the compartment boundary has the capacity to organize the development of both compartments. Finally, we report evidence suggesting that dpp may exert its organizing influence by acting as a gradient morphogen in contrast to hh which appears to act principally as a short range inducer of dpp.
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Manak, J. R., L. D. Mathies, and M. P. Scott. "Regulation of a decapentaplegic midgut enhancer by homeotic proteins." Development 120, no. 12 (December 1, 1994): 3605–19. http://dx.doi.org/10.1242/dev.120.12.3605.
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The clustered homeotic genes encode transcription factors that regulate pattern formation in all animals, conferring cell fates by coordinating the activities of downstream ‘target’ genes. In the Drosophila midgut, the Ultrabithorax (Ubx) protein activates and the abdominalA (abd-A) protein represses transcription of the decapentaplegic (dpp) gene, which encodes a secreted signalling protein of the TGF beta class. We have identified an 813 bp dpp enhancer which is capable of driving expression of a lacZ gene in a correct pattern in the embryonic midgut. The enhancer is activated ectopically in the visceral mesoderm by ubiquitous expression of Ubx or Antennapedia but not by Sex combs reduced protein. Ectopic expression of abd-A represses the enhancer. Deletion analysis reveals regions required for repression and activation. A 419 bp subfragment of the 813 bp fragment also drives reporter gene expression in an appropriate pattern, albeit more weakly. Evolutionary sequence conservation suggests other factors work with homeotic proteins to regulate dpp. A candidate cofactor, the extradenticle protein, binds to the dpp enhancer in close proximity to homeotic protein binding sites. Mutation of either this site or another conserved motif compromises enhancer function. A 45 bp fragment of DNA from within the enhancer correctly responds to both UBX and ABD-A in a largely tissue-specific manner, thus representing the smallest in vivo homeotic response element (HOMRE) identified to date.
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Yang, X., M. van Beest, H. Clevers, T. Jones, D. A. Hursh, and M. A. Mortin. "decapentaplegic is a direct target of dTcf repression in the Drosophila visceral mesoderm." Development 127, no. 17 (September 1, 2000): 3695–702. http://dx.doi.org/10.1242/dev.127.17.3695.
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Drosophila T cell factor (dTcf) mediates transcriptional activation in the presence of Wingless signalling and repression in its absence. Wingless signalling is required for the correct expression of decapentaplegic (dpp), a Transforming Growth Factor (beta) family member, in parasegments 3 and 7 of the Drosophila visceral mesoderm. Here we demonstrate that a dpp enhancer element, which directs expression of a reporter gene in the visceral mesoderm in a pattern indistinguishable from dpp, has two functional dTcf binding sites. Mutations that reduce or eliminate Wingless signalling abolish dpp reporter gene expression in parasegment 3 and reduce it in parasegment 7 while ectopic expression of Wingless signalling components expand reporter gene expression anteriorly in the visceral mesoderm. However, mutation of the dTcf binding sites in the dpp enhancer results in ectopic expression of reporter gene expression throughout the visceral mesoderm, with no diminution of expression in the endogenous sites of expression. These results demonstrate that the primary function of dTcf binding to the dpp enhancer is repression throughout the visceral mesoderm and that activation by Wingless signalling is probably not mediated via these dTcf binding sites to facilitate correct dpp expression in the visceral mesoderm.
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Yu, K., M. A. Sturtevant, B. Biehs, V. Francois, R. W. Padgett, R. K. Blackman, and E. Bier. "The Drosophila decapentaplegic and short gastrulation genes function antagonistically during adult wing vein development." Development 122, no. 12 (December 1, 1996): 4033–44. http://dx.doi.org/10.1242/dev.122.12.4033.
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TGF-beta-related signaling pathways play diverse roles during vertebrate and invertebrate development. A common mechanism for regulating the activity of TGF-beta family members is inhibition by extracellular antagonists. Recently, the Drosophila short gastrulation (sog) gene was shown to encode a predicted diffusible factor which antagonizes signaling mediated by the TGF-beta-like Decapentaplegic (Dpp) pathway in the early blastoderm embryo. sog and dpp, which are among the earliest zygotic genes to be activated, are expressed in complementary dorsal-ventral domains. The opposing actions of sog and dpp in the early embryo have been highly conserved during evolution as their vertebrate counterparts, chordin and BMP-4, function homologously to define neural versus non-neural ectoderm in Xenopus. Here we exploit the genetically sensitive adult wing vein pattern to investigate the generality of the antagonistic relationship between sog and dpp. We show that dpp is expressed in vein primordia during pupal wing development and functions to promote vein formation. In contrast, sog is expressed in complementary intervein cells and suppresses vein formation. sog and dpp function during the same phenocritical periods (i.e. 16–28 hours after pupariation) to influence the vein versus intervein cell fate choice. The conflicting activities of dpp and sog are also revealed by antagonistic dosage-sensitive interactions between these two genes during vein development. Analysis of vein and intervein marker expression in dpp and sog mutant wings suggests that dpp promotes vein fates indirectly by activating the vein gene rhomboid (rho), and that sog functions by blocking an autoactivating Dpp feedback loop. These data support the view that Sog is a dedicated Dpp antagonist.
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Arquier, Nathalie, Laurent Perrin, Pascal Manfruelli, and Michel Sémériva. "TheDrosophilatumor suppressor genelethal(2)giant larvaeis required for the emission of the Decapentaplegic signal." Development 128, no. 12 (June 15, 2001): 2209–20. http://dx.doi.org/10.1242/dev.128.12.2209.
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The Drosophila tumor suppressor gene lethal(2) giant larvae (lgl) encodes a cytoskeletal protein required for the change in shape and polarity acquisition of epithelial cells, and also for asymmetric division of neuroblasts. We show here that lgl participates in the emission of Decapentaplegic (Dpp), a member of the transforming growth factor β (TGFβ) family, in various developmental processes.During embryogenesis, lgl is required for the dpp-dependent transcriptional activation of zipper (zip), which encodes the non-muscle myosin heavy chain (NMHC), in the dorsalmost ectodermal cells – the leading edge cells. The embryonic expression of known targets of the dpp signaling pathway, such as labial or tinman was abolished or strongly reduced in lgl mutants. lgl mutant cuticles exhibited phenotypes resembling those observed in mutated partners of the dpp signaling pathway. In addition, lgl was required downstream of dpp and upstream of its receptor Thickveins (Tkv) for the dorsoventral patterning of the ectoderm. During larval development, the expression of spalt, a dpp target, was abolished in mutant wing discs, while it was restored by a constitutively activated form of Tkv (TkvQ253D). Taking into account that the activation of dpp expression was unaffected in the mutant, this suggests that lgl function is not required downstream of the Dpp receptor. Finally, the function of lgl responsible for the activation of Spalt expression appeared to be required only in the cells that produce Dpp, and lgl mutant somatic clones behaved non autonomously. We therefore position the activity of lgl in the cells that produce Dpp, and not in those that respond to the Dpp signal. These results are consistent with a same role for lgl in exocytosis and secretion as that proposed for its yeast ortholog sro7/77 and lgl might function in parallel or independently of its well-documented role in the control of epithelial cell polarity.
