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Relevant bibliographies by topics / Caenorhabditis elegans Transcription factors

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Academic literature on the topic 'Caenorhabditis elegans Transcription factors'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "Caenorhabditis elegans Transcription factors"

1

Krpelanová, Eva. "Functional analysis of SP transcription factors in Caenorhabditis elegans." Blood Cells, Molecules, and Diseases 38, no. 2 (March 2007): 149–50. http://dx.doi.org/10.1016/j.bcmd.2006.10.073.

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Crum, T. L., and P. G. Okkema. "SUMOylation-dependent function of a T-box transcriptional repressor in Caenorhabditis elegans." Biochemical Society Transactions 35, no. 6 (November 23, 2007): 1424–26. http://dx.doi.org/10.1042/bst0351424.

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T-box transcription factors are crucial developmental regulators, and they have not previously been associated with SUMOylation. In Caenorhabditis elegans, the Tbx2 subfamily member TBX-2 (T-box protein 2) is required for anterior pharyngeal muscle development. TBX-2 interacts with SUMOylation pathway enzymes, and loss of these enzymes phenocopies tbx-2 mutants. We hypothesize that TBX-2 functions as a SUMOylation-dependent transcriptional repressor. TBX-2 contains two consensus SUMOylation sites conserved in many T-box transcriptional repressors, and we suggest that the function of these T-box factors may similarly involve SUMOylation.

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Klotz. "FOXO Transcription Factors: Regulators of Metabolism and Stress Resistance." Proceedings 11, no. 1 (April 16, 2019): 11. http://dx.doi.org/10.3390/proceedings2019011011.

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FOXO (Forkhead box, class O) proteins are transcriptional regulators ubiquitously expressed in mammalian cells with roles in modulating fuel metabolism, stress resistance and cell death. FOXO transcription factors are regulated by redox processes at several levels, including enzymatic and nonenzymatic posttranslational modification. Target genes controlled by FOXO proteins include genes encoding antioxidant proteins, thus likely contributing to the key role FOXOs play in the cellular response to oxidative stress. Here, an overview is provided on (i) the modulation of FOXO proteins by thiol depleting agents, (ii) consequences of thiol depletion for stress resistance and life span of a model organism, Caenorhabditis elegans and (iii) the role of FOXO proteins therein.

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Christensen, Elyse L., Alexandra Beasley, Jessica Radchuk, Zachery E. Mielko, Elicia Preston, Sidney Stuckett, John I. Murray, and Martin L. Hudson. "ngn-1/neurogenin Activates Transcription of Multiple Terminal Selector Transcription Factors in the Caenorhabditis elegans Nervous System." G3: Genes|Genomes|Genetics 10, no. 6 (April 9, 2020): 1949–62. http://dx.doi.org/10.1534/g3.120.401126.

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Proper nervous system development is required for an organism’s survival and function. Defects in neurogenesis have been linked to neurodevelopmental disorders such as schizophrenia and autism. Understanding the gene regulatory networks that orchestrate neural development, specifically cascades of proneural transcription factors, can better elucidate which genes are most important during early neurogenesis. Neurogenins are a family of deeply conserved factors shown to be both necessary and sufficient for the development of neural subtypes. However, the immediate downstream targets of neurogenin are not well characterized. The objective of this study was to further elucidate the role of ngn-1/neurogenin in nervous system development and to identify its downstream transcriptional targets, using the nematode Caenorhabditis elegans as a model for this work. We found that ngn-1 is required for axon outgrowth, nerve ring architecture, and neuronal cell fate specification. We also showed that ngn-1 may have roles in neuroblast migration and epithelial integrity during embryonic development. Using RNA sequencing and comparative transcriptome analysis, we identified eight transcription factors (hlh-34/NPAS1, unc-42/PROP1, ceh-17/PHOX2A, lim-4/LHX6, fax-1/NR2E3, lin-11/LHX1, tlp-1/ZNF503, and nhr-23/RORB) whose transcription is activated, either directly or indirectly, by ngn-1. Our results show that ngn-1 has a role in transcribing known terminal regulators that establish and maintain cell fate of differentiated neural subtypes and confirms that ngn-1 functions as a proneural transcription factor in C. elegans neurogenesis.

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Cherian, Jerrin R., Katherine V. Adams, and Lisa N. Petrella. "Wnt Signaling Drives Ectopic Gene Expression and Larval Arrest in the Absence of the Caenorhabditis elegans DREAM Repressor Complex." G3: Genes|Genomes|Genetics 10, no. 2 (December 16, 2019): 863–74. http://dx.doi.org/10.1534/g3.119.400850.

