Academic literature on the topic 'Decapentaplegic (Dpp)'
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Journal articles on the topic "Decapentaplegic (Dpp)"
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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.
Dissertations / Theses on the topic "Decapentaplegic (Dpp)"
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Shen, Jie. "The role of Decapentaplegic (Dpp) in Drosophila wing development." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2004. http://nbn-resolving.de/urn:nbn:de:swb:14-1102321765343-79763.
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Decapentaplegic (Dpp), a member of the TGF-[Beta] superfamily, acts as a morphogen to direct cell differentiation, determine cell fate and promote cell survival and proliferation in Drosophila wing development. To investigate the role of Dpp in Drosophila wing development, three aspects of the patterning role of Dpp have been analyzed. First, I investigated the cellular responses to Dpp signaling by a loss of function strategy. The consequences of lacking Dpp signal transduction on cell morphology and tissue integrity were analyzed. Second, I investigated whether Dpp signaling is down-stream of Hh signaling to maintain the normal cell segregation at the A/P boundary by clonal analysis. Third, I investigated whether cross talk among the Hh, Dpp and Wg signaling pathways exists and what its relevance for wing patterning is. To investigate the role of Dpp in Drosophila wing development, the general strategies are to look at the phenotypes of loss-of-function and gain-of-function. Mutant clones lacking Dpp signal transduction by knock down Dpp receptor Thick veins (Tkv) do not survive in wing blade due to JNK dependent apoptosis. To get larger mutant clones for analysis, JNK pathway was inhibited by knock down bsk (encodes JNK) in mutant clones lacking Dpp signaling using FLP-FRT system. Clones double mutant for tkv and bsk did not undergo apoptosis, but recovered at very low frequencies compared to sibling clones. Here, I showed that the low recovery of tkv bsk double mutant clones are due to the extrusion of mutant cells. The extrusion of tkv bsk double mutant cells correlated with changes in the actin cytoskeleton and a dramatic loss of the apical microtubule web normally present in these cells. These results suggest that Dpp signaling is required for cell morphogenesis in Drosophila wing development. We propose that Dpp acts as a survival factor in the wing disc epithelium by orchestrating proper cytoskeletal organization and maintaining normal cell-cell contact. Drosophila wing is subdivided into anterior (A) and posterior (P) compartments. This developing into adjacent compartments is crucial for the patterning of Drosophila wing. Previous study has shown that Hedgehog (Hh) signaling is required in A cells to maintain the A/P boundary and is sufficient to specify A type cell sorting. A previous study has in addition implicated the signaling molecule Decapentaplegic (Dpp) in maintaining the A/P boundary. However, this study did not address whether and in which cells, A and/or P, Dpp signal transduction was required to maintain this boundary. Here, I have analyzed the role of components of the Dpp signal transduction pathway and the relation of Dpp and Hh signaling in maintaining the A/P boundary by clonal analysis. I showed that Dpp signaling mediated by the Dpp target gene, T-box protein Optomotor-blind (Omb), is required in A cells, but not in P cells, to maintain the normal position of the A/P boundary. During patterning formation, it is essential for cells to receive precise positional information to pattern the tissue. It has been proposed for a long time that different signaling pathways such as Hedgehog (Hh), Dpp and Wingless (Wg) signaling pathways provide positional information for tissue patterning in an integrated manner. Recently, evidence of interactions between Hh and Dpp as well as Wg and Hh signaling pathways has been reported in Drosophila wing. Here, I have identified additional interactions among Hh, Dpp and Notch/Wg signaling. We propose that the selector gene engrailed, Hh and Dpp signaling interact with each other to regulate target genes expression and thus to pattern the wing along the A/P axis. Further more, I showed that Dpp signaling is also participating in the patterning along the D/V axis by interaction with the selector gene apterous and Notch/Wg signaling.
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Pantazis, Periklis. "Role of endocytic trafficking during Dpp gradient formation." [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11611845.
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Bollenbach, Tobias. "Formation of morphogen gradients." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2005. http://nbn-resolving.de/urn:nbn:de:swb:14-1131092485542-81424.