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Schwyter, D. H., J. D. Huang, T. Dubnicoff, and A. J. Courey. "The decapentaplegic core promoter region plays an integral role in the spatial control of transcription." Molecular and Cellular Biology 15, no. 7 (July 1995): 3960–68. http://dx.doi.org/10.1128/mcb.15.7.3960.
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The Drosophila melanogaster decapentaplegic (dpp) gene encodes a transforming growth factor beta-related cell signaling molecule that plays a critical role in dorsal/ventral pattern formation. The dpp expression pattern in the Drosophila embryo is dynamic, consisting of three phases. Phase I, in which dpp is expressed in a broad dorsal domain, depends on elements in the dpp second intron that interact with the Dorsal transcription factor to repress transcription ventrally. In contrast, phases II and III, in which dpp is expressed first in broad longitudinal stripes (phase II) and subsequently in narrow longitudinal stripes (phase III), depend on multiple independent elements in the dpp 5'-flanking region. Several aspects of the normal dpp expression pattern appear to depend on the unique properties of the dpp core promoter. For example, this core promoter (extending from -22 to +6) is able to direct a phase II expression pattern in the absence of additional upstream or downstream regulatory elements. In addition, a ventral-specific enhancer in the dpp 5'-flanking region that binds the Dorsal factor activates the heterologous hsp70 core promoter but not the dpp core promoter. Thus, the dpp core promoter region may contribute to spatially regulated transcription both by interacting directly with spatially restricted activators and by modifying the activity of proteins bound to enhancer elements.
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Rakshit, Arpita, and Rabindra Nath Chatterjee. "Molecular evolutionary analysis of decapentaplegic (dpp) gene in Drosophilidae." Nucleus 57, no. 1 (March 25, 2014): 61–65. http://dx.doi.org/10.1007/s13237-014-0104-1.
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Gelbart, William M. "The decapentaplegic gene: a TGF-β homologue controlling pattern formation in Drosophila." Development 107, Supplement (April 1, 1989): 65–74. http://dx.doi.org/10.1242/dev.107.supplement.65.
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The type β transforming growth factor (TGF-β) family of secreted factors encompasses a wide range of structurally related proteins that control the state of determination or differentiation in a wide variety of cell types. For all members of the family that have been studied at the protein level, the active moieties arise as dimers of the C-terminal ∼110 amino acid fragment derived from much longer precursor polypeptides. The hallmark of the family is a series of 7 completely conserved cysteine residues in the C-terminus; other conserved amino acid sequences generally cluster in the vicinity of 6 of these 7 cysteines. This report focuses on our current understanding of the genetic structure and developmental role of the decapentaplegic (dpp) gene in Drosophila, the only member of the TGF-β family thus far identified in invertebrates. The dpp polypeptide bears a sufficiently close relationship to two bone morphogenesis proteins (BMP-2A and BMP-2B) identified in mammals (Wozney et al. 1988, Science 242, 1528–1534) to warrant the suggestion that dpp and the BMP-2s are the descendants of a common ancestral gene. The protein-coding information for dpp is contained within a 6 kb DNA segment. An elaborate cis-regulatory apparatus, encompassing a >55 kb DNA segment, has evolved to control expression of the dpp gene, which is required for determination of dorsal ectoderm in the early embryo, for normal distal outgrowth of the adult appendages, and for sundry other developmental events, which are currently less welldefined. Studies of chimeric individuals and observations of transcript accumulation in situ have demonstrated that the dpp gene is expressed along the A/P boundary of the imaginal disks. A possible role of dpp in elaborating positional information in imaginal disk development is discussed.
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Hursh, D. A., R. W. Padgett, and W. M. Gelbart. "Cross regulation of decapentaplegic and Ultrabithorax transcription in the embryonic visceral mesoderm of Drosophila." Development 117, no. 4 (April 1, 1993): 1211–22. http://dx.doi.org/10.1242/dev.117.4.1211.
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The Drosophila decapentaplegic gene (dpp) encodes a TGF-beta family member involved in signal transduction during embryonic midgut formation. The shortvein (shv) class of cis-regulatory dpp mutants disrupt expression in parasegments 4 and 7 (ps4 and ps7) of the embryonic visceral mesoderm (VM) surrounding the gut and cause abnormalities in gut morphogenesis. We demonstrate that cis-regulatory elements directing expression in ps4 and ps7 are separable and identify DNA fragments that generate ps4 and ps7 expression patterns using reporter gene constructs. dpp reporter gene expression in both ps4 and ps7 is autoregulated as it requires endogenous dpp+ activity. Reporter gene ps7 expression requires the wild-type action of Ultra-bithorax (Ubx), and abdominal-A. Furthermore, the expression of certain Ubx reporter genes is coincident with dpp in the VM. Both the mis-expression of Ubx reporter genes in the developing gastric caecae at ps4 and its normal expression in ps7 are dependent upon endogenous dpp+ activity. We conclude that dpp both responds to and regulates Ubx in ps7 of the visceral mesoderm and that Ubx autoregulation within this tissue may be indirect as it requires more components than have previously been thought.
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Hepker, J., R. K. Blackman, and R. Holmgren. "Cubitus interruptus is necessary but not sufficient for direct activation of a wing-specific decapentaplegic enhancer." Development 126, no. 16 (August 15, 1999): 3669–77. http://dx.doi.org/10.1242/dev.126.16.3669.
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In Drosophila, the imaginal discs are the primordia for adult appendages. Their proper formation is dependent upon the activation of the decapentaplegic (dpp) gene in a stripe of cells just anterior to the compartment boundary. In imaginal discs, the dpp gene has been shown to be activated by Hedgehog signal transduction. However, an initial analysis of its enhancer region suggests that its regulation is complex and depends upon additional factors. In order to understand how multiple factors regulate dpp expression, we chose to focus on a single dpp enhancer element, the dpp heldout enhancer, from the 3′ cis regulatory disc region of the dpp locus. In this report, we present a molecular analysis of this 358 bp wing- and haltere-specific dpp enhancer, which demonstrates a direct transcriptional requirement for the Cubitus interruptus (Ci) protein. The results suggest that, in addition to regulation by Ci, expression of the dpp heldout enhancer is spatially determined by Drosophila TCF (dTCF) and the Vestigial/Scalloped selector system and that temporal control is provided by dpp autoregulation. Consistent with the unexpectedly complex regulation of the dpp heldout enhancer, analysis of a Ci consensus site reporter construct suggests that Ci, a mediator of Hedgehog transcriptional activation, can only transactivate in concert with other factors.
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Chanut, F., and U. Heberlein. "Role of decapentaplegic in initiation and progression of the morphogenetic furrow in the developing Drosophila retina." Development 124, no. 2 (January 15, 1997): 559–67. http://dx.doi.org/10.1242/dev.124.2.559.
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Morphogenesis in the Drosophila retina initiates at the posterior margin of the eye imaginal disc by an unknown mechanism. Upon initiation, a wave of differentiation, its forward edge marked by the morphogenetic furrow (MF), proceeds anteriorly across the disc. Progression of the MF is driven by hedgehog (hh), expressed by differentiating photoreceptor cells. The TGF-beta homolog encoded by decapentaplegic (dpp) is expressed at the disc's posterior margin prior to initiation and in the furrow, under the control of hh, during MF progression. While dpp has been implicated in eye disc growth and morphogenesis, its precise role in retinal differentiation has not been determined. To address the role of dpp in initiation and progression of retinal differentiation we analyzed the consequences of reduced and increased dpp function during eye development. We find that dpp is not only required for normal MF initiation, but is sufficient to induce ectopic initiation of differentiation. Inappropriate initiation is normally inhibited by wingless (wg). Loss of dpp function is accompanied by expansion of wg expression, while increased dpp function leads to loss of wg transcription. In addition, dpp is required to maintain, and sufficient to induce, its own expression along the disc's margins. We postulate that dpp autoregulation and dpp-mediated inhibition of wg expression are required for the coordinated regulation of furrow initiation and progression. Finally, we show that in the later stages of retinal differentiation, reduction of dpp function leads to an arrest in MF progression.
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Wiersdorff, V., T. Lecuit, S. M. Cohen, and M. Mlodzik. "Mad acts downstream of Dpp receptors, revealing a differential requirement for dpp signaling in initiation and propagation of morphogenesis in the Drosophila eye." Development 122, no. 7 (July 1, 1996): 2153–62. http://dx.doi.org/10.1242/dev.122.7.2153.
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Decapentaplegic (Dpp), a member of the TGF-betta family of cytokines, has been implicated in many patterning processes in Drosophila, including the initial steps of pattern formation in the developing eye. We show that the Mothers against dpp (Mad) gene is required for dpp signaling during eye development. Clonal analysis demonstrates a cell-autonomous function for Mad and genetic interactions indicate that Mad is an essential component of the signal transduction pathway downstream of the Dpp receptors in responding cells. Mad-mediated dpp signaling is absolutely required for the initiation of the morphogenetic furrow in the eye, but has only a minor role in its subsequent propagation across the eye
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Inoue, Hirofumi, Takeshi Imamura, Yasuhiro Ishidou, Masao Takase, Yoshiyuki Udagawa, Yoshitomo Oka, Kazuhide Tsuneizumi, Tetsuya Tabata, Kohei Miyazono, and Masahiro Kawabata. "Interplay of Signal Mediators of Decapentaplegic (Dpp): Molecular Characterization of Mothers against dpp, Medea, and Daughters against dpp." Molecular Biology of the Cell 9, no. 8 (August 1998): 2145–56. http://dx.doi.org/10.1091/mbc.9.8.2145.
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Decapentaplegic (Dpp) plays an essential role inDrosophila development, and analyses of the Dpp signaling pathway have contributed greatly to understanding of the actions of the TGF-β superfamily. Intracellular signaling of the TGF-β superfamily is mediated by Smad proteins, which are now grouped into three classes. Two Smads have been identified inDrosophila. Mothers against dpp (Mad) is a pathway-specific Smad, whereas Daughters against dpp (Dad) is an inhibitory Smad genetically shown to antagonize Dpp signaling. Here we report the identification of a common mediator Smad inDrosophila, which is closely related to human Smad4. Mad forms a heteromeric complex with Drosophila Smad4 (Medea) upon phosphorylation by Thick veins (Tkv), a type I receptor for Dpp. Dad stably associates with Tkv and thereby inhibits Tkv-induced Mad phosphorylation. Dad also blocks hetero-oligomerization and nuclear translocation of Mad. We also show that Mad exists as a monomer in the absence of Tkv stimulation. Tkv induces homo-oligomerization of Mad, and Dad inhibits this step. Finally, we propose a model for Dpp signaling by Drosophila Smad proteins.
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Newfeld, Stuart J., and Norma T. Takaesu. "Local Transposition of a hobo Element Within the decapentaplegic Locus of Drosophila." Genetics 151, no. 1 (January 1, 1999): 177–87. http://dx.doi.org/10.1093/genetics/151.1.177.
Full textAbstract:
Abstract We have efficiently mobilized a phenotypically silent hobo transgene inserted within the cis-regulatory heldout region of the decapentaplegic (dpp) locus in Drosophila melanogaster. The goal of our experiment was to identify germline transmission of a local transposition event within the dpp locus that meets two specific criteria. First, excision of the hobo construct does not generate an adult mutant phenotype, suggesting minimal alteration to the original site of insertion. Second, we required a new insertion of the hobo transgene into the Haploinsufficient region of the locus ∼25 kb away. Genetic and molecular criteria are used to evaluate candidate germlines. In a pilot study, this local transposition event occurred independently in two individuals. Both of the transposition events appear to be new insertions into the dpp transcription unit. One insertion is between the two protein-coding exons, and the other is in the 3′-untranslated region of exon three. Strains carrying these insertions are valuable new reagents for the analysis of dpp function and molecular evolution. These results further support the use of the hobo system as an important tool in Drosophila genetics.
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Burke, R., and K. Basler. "Dpp receptors are autonomously required for cell proliferation in the entire developing Drosophila wing." Development 122, no. 7 (July 1, 1996): 2261–69. http://dx.doi.org/10.1242/dev.122.7.2261.
Full textAbstract:
The mammalian growth factor TGFbeta negatively regulates cell proliferation in various systems. Here we provide evidence that another TGFbeta superfamily member, Drosophila Decapentaplegic (Dpp), stimulates cell proliferation. In the developing wing blade, somatic clones lacking the Dpp receptors Punt or Thick veins (Tkv), or lacking Schnurri, a transcription factor involved in Dpp signal interpretation, fail to grow when induced early in larval development. Furthermore the spatial requirement for these signaling components indicates that Dpp has to travel several cell diameters from its source in order to reach all cells that require its signal. The requirement for Tkv also depends on the distance of cells from the source of the Dpp signal. We propose that Dpp can act at a distance to positively control cell proliferation.
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Lecuit, T., and S. M. Cohen. "Dpp receptor levels contribute to shaping the Dpp morphogen gradient in the Drosophila wing imaginal disc." Development 125, no. 24 (December 15, 1998): 4901–7. http://dx.doi.org/10.1242/dev.125.24.4901.
Full textAbstract:
Axis formation in the Drosophila wing depends on the localized expression of the secreted signaling molecule Decapentaplegic (Dpp). Dpp acts directly at a distance to specify discrete spatial domains, suggesting that it functions as a morphogen. Expression levels of the Dpp receptor thick veins (tkv) are not uniform along the anterior-posterior axis of the wing imaginal disc. Receptor levels are low where Dpp induces its targets Spalt and Omb in the wing pouch. Receptor levels increase in cells farther from the source of Dpp in the lateral regions of the disc. We present evidence that Dpp signaling negatively regulates tkv expression and that the level of receptor influences the effective range of the Dpp gradient. High levels of tkv sensitize cells to low levels of Dpp and also appear to limit the movement of Dpp outside the wing pouch. Thus receptor levels help to shape the Dpp gradient.