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Morphogens are signaling molecules that play a key role in animal development. They spread from a restricted source into an adjacent target tissue forming a concentration gradient. The fate of cells in the target tissue is determined by the local concentration of such morphogens. Morphogen transport through the tissue has been studied in experiments which lead to the suggestion of several transport mechanisms. While diffusion in the extracellular space contributes to transport, recent experiments on the morphogen Decapentaplegic (Dpp) in the fruit fly Drosophila provide evidence for the importance of a cellular transport mechanism that was termed "planar transcytosis". In this mechanism, morphogens are transported through cells by repeated rounds of internalization and externalization. Starting from a microscopic theoretical description of these processes, we derive systems of nonlinear transport equations which describe the interplay of transcytosis and passive diffusion. We compare the results of numerical calculations based on this theoretical description of morphogen transport to recent experimental data on the morphogen Dpp in the Drosophila wing disk. Agreement with the experimental data is only achieved if the parameters entering the theoretical description are chosen such that transcytosis contributes strongly to transport. Analyzing the derived transport equations, we find that transcytosis leads to an increased robustness of the created gradients with respect to morphogen over-expression. Indications for this kind of robustness have been found in experiments. Furthermore, we theoretically investigate morphogen gradient formation in disordered systems. Here, an important question is how the position of concentration thresholds can be defined with high precision in the noisy environment present in typical developing tissues. Among other things, we find that the dimensionality of the system in which the gradient is formed plays an important role for the precision. Comparing gradients formed by transcytosis to those formed by extracellular diffusion, we find substantial differences that may result in a higher precision of gradients formed by transcytosis. Finally, we suggest several experiments to test the theoretical predictions of this work.
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Szuplewski, Sébastien. "Etude du facteur de transcription à domaine bZIP de Drosophila melanogaster : vrille." Paris 11, 2002. http://www.theses.fr/2002PA112109.
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Le gène decapentaplegic (dpp) code l'orthologue de Drosophila melanogaster des facteurs sécrétes de la super-famille des TGF-β, BMP-2 et -4. Il est requis tout au long du développement de la drosophile dans divers processus, tels que la mise en place de plans d'organisation, la différenciation, l'adhésion et la migration cellulaire, le contrôle de la croissance cellulaire, de la prolifération et de la mort cellulaire programmée. Les gènes vrille et cyclope ont été isolés car leurs allèles mutants se comportent comme des enhancers maternels dominants du phénotype de ventralisation de dpp. Le gène vrille (vri) code un facteur de transcription à domaine bZIP. Ce domaine en fait l'orthologue des protéines de vertébrés Gene 9 et E4BP4/NFIL3A. Le but de cette thèse était de déterminer les fonctions de Vrille au cours du développement de la drosophile et en particulier de préciser son rôle en relation avec la voie de signalisation Dpp. Les interactions entre allèles mutants de vri et de dpp au cours de l'embryogenèse et de la morphogénèse alaire pouvaient suggérer un rôle général de Vrille dans la voie de signalisation de Dpp. Or, l'analyse des cuticules des embryons dépourvus des composantes maternelle et zygotique de vri semblait exclure un rôle de vri dans la mise en place de la polarité dorso-ventrale et/ou la différenciation des tissus dorsaux, contrairement à dpp. L'analyse des phénotypes des mutants et de la surexpression de vri a permis de confirmer que Vrille n'est pas un facteur général de la voie de signalisation Dpp. En effet, les embryons homozygotes mutants pour vri ne présentent pas de défauts comparables à ceux des embryons homozygotes mutants pour dpp au niveau de l'intestin moyen et des trachées. De même, la surexpression de vri ne mime pas celle de dpp. L'interaction génétique entre dpp et vri au cours de la morphogenèse alaire pourrait avoir lieu au cours de la croissance du tissus alaire. En effet, l'analyse des phénotypes des allèles mutants de vri et de sa surexpression suggère un rôle de Vrille dans la croissance tissulaire. Une autre partie de mon travail était de tester la capacité de Vrille à former des hétérodimères avec d'autres facteurs de transcription à domaine bZIP. La protéine Vrille est capable de s'hétérodimériser in vitro avec dCREB-A et DFosThe decapentaplegic (dpp) gene encodes the Drosophila melanogaster homolog of the secreted factors BMP-2 et -4, which belong to the TGF-β superfamilly. It is involved in various processes during Drosophile development such as patterning, cell differenciation, adhesion and migration, or control of cell growth, proliferation and programmed cell death. The vrille and cyclope genes were isolated because they act as dominant maternal enhancers of the dpp ventralised embryonic phenotype. The vrille (vri) gene encodes a bZIP transcription factor. The bZIP do main of Vri represents a Gene 9 and E4BP4/NFIL3A bZIP domain ortholog. The goal of this thesis was to determine the functions of Vrille during Drosophila development, in particular in relation to the Dpp pathway. In addition to their interaction during embryogenesis, vri and dpp interact during wing morphogenesis could suggesting a general role of Vri in the Dpp pathway. However, the germline clone analysis seems to exclude a role of vri du ring the dorso-ventral patterning of the embryo, in contrast to the Dpp pathway. Similarly, the midgut and the trachae of vri mutant embryos do not present a dpp-like phenotype ; and vri overexpression does not mimic the phenotype of the dpp overexpression in various tissue tested. In conclusion, vri is not a general component of the Dpp pathway. The vri and dpp gene could interact for wing imaginal disc growth. In fact, the phenotypes observed during clonal and overexpression analysis are consistent with the hypothesis that vri is required for normal cell growth and proliferation. Another part of my work was to test the capacity of Vrille to form heterodimers with another bZIP transcription factors. I show in vitro that Vrille can interact with dCREB-A and DFos
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Bittig, Thomas. "Morphogenetic signaling in growing tissues." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2008. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1222339699038-97723.
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During the development of multicellular organisms, organs grow to well-defined shapes and sizes. The proper size and patterning of tissues are ensured by signaling molecules as e.g. morphogens. Secreted from a restricted source, morphogens spread into the adjacent target tissue where they form a graded concentration profile. Upon binding of the morphogens to receptors on the cell surfaces, the morphogenetic signal is transduced inside the cell via the phosphorylation of transcription factors, which subsequently regulate the expression of different target genes. Thus, cell fates are determined by the local concentration of such morphogens. In this work, we investigate three key aspects of morphogenetic signaling processes in growing tissues. First, we study the mechanics of tissue growth via cell division and cell death. We examine the rearrangements of cells on large scales and times by developing a continuum theory which describes the growing tissue as an active complex fluid. In our description we include anisotropic stresses generated by oriented cell division, and we show that average cellular trajectories exhibit anisotropic scaling behaviors. Our description is used to study experimentally measured shape changes of the developing wing disk of the fruit fly Drosophila melanogaster. Second, we focus on the spreading of morphogens in growing tissues. We show that the flow field of cell movements due to oriented cell division and cell death causes a drift term in the morphogen transport equation, which captures the stretching and dilution of the concentration profile. Comparing our theoretical results to recent experiments in the Drosophila wing disk, we find that the transport of the morphogen Dpp is mainly intracellular. We moreover show that the decay length of the Dpp gradient increases during development as a result of changing degradation rate and diffusion coefficient, whereas the drift of molecules due to growth is negligible. Thus growth does not affect the decay length of the gradient, but the decay length of the gradient might affect the tissue growth rate as discussed in this work. Finally, we develop a microscopic theoretical description of the intracellular transduction machinery of morphogenetic signals within an individual cell. Our description captures the kinetics of the trafficking of proteins between different cellular compartments in response to receptor-bound signaling molecules. Analyzing experimental data at the Drosophila neuromuscular junction, we show that the morphogenetic signaling is modulated by synaptic signaling via neuronal action potentials.
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Pantazis, Periklis. "Role of endocytic trafficking during Dpp gradient formation." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2004. http://nbn-resolving.de/urn:nbn:de:swb:14-1106665288062-25959.