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Johnston, L. A., and G. Schubiger. "Ectopic expression of wingless in imaginal discs interferes with decapentaplegic expression and alters cell determination." Development 122, no. 11 (November 1, 1996): 3519–29. http://dx.doi.org/10.1242/dev.122.11.3519.
Full textAbstract:
We have expressed the segment polarity gene wingless (wg) ectopically in imaginal discs to examine its regulation of both ventral patterning and transdetermination. By experimentally manipulating the amount of Wg protein, we show that different thresholds of Wg activity elicit different outcomes, which are mediated by regulation of decapentaplegic (dpp) expression and result in alterations in the expression of homeotic genes. A high level of Wg activity leads to loss of all dorsal pattern elements and the formation of a complete complement of ventral pattern elements on the dorsal side of legs, and is correlated with repression of dpp expression. wg expression in dorsal cells of each disc also leads to dose-dependent transdetermination in those cells in homologous discs such as the labial, antennal and leg, but not in cells of dorsally located discs. When dpp expression is repressed by high levels of Wg, transdetermination does not occur, confirming that dpp participates with wg to induce transdetermination. These and other experiments suggest that dorsal expression of wg alters disc patterning and disc cell determination by modulating the expression of dpp. The dose-dependent effects of wg on dpp expression, ventralization of dorsal cells and transdetermination support a model in which wg functions as a morphogen in imaginal discs.
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Wharton, K. A., R. P. Ray, and W. M. Gelbart. "An activity gradient of decapentaplegic is necessary for the specification of dorsal pattern elements in the Drosophila embryo." Development 117, no. 2 (February 1, 1993): 807–22. http://dx.doi.org/10.1242/dev.117.2.807.
Full textAbstract:
decapentaplegic (dpp) is a zygotically expressed gene encoding a TGF-beta-related ligand that is necessary for dorsal-ventral patterning in the Drosophila embryo. We show here that dpp is an integral part of a gradient that specifies many different cell fates via intercellular signalling. There is a graded requirement for dpp activity in the early embryo: high levels of dpp activity specify the amnioserosa, while progressively lower levels specify dorsal and lateral ectoderm. This potential for dpp to specify cell fate is highly dosage sensitive. In the wild-type embryo, increasing the gene dosage of dpp can shift cell fates along the dorsal-ventral axis. Furthermore, in mutant embryos, in which only a subset of the dorsal-ventral pattern elements are represented, increasing the gene dosage of dpp can specifically transform those pattern elements into more dorsal ones. We present evidence that the zygotic dpp gradient and the maternal dorsal gradient specify distinct, non-overlapping domains of the dorsal-ventral pattern.
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Sanicola, M., J. Sekelsky, S. Elson, and W. M. Gelbart. "Drawing a stripe in Drosophila imaginal disks: negative regulation of decapentaplegic and patched expression by engrailed." Genetics 139, no. 2 (February 1, 1995): 745–56. http://dx.doi.org/10.1093/genetics/139.2.745.
Full textAbstract:
Abstract During development of the Drosophila adult appendage precursors, the larval imaginal disks, the decapentaplegic (dpp) gene is expressed in a stripe just anterior to the anterior/posterior (A/P) compartment boundary. Here, we investigate the genetic controls that lead to production of this stripe. We extend previous observations on leaky engrailed (en) mutations by showing that mutant clones completely lacking both en and invected (inv) activity ectopically express dpp-lacZ reporter genes in the posterior compartment, where dpp activity ordinarily is repressed. Similarly, patched (ptc) is also ectopically expressed in such posterior compartment en-inv- null clones. In contrast, these en-inv- clones exhibit loss of hedgehog (hh) expression. We suggest that the absence of dpp expression in the posterior compartment is due to direct repression by en. Ubiquitious expression of en in imaginal disks, produced by a hs-en construct, eliminates the expression of dpp-lacZ in its normal A/P boundary stripe. We identify three in vitro Engrailed binding sites in one of our dpp-lacZ reporter gene. Mutagenesis of these Engrailed binding sites results in ectopic expression of this reporter gene, but does not alter the normal stripe of expression at the A/P boundary. We propose that the en-hh-ptc regulatory loop that is responsible for segmental expression of wingless in the embryo is reutilized in imaginal disks to create a stripe of dpp expression along the A/P compartment boundary.
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Panganiban, G. E., R. Reuter, M. P. Scott, and F. M. Hoffmann. "A Drosophila growth factor homolog, decapentaplegic, regulates homeotic gene expression within and across germ layers during midgut morphogenesis." Development 110, no. 4 (December 1, 1990): 1041–50. http://dx.doi.org/10.1242/dev.110.4.1041.
Full textAbstract:
The decapentaplegic (dpp) gene product, a member of the transforming growth factor-beta family, is required in Drosophila embryos for normal gastrulation and the establishment of dorsal-ventral polarity in the embryo. dpp is also expressed at specific positions in the visceral mesoderm along the developing midgut. We find that mutations that eliminate the visceral mesoderm expression of dpp lead to defects in midgut morphogenesis and alter the spatially localized expression of the homeotic genes Sex combs reduced (Scr), Ultrabithorax (Ubx), and Antennapedia (Antp) in the visceral mesoderm. The extracellular dpp protein migrates from the visceral mesoderm across the apposing endodermal cell layer in a region of the endoderm that expresses the homeotic gene labial (lab). Mesodermal expression of dpp is required for the expression of lab in these endodermal cells indicating that dpp mediates an inductive interaction between the two germ layers. We propose that extracellular dpp protein regulates gut morphogenesis, in part, by regulating homeotic gene expression in the visceral mesoderm and endoderm of the developing midgut.
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Jazwinska, A., C. Rushlow, and S. Roth. "The role of brinker in mediating the graded response to Dpp in early Drosophila embryos." Development 126, no. 15 (August 1, 1999): 3323–34. http://dx.doi.org/10.1242/dev.126.15.3323.
Full textAbstract:
Brinker (Brk), a novel protein with features of a transcriptional repressor, regulates the graded response to Decapentaplegic (Dpp) in appendage primordia of Drosophila. Here, we show that in the embryo brk also has differential effects on Dpp target genes, depending on the level of Dpp activity required for their activation. Low-level target genes, like dpp itself, tolloid and early zerknullt, show strong ectopic expression in ventrolateral regions of brk mutant embryos; intermediate-level target genes like pannier show weak ectopic expression, while high-level target genes like u-shaped and rhomboid are not affected. Ectopic target gene activation in the absence of brk is independent of Dpp, Tkv and Medea, indicating that Dpp signaling normally antagonizes brk's repression of these target genes. brk is expressed like short gastrulation (sog) in ventrolateral regions of the embryo abutting the dpp domain. Here, both brk and sog antagonize the antineurogenic activity of Dpp so that only in brk sog double mutants is the neuroectoderm completely deleted.
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Maves, L., and G. Schubiger. "A molecular basis for transdetermination in Drosophila imaginal discs: interactions between wingless and decapentaplegic signaling." Development 125, no. 1 (January 1, 1998): 115–24. http://dx.doi.org/10.1242/dev.125.1.115.
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We are investigating how Drosophila imaginal disc cells establish and maintain their appendage-specific determined states. We have previously shown that ectopic expression of wingless (wg) induces leg disc cells to activate expression of the wing marker Vestigial (Vg) and transdetermine to wing cells. Here we show that ectopic wg expression non-cell-autonomously induces Vg expression in leg discs and that activated Armadillo, a cytosolic transducer of the Wg signal, cell-autonomously induces Vg expression in leg discs, indicating that this Vg expression is directly activated by Wg signaling. We find that ubiquitous expression of wg in leg discs can induce only dorsal leg disc cells to express Vg and transdetermine to wing. Dorsal leg disc cells normally express high levels of decapentaplegic (dpp) and its downstream target, optomotor-blind (omb). We find that high levels of dpp expression, which are both necessary and sufficient for dorsal leg development, are required for wg-induced transdetermination. We show that dorsalization of ventral leg disc cells, through targeted expression of either dpp or omb, is sufficient to allow wg to induce Vg expression and wing fate. Thus, dpp and omb promote both dorsal leg cell fate as well as transdetermination-competent leg disc cells. Taken together, our results show that the Wg and Dpp signaling pathways cooperate to induce Vg expression and leg-towing transdetermination. We also show that a specific vg regulatory element, the vg boundary enhancer, is required for transdetermination. We propose that an interaction between Wg and Dpp signaling can explain why leg disc cells transdetermine to wing and that our results have implications for normal leg and wing development.
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Newfeld, S. J., A. Mehra, M. A. Singer, J. L. Wrana, L. Attisano, and W. M. Gelbart. "Mothers against dpp participates in a DDP/TGF-beta responsive serine-threonine kinase signal transduction cascade." Development 124, no. 16 (August 15, 1997): 3167–76. http://dx.doi.org/10.1242/dev.124.16.3167.
Full textAbstract:
Mothers against dpp (Mad) is the prototype of a family of genes required for signaling by TGF-beta related ligands. In Drosophila, Mad is specifically required in cells responding to Decapentaplegic (DPP) signals. We further specify the role of Mad in DPP-mediated signaling by utilizing tkvQ199D, an activated form of the DPP type I receptor serine-threonine kinase thick veins (tkv). In the embryonic midgut, tkvQ199D mimics DPP-mediated inductive interactions. Homozygous Mad mutations block signaling by tkvQ199D. Appropriate responses to signaling by tkvQ199D are restored by expression of MAD protein in DPP-target cells. Endogenous MAD is phosphorylated in a ligand-dependent manner in Drosophila cell culture. DPP overexpression in the embryonic midgut induces MAD nuclear accumulation; after withdrawal of the overexpressed DPP signal, MAD is detected only in the cytoplasm. However, in three different tissues and developmental stages actively responding to endogenous DPP, MAD protein is detected in the cytoplasm but not in the nucleus. From these observations, we discuss possible roles for MAD in a DPP-dependent serine-threonine kinase signal transduction cascade integral to the proper interpretation of DPP signals.
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Sekelsky, J. J., S. J. Newfeld, L. A. Raftery, E. H. Chartoff, and W. M. Gelbart. "Genetic characterization and cloning of mothers against dpp, a gene required for decapentaplegic function in Drosophila melanogaster." Genetics 139, no. 3 (March 1, 1995): 1347–58. http://dx.doi.org/10.1093/genetics/139.3.1347.
Full textAbstract:
Abstract The decapentaplegic (dpp) gene of Drosophila melanogaster encodes a growth factor that belongs to the transforming growth factor-beta (TGF-beta) superfamily and that plays a central role in multiple cell-cell signaling events throughout development. Through genetic screens we are seeking to identify other functions that act upstream, downstream or in concert with dpp to mediate its signaling role. We report here the genetic characterization and cloning of Mothers against dpp (Mad), a gene identified in two such screens. Mad loss-of-function mutations interact with dpp alleles to enhance embryonic dorsal-ventral patterning defects, as well as adult appendage defects, suggesting a role for Mad in mediating some aspect of dpp function. In support of this, homozygous Mad mutant animals exhibit defects in midgut morphogenesis, imaginal disk development and embryonic dorsal-ventral patterning that are very reminiscent of dpp mutant phenotypes. We cloned the Mad region and identified the Mad transcription unit through germline transformation rescue. We sequenced a Mad cDNA and identified three Mad point mutations that alter the coding information. The predicted MAD polypeptide lacks known protein motifs, but has strong sequence similarity to three polypeptides predicted from genomic sequence from the nematode Caenorhabditis elegans. Hence, MAD is a member of a novel, highly conserved protein family.
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Kopp, A., R. K. Blackman, and I. Duncan. "Wingless, decapentaplegic and EGF receptor signaling pathways interact to specify dorso-ventral pattern in the adult abdomen of Drosophila." Development 126, no. 16 (August 15, 1999): 3495–507. http://dx.doi.org/10.1242/dev.126.16.3495.
Full textAbstract:
Adult abdominal segments of Drosophila are subdivided along the dorso-ventral axis into a dorsal tergite, a ventral sternite and ventro-lateral pleural cuticle. We report that this pattern is largely specified during the pupal stage by Wingless (Wg), Decapentaplegic (Dpp) and Drosophila EGF Receptor (DER) signaling. Expression of wg and dpp is activated at the posterior edge of the anterior compartment by Hedgehog signaling. Within this region, wg and dpp are expressed in domains that are mutually exclusive along the dorso-ventral axis: wg is expressed in the sternite and medio-lateral tergite, whereas dpp expression is confined to the pleura and the dorsal midline. Neither gene is expressed in the lateral tergite. Shirras and Couso (1996, Dev. Biol. 175, 24–36) have shown that tergite and sternite cell fates are specified by Wg signaling. We find that DER acts synergistically with Wg to promote tergite and sternite identities, and that Wg and DER activities are opposed by Dpp signaling, which promotes pleural identity. Wg and Dpp interact antagonistically at two levels. First, their expression is confined to complementary domains by mutual transcriptional repression. Second, Wg and Dpp compete directly with one another by exerting opposite effects on cell fate. DER signaling does not affect the expression of wg or dpp, indicating that it interacts with Wg and Dpp at the level of cell fate determination. Within the tergite, the requirements for Wg and DER function are roughly complementary: Wg is required mainly in the medial region, whereas DER is most important laterally. Finally, we show that Dpp signaling at the dorsal midline controls dorso-ventral patterning within the tergite by promoting pigmentation in the medial region.
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Curtiss, J., and M. Mlodzik. "Morphogenetic furrow initiation and progression during eye development in Drosophila: the roles of decapentaplegic, hedgehog and eyes absent." Development 127, no. 6 (March 15, 2000): 1325–36. http://dx.doi.org/10.1242/dev.127.6.1325.