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Morphogens are secreted signalling molecules that are expressed in restricted groups of cells within the developing tissue. From there, they are secreted and travel throughout the target field and form concentration gradients. These concentration profiles endow receiving cells with positional information. A number of experiments in Drosophila demonstrated that the morphogen Decapentaplegic (Dpp) forms activity gradients by inducing the expression of several target genes above distinct concentration thresholds at different distances from the source. This way, Dpp contributes to developmental fates in the target field such as the Drosophila wing disc. Although the tissue distribution as well as the actual shape and size of the Dpp morphogen concentration gradient has been visualized, the cell biological mechanisms through which the morphogen forms and maintains a gradient are still a subject of debate. Two hypotheses as to the dominant mechanism of movement have been proposed that can account for Dpp spreading throughout the Drosophila wing imaginal target tissue: extracellular diffusion and planar transcytosis, i. e. endocytosis and resecretion of the ligand that is thereby transported through the cells. Here, I present data indicating that implications of a theoreticalanalysis of Dpp spreading, where Dpp transport through the target tissue is solely based on extracellular diffusion taking into account receptor binding and subsequent internalization, are inconsistent with experimental results. By performing Fluorescence Recovery After Photobleaching (FRAP) experiments, I demonstrate a key role of Dynamin-mediated endocytosis for Dpp gradient formation. In addition, I show that most of GFP-Dpp traffics through endocytic compartments at the receiving epithelial cells, probably recycled through apical recycling endosomes (ARE). Finally, a Dpp recycling assay based on subcellular photouncage of ligand is presented to address specifically the Dpp recycling event at the receiving cells.
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Marcillière, Sophie. "Caractérisation génétique et moléculaire d'un nouveau gène impliqué dans la régulation de decapentaplegic chez Drosophila melanogaster." Paris 6, 2002. http://www.theses.fr/2002PA066245.
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Lecuit, Thomas. "Etude des proprietes organisatrices du facteur de croissance decapentaplegic (dpp)/tgf, au cours du developpement des membres de la drosophile." Paris 6, 1998. http://www.theses.fr/1998PA066713.
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La decouverte que certains groupes de cellules possedent des proprietes inductrices au cours du developpement eut une importance considerable. Elle posait en effet les jalons d'une approche experimentale et rationnelle du developpement. Des questions importantes furent alors clairement posees : quelle est la nature des signaux de communication entre les cellules et quels sont leurs modes de fonctionnement ? utilisant la drosophile comme animal modele, nous nous sommes interesses au gene decapentaplegic (dpp), un homologue de tgf, qui organise la formation de plusieurs axes des membres. Nous montrons tout d'abord que dpp controle directement et a distance l'identite des cellules de l'aile de long de l'axe antero-posterieur. Dpp presente aussi une activite en gradient et l'identite cellulaire est determinee par la concentration locale de dpp. Ces proprietes font de dpp un exemple de morphogene. Par ailleurs, nous montrons que l'interaction cooperative entre les facteurs de croissance dpp et wingless au cours du developpement de la patte, induit aussi une activite de type morphogene dont les proprietes organisatrices se distinguent de celles de chacun de ces genes pris de facon isolee. Nous concluons aussi que la capacite qu'ont les cellules de memoriser certains aspects de l'action passee de dpp et wg joue aussi un role important (effet de memoire cellulaire). Enfin, nous proposons plusieurs modeles pour la formation de tels gradients de concentration. En particulier, au dela de phenomenes de diffusion et de transport actif, nous dirigeons notre attention sur le possible role actif de la division cellulaire comme facteur de dilution et de dispersion au cours de la formation du gradient.
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Shen, Jie [Verfasser]. "The role of decapentaplegic (Dpp) in Drosophila wing development / von Jie Shen." 2004. http://d-nb.info/973397217/34.
Full textBook chapters on the topic "Decapentaplegic (Dpp)"
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"dpp (decapentaplegic)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 559. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4876.
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"Decapentaplegic (DPP)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 480. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4202.
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