Full textAbstract:
The Drosophila signaling factor decapentaplegic (dpp) mediates the effects of hedgehog (hh) in tissue patterning by regulating the expression of tissue-specific genes. In the eye disc, the transcription factors eyeless (ey), eyes absent (eya), sine oculis (so) and dachshund (dac) participate with these signaling molecules in a complex regulatory network that results in the initiation of eye development. Our analysis of functional relationships in the early eye disc indicates that hh and dpp play no role in regulating ey, but are required for eya, so and dac expression. We show that restoring expression of eya in loss-of-function dpp mutant backgrounds is sufficient to induce so and dac expression and to rescue eye development. Thus, once expressed, eya can carry out its functions in the absence of dpp. These experiments indicate that dpp functions downstream of or in parallel with ey, but upstream of eya, so and dac. Additional control is provided by a feedback loop that maintains expression of eya and so and includes dpp. The fact that exogenous overexpression of ey, eya, so and dac interferes with wild-type eye development demonstrates the importance of such a complicated mechanism for maintaining proper levels of these factors during early eye development. Whereas initiation of eye development fails in either Hh or Dpp signaling mutants, the subsequent progression of the morphogenetic furrow is only slowed down. However, we find that clones that are simultaneously mutant for Hh and Dpp signaling components completely block furrow progression and eye differentiation, suggesting that Hh and Dpp serve partially redundant functions in this process. Interestingly, furrow-associated expression of eya, so and dac is not affected by double mutant tissue, suggesting that some other factor(s) regulates their expression during furrow progression.
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Newfeld, S. J., E. H. Chartoff, J. M. Graff, D. A. Melton, and W. M. Gelbart. "Mothers against dpp encodes a conserved cytoplasmic protein required in DPP/TGF-beta responsive cells." Development 122, no. 7 (July 1, 1996): 2099–108. http://dx.doi.org/10.1242/dev.122.7.2099.
Full textAbstract:
The proteins necessary for signal transduction in cells responding to ligands of the TGF-beta family are largely unknown. We have previously identified Mad (Mothers against dpp), a gene that interacts with the TGF-beta family member encoded by decapentaplegic (dpp) in Drosophila. Assay of Mad's role in the DPP-dependent events of embryonic midgut development demonstrates that Mad is required for any response of the visceral mesoderm or endoderm to DPP signals from the visceral mesoderm. Replacement of the normal DPP promoter with a heterologous (hsp70) promoter fails to restore DPP-dependent responses in Mad mutant midguts. Experiments utilizing Mad transgenes regulated by tissue-specific promoters show that MAD is required specifically in cells responding to DPP. Immunohistochemical studies localize MAD to the cytoplasm in all tissues examined. Experiments in Xenopus embryos demonstrate that Drosophila MAD can function in the signaling pathway of BMP-4, a vertebrate homolog of dpp. Based on these results, we propose that Mad is a highly conserved and essential element of the DPP signal transduction pathway.
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Wasik, Bethany R., and Armin P. Moczek. "Decapentaplegic (dpp) regulates the growth of a morphological novelty, beetle horns." Development Genes and Evolution 221, no. 1 (March 12, 2011): 17–27. http://dx.doi.org/10.1007/s00427-011-0355-7.
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Heslip, T. R., H. Theisen, H. Walker, and J. L. Marsh. "Shaggy and dishevelled exert opposite effects on Wingless and Decapentaplegic expression and on positional identity in imaginal discs." Development 124, no. 5 (March 1, 1997): 1069–78. http://dx.doi.org/10.1242/dev.124.5.1069.
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The finding that Wingless (WG) and Decapentaplegic (DPP) suppress each others transcription provides a mechanism for creating developmental territories in fields of cells. Here, we address the mechanism of that antagonism. The dishevelled (dsh) and shaggy (sgg) genes encode intracellular proteins generally thought of as downstream of WG signaling. We have investigated the effects of changing either DSH or SGG activity on both cell fate and wg and dpp expression. At the level of cell fate in discs, DSH antagonizes SGG activity. At the level of gene expression, SGG positively regulates dpp expression and negatively regulates wg expression while DSH activity suppresses dpp expression and promotes wg expression. Sharp borders of gene expression correlating precisely with clone boundaries suggest that the effects of DSH and SGG on transcription of wg and dpp are not mediated by secreted factors but rather act through intracellular effectors. The interactions described here suggest a model for the antagonism between WG and DPP that is mediated via SGG. The model incorporates autoactivation and lateral inhibition, which are properties required for the production of stable patterns. The regulatory interactions described exhibit extensive ability to organize new pattern in response to manipulation or injury.
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Jackson, S. M., H. Nakato, M. Sugiura, A. Jannuzi, R. Oakes, V. Kaluza, C. Golden, and S. B. Selleck. "dally, a Drosophila glypican, controls cellular responses to the TGF-beta-related morphogen, Dpp." Development 124, no. 20 (October 15, 1997): 4113–20. http://dx.doi.org/10.1242/dev.124.20.4113.
Full textAbstract:
Decapentaplegic (Dpp) is a Drosophila member of the Transforming Growth Factor-beta (TGF-beta)/Bone Morphogenetic Protein (BMP) superfamily of growth factors. Dpp serves as a classical morphogen, where concentration gradients of this secreted factor control patterning over many cell dimensions. Regulating the level of Dpp signaling is therefore critical to its function during development. One type of molecule proposed to modulate growth factor signaling at the cell surface are integral membrane proteoglycans. We show here that division abnormally delayed (dally), a Drosophila member of the glypican family of integral membrane proteoglycans is required for normal Dpp signaling during development, affecting cellular responses to this morphogen. Ectopic expression of dally+ can alter the patterning activity of Dpp, suggesting a role for dally+ in modulating Dpp signaling strength. These findings support a role for members of the glypican family in controlling TGF-beta/BMP activity in vivo by affecting signaling at the cell surface.
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Luo, Lichao, Huashan Wang, Chao Fan, Sen Liu, and Yu Cai. "Wnt ligands regulate Tkv expression to constrain Dpp activity in the Drosophila ovarian stem cell niche." Journal of Cell Biology 209, no. 4 (May 25, 2015): 595–608. http://dx.doi.org/10.1083/jcb.201409142.
Full textAbstract:
Stem cell self-renewal versus differentiation is regulated by the niche, which provides localized molecules that favor self-renewal. In the Drosophila melanogaster female germline stem cell (GSC) niche, Decapentaplegic (Dpp), a fly transforming growth factor β molecule and well-established long-range morphogen, acts over one cell diameter to maintain the GSCs. Here, we show that Thickveins (Tkv; a type I receptor of Dpp) is highly expressed in stromal cells next to Dpp-producing cells and functions to remove excess Dpp outside the niche, thereby spatially restricting its activity. Interestingly, Tkv expression in these stromal cells is regulated by multiple Wnt ligands that are produced by the niche. Our data demonstrate a self-restraining mechanism by which the Drosophila ovarian GSC niche acts to define its own boundary.
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Chen, Y., M. J. Riese, M. A. Killinger, and F. M. Hoffmann. "A genetic screen for modifiers of Drosophila decapentaplegic signaling identifies mutations in punt, Mothers against dpp and the BMP-7 homologue, 60A." Development 125, no. 9 (May 1, 1998): 1759–68. http://dx.doi.org/10.1242/dev.125.9.1759.
Full textAbstract:
decapentaplegic (dpp) is a Transforming Growth Factor beta (TGF-beta)-related growth factor that controls multiple developmental processes in Drosophila. To identify components involved in dpp signaling, we carried out a genetic screen for dominant enhancer mutations of a hypomorphic allele of thick veins (tkv), a type I receptor for dpp. We recovered new alleles of tkv, punt, Mothers against dpp (Mad) and Medea (Med), all of which are known to mediate dpp signaling. We also recovered mutations in the 60A gene which encodes another TGF-beta-related factor in Drosophila. DNA sequence analysis established that all three 60A alleles were nonsense mutations in the prodomain of the 60A polypeptide. These mutations in 60A caused defects in midgut morphogenesis and fat body differentiation. We present evidence that when dpp signaling is compromised, lowering the level of 60A impairs several dpp-dependent developmental processes examined, including the patterning of the visceral mesoderm, the embryonic ectoderm and the imaginal discs. These results provide the first in vivo evidence for the involvement of 60A in the dpp pathway. We propose that 60A activity is required to maintain optimal signaling capacity of the dpp pathway, possibly by forming biologically active heterodimers with Dpp proteins.
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Zecca, Myriam, and Gary Struhl. "A unified mechanism for the control of Drosophila wing growth by the morphogens Decapentaplegic and Wingless." PLOS Biology 19, no. 3 (March 3, 2021): e3001111. http://dx.doi.org/10.1371/journal.pbio.3001111.
Full textAbstract:
Development of the Drosophila wing—a paradigm of organ development—is governed by 2 morphogens, Decapentaplegic (Dpp, a BMP) and Wingless (Wg, a Wnt). Both proteins are produced by defined subpopulations of cells and spread outwards, forming gradients that control gene expression and cell pattern as a function of concentration. They also control growth, but how is unknown. Most studies have focused on Dpp and yielded disparate models in which cells throughout the wing grow at similar rates in response to the grade or temporal change in Dpp concentration or to the different amounts of Dpp “equalized” by molecular or mechanical feedbacks. In contrast, a model for Wg posits that growth is governed by a progressive expansion in morphogen range, via a mechanism in which a minimum threshold of Wg sustains the growth of cells within the wing and recruits surrounding “pre-wing” cells to grow and enter the wing. This mechanism depends on the capacity of Wg to fuel the autoregulation of vestigial (vg)—the selector gene that specifies the wing state—both to sustain vg expression in wing cells and by a feed-forward (FF) circuit of Fat (Ft)/Dachsous (Ds) protocadherin signaling to induce vg expression in neighboring pre-wing cells. Here, we have subjected Dpp to the same experimental tests used to elucidate the Wg model and find that it behaves indistinguishably. Hence, we posit that both morphogens act together, via a common mechanism, to control wing growth as a function of morphogen range.
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Wisotzkey, R. G., A. Mehra, D. J. Sutherland, L. L. Dobens, X. Liu, C. Dohrmann, L. Attisano, and L. A. Raftery. "Medea is a Drosophila Smad4 homolog that is differentially required to potentiate DPP responses." Development 125, no. 8 (April 15, 1998): 1433–45. http://dx.doi.org/10.1242/dev.125.8.1433.
Full textAbstract:
Mothers against dpp (Mad) mediates Decapentaplegic (DPP) signaling throughout Drosophila development. Here we demonstrate that Medea encodes a MAD-related protein that functions in DPP signaling. MEDEA is most similar to mammalian Smad4 and forms heteromeric complexes with MAD. Like dpp, Medea is essential for embryonic dorsal/ventral patterning. However, Mad is essential in the germline for oogenesis whereas Medea is dispensable. In the wing primordium, loss of Medea most severely affects regions receiving low DPP signal. MEDEA is localized in the cytoplasm, is not regulated by phosphorylation, and requires physical association with MAD for nuclear translocation. Furthermore, inactivating MEDEA mutations prevent nuclear translocation either by preventing interaction with MAD or by trapping MAD/MEDEA complexes in the cytosol. Thus MAD-mediated nuclear translocation is essential for MEDEA function. Together these data show that, while MAD is essential for mediating all DPP signals, heteromeric MAD/MEDEA complexes function to modify or enhance DPP responses. We propose that this provides a general model for Smad4/MEDEA function in signaling by the TGF-beta family.
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Ducuing, Antoine, Charlotte Keeley, Bertrand Mollereau, and Stéphane Vincent. "A DPP-mediated feed-forward loop canalizes morphogenesis during Drosophila dorsal closure." Journal of Cell Biology 208, no. 2 (January 19, 2015): 239–48. http://dx.doi.org/10.1083/jcb.201410042.
Full textAbstract:
Development is robust because nature has selected various mechanisms to buffer the deleterious effects of environmental and genetic variations to deliver phenotypic stability. Robustness relies on smart network motifs such as feed-forward loops (FFLs) that ensure the reliable interpretation of developmental signals. In this paper, we show that Decapentaplegic (DPP) and JNK form a coherent FFL that controls the specification and differentiation of leading edge cells during Drosophila melanogaster dorsal closure (DC). We provide molecular evidence that through repression by Brinker (Brk), the DPP branch of the FFL filters unwanted JNK activity. High-throughput live imaging revealed that this DPP/Brk branch is dispensable for DC under normal conditions but is required when embryos are subjected to thermal stress. Our results indicate that the wiring of DPP signaling buffers against environmental challenges and canalizes cell identity. We propose that the main function of DPP pathway during Drosophila DC is to ensure robust morphogenesis, a distinct function from its well-established ability to spread spatial information.
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Peri, F., and S. Roth. "Combined activities of Gurken and decapentaplegic specify dorsal chorion structures of the Drosophila egg." Development 127, no. 4 (February 15, 2000): 841–50. http://dx.doi.org/10.1242/dev.127.4.841.
Full textAbstract:
During Drosophila oogenesis Gurken, associated with the oocyte nucleus, activates the Drosophila EGF receptor in the follicular epithelium. Gurken first specifies posterior follicle cells, which in turn signal back to the oocyte to induce the migration of the oocyte nucleus from a posterior to an anterior-dorsal position. Here, Gurken signals again to specify dorsal follicle cells, which give rise to dorsal chorion structures including the dorsal appendages. If Gurken signaling is delayed and starts after stage 6 of oogenesis the nucleus remains at the posterior pole of the oocyte. Eggs develop with a posterior ring of dorsal appendage material that is produced by main-body follicle cells expressing the gene Broad-Complex. They encircle terminal follicle cells expressing variable amounts of the TGFbeta homologue, decapentaplegic. By ectopically expressing decapentaplegic and clonal analysis with Mothers against dpp we show that Decapentaplegic signaling is required for Broad-Complex expression. Thus, the specification and positioning of dorsal appendages along the anterior-posterior axis depends on the intersection of both Gurken and Decapentaplegic signaling. This intersection also induces rhomboid expression and thereby initiates the positive feedback loop of EGF receptor activation, which positions the dorsal appendages along the dorsal-ventral egg axis.
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Campbell, G., and A. Tomlinson. "Initiation of the proximodistal axis in insect legs." Development 121, no. 3 (March 1, 1995): 619–28. http://dx.doi.org/10.1242/dev.121.3.619.
Full textAbstract:
Much of the cell-cell communication that controls assignment of cell fates during animal development appears to be mediated by extracellular signaling molecules. The formation of the proximodistal (P/D) axis of the legs of flies is controlled by at least two such molecules, a Wnt and a TGFbeta, encoded by the wingless (wg) and decapentaplegic (dpp) genes, respectively. The P/D axis appears to be initiated from the site where cells expressing wg are in close association with those expressing dpp. Support for this hypothesis comes from two sources: classical grafting experiments in cockroaches and ectopic protein expression in Drosophila.
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Su, Maureen A., Robert G. Wisotzkey, and Stuart J. Newfeld. "A Screen for Modifiers of decapentaplegic Mutant Phenotypes Identifies lilliputian, the Only Member of the Fragile-X/Burkitt's Lymphoma Family of Transcription Factors in Drosophila melanogaster." Genetics 157, no. 2 (February 1, 2001): 717–25. http://dx.doi.org/10.1093/genetics/157.2.717.
Full textAbstract:
Abstract The decapentaplegic (dpp) gene directs numerous developmental events in Drosophila melanogaster. dpp encodes a member of the Transforming Growth Factor-β family of secreted signaling molecules. At this time, mechanisms of dpp signaling have not yet been fully described. Therefore we conducted a genetic screen for new dpp signaling pathway components. The screen exploited a transvection-dependent dpp phenotype: heldout wings. The screen generated 30 mutations that appear to disrupt transvection at dpp. One of the mutations is a translocation with a recessive lethal breakpoint in cytological region 23C1-2. Genetic analyses identified a number of mutations allelic to this breakpoint. The 23C1-2 complementation group includes several mutations in the newly discovered gene lilliputian (lilli). lilli mutations that disrupt the transvection-dependent dpp phenotype are also dominant maternal enhancers of recessive embryonic lethal alleles of dpp and screw. lilli zygotic mutant embryos exhibit a partially ventralized phenotype similar to dpp embryonic lethal mutations. Phylogenetic analyses revealed that lilli encodes the only Drosophila member of a family of transcription factors that includes the human genes causing Fragile-X mental retardation (FMR2) and Burkitt's Lymphoma (LAF4). Taken together, the genetic and phylogenetic data suggest that lilli may be an activator of dpp expression in embryonic dorsal-ventral patterning and wing development.
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Raftery, L. A., M. Sanicola, R. K. Blackman, and W. M. Gelbart. "The relationship of decapentaplegic and engrailed expression in Drosophila imaginal disks: do these genes mark the anterior-posterior compartment boundary?" Development 113, no. 1 (September 1, 1991): 27–33. http://dx.doi.org/10.1242/dev.113.1.27.
Full textAbstract:
Imaginal disks, the primordia of the adult appendages in Drosophila, are divided into anterior and posterior compartments. However, the developmental role of such compartments remains unclear. The expression of decapentaplegic (dpp), a pattern formation gene required for imaginal disk development, has the intriguing property of being expressed in a line at or near the boundary between these compartments. Here, we compare the distribution of dpp-driven reporter gene expression to the pattern of expression of the engrailed (en) gene, known to be required for the maintenance of the compartment boundary. Using confocal microscopy to obtain single cell resolution, we have determined that the majority of the en+ imaginal disk cells expressing the dpp-driven reporter genes about those cells expressing en, while a small percentage of dpp reporter gene expressing cells also express en. In posterior regions of en mutant disks, where compartmentalization is abnormal, we observe ectopic expression of the dpp-driven reporter genes. We conclude that the pattern of dpp expression in imaginal disks is delimited in part through the direct or indirect repression by engrailed. Our results lead us to question the widely held assumption that the anterior edge of en expression demarcates the A/P compartment boundary.
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Ferguson, E. L., and K. V. Anderson. "Localized enhancement and repression of the activity of the TGF-beta family member, decapentaplegic, is necessary for dorsal-ventral pattern formation in the Drosophila embryo." Development 114, no. 3 (March 1, 1992): 583–97. http://dx.doi.org/10.1242/dev.114.3.583.
Full textAbstract:
Seven zygotically active genes are required for normal patterning of the dorsal 40% of the Drosophila embryo. Among these genes, decapentaplegic (dpp) has the strongest mutant phenotype: in the absence of dpp, all cells in the dorsal and dorsolateral regions of the embryo adopt fates characteristic of more ventrally derived cells (Irish and Gelbart (1987) Genes Dev. 1, 868–879). Here we describe the phenotypes caused by alleles of another of this set of genes, tolloid, and show that tolloid is required for dorsal, but not dorsolateral, pattern. Extragenic suppressors of tolloid mutations were isolated that proved to be mutations that elevate dpp activity. We studied the relationship between tolloid and dpp by analyzing the phenotypes of tolloid embryos with elevated numbers of the dpp gene and found that doubling the dpp+ gene dosage completely suppressed weak tolloid mutants and partially suppressed the phenotypes of tolloid null mutants. We conclude that the function of tolloid is to increase dpp activity. We also examined the effect of doubling dpp+ gene dosage on the phenotypes caused by other mutations affecting dorsal development. Like tolloid, the phenotypes of mutant embryos lacking shrew gene function were suppressed by elevated dpp, indicating that shrew also acts upstream of dpp to increase dpp activity. In contrast, increasing the number of copies of the dpp gene enhanced the short gastrulation (sog) mutant phenotype, causing ventrolateral cells to adopt dorsal fates. This indicates that sog gene product normally blocks dpp activity ventrally. We propose that the tolloid, shrew and sog genes are required to generate a gradient of dpp activity, which directly specifies the pattern of the dorsal 40% of the embryo.
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Araujo, H., and E. Bier. "sog and dpp exert opposing maternal functions to modify toll signaling and pattern the dorsoventral axis of the Drosophila embryo." Development 127, no. 16 (August 15, 2000): 3631–44. http://dx.doi.org/10.1242/dev.127.16.3631.
Full textAbstract:
The short gastrulation (sog) and decapentaplegic (dpp) genes function antagonistically in the early Drosophila zygote to pattern the dorsoventral (DV) axis of the embryo. This interplay between sog and dpp determines the extent of the neuroectoderm and subdivides the dorsal ectoderm into two territories. Here, we present evidence that sog and dpp also play opposing roles during oogenesis in patterning the DV axis of the embryo. We show that maternally produced Dpp increases levels of the I(kappa)B-related protein Cactus and reduces the magnitude of the nuclear concentration gradient of the NF(kappa)B-related Dorsal protein, and that Sog limits this effect. We present evidence suggesting that Dpp signaling increases Cactus levels by reducing a signal-independent component of Cactus degradation. Epistasis experiments reveal that sog and dpp act downstream of, or in parallel to, the Toll receptor to reduce translocation of Dorsal protein into the nucleus. These results broaden the role previously defined for sog and dpp in establishing the embryonic DV axis and reveal a novel form of crossregulation between the NF(kappa)B and TGF(beta) signaling pathways in pattern formation.