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Establishment and maintenance of proper gene expression is a requirement for normal growth and development. The DREAM complex in Caenorhabditis elegans functions as a transcriptional repressor of germline genes in somatic cells. At 26°, DREAM complex mutants show increased misexpression of germline genes in somatic cells and High Temperature Arrest (HTA) of worms at the first larval stage. To identify transcription factors required for the ectopic expression of germline genes in DREAM complex mutants, we conducted an RNA interference screen against 123 transcription factors capable of binding DREAM target promoter loci for suppression of the HTA phenotype in lin-54 mutants. We found that knock-down of 15 embryonically expressed transcription factors suppress the HTA phenotype in lin-54 mutants. Five of the transcription factors found in the initial screen have associations with Wnt signaling pathways. In a subsequent RNAi suppression screen of Wnt signaling factors we found that knock-down of the non-canonical Wnt/PCP pathway factors vang-1, prkl-1 and fmi-1 in a lin-54 mutant background resulted in strong suppression of the HTA phenotype. Animals mutant for both lin-54 and vang-1 showed almost complete suppression of the HTA phenotype, pgl-1 misexpression, and fertility defects associated with lin-54 single mutants at 26°. We propose a model whereby a set of embryonically expressed transcription factors, and the Wnt/PCP pathway, act opportunistically to activate DREAM complex target genes in somatic cells of DREAM complex mutants at 26°.

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Zečić, Aleksandra, and Bart P. Braeckman. "DAF-16/FoxO in Caenorhabditis elegans and Its Role in Metabolic Remodeling." Cells 9, no. 1 (January 2, 2020): 109. http://dx.doi.org/10.3390/cells9010109.

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DAF-16, the only forkhead box transcription factors class O (FoxO) homolog in Caenorhabditis elegans, integrates signals from upstream pathways to elicit transcriptional changes in many genes involved in aging, development, stress, metabolism, and immunity. The major regulator of DAF-16 activity is the insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) pathway, reduction of which leads to lifespan extension in worms, flies, mice, and humans. In C. elegans daf-2 mutants, reduced IIS leads to a heterochronic activation of a dauer survival program during adulthood. This program includes elevated antioxidant defense and a metabolic shift toward accumulation of carbohydrates (i.e., trehalose and glycogen) and triglycerides, and activation of the glyoxylate shunt, which could allow fat-to-carbohydrate conversion. The longevity of daf-2 mutants seems to be partially supported by endogenous trehalose, a nonreducing disaccharide that mammals cannot synthesize, which points toward considerable differences in downstream mechanisms by which IIS regulates aging in distinct groups.

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Estes, Kathleen A., Tiffany L. Dunbar, Jennifer R. Powell, Frederick M. Ausubel, and Emily R. Troemel. "bZIP transcription factor zip-2 mediates an early response to Pseudomonas aeruginosa infection in Caenorhabditis elegans." Proceedings of the National Academy of Sciences 107, no. 5 (January 21, 2010): 2153–58. http://dx.doi.org/10.1073/pnas.0914643107.

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Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen.

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Spieth, J., Y. H. Shim, K. Lea, R. Conrad, and T. Blumenthal. "elt-1, an embryonically expressed Caenorhabditis elegans gene homologous to the GATA transcription factor family." Molecular and Cellular Biology 11, no. 9 (September 1991): 4651–59. http://dx.doi.org/10.1128/mcb.11.9.4651.

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The short, asymmetrical DNA sequence to which the vertebrate GATA family of transcription factors binds is present in some Caenorhabditis elegans gene regulatory regions: it is required for activation of the vitellogenin genes and is also found just 5' of the TATA boxes of tra-2 and the msp genes. In vertebrates GATA-1 is specific to erythroid lineages, whereas GATA-2 and GATA-3 are present in multiple tissues. In an effort to identify the trans-acting factors that may recognize this sequence element in C. elegans, we used a degenerate oligonucleotide to clone a C. elegans homolog to this gene. We call this gene elt-1 (erythrocytelike transcription factor). It is single copy and specifies a 1.75-kb mRNA that is present predominantly, if not exclusively, in embryos. The region of elt-1 encoding two zinc fingers is remarkably similar to the DNA-binding domain of the vertebrate GATA-binding proteins. However, outside of the DNA-binding domains the amino acid sequences are quite divergent. Nevertheless, introns are located at identical or nearly identical positions in elt-1 and the mouse GATA-1 gene. In addition, elt-1 mRNA is trans-spliced to the 22-base untranslated leader, SL1. The DNA upstream of the elt-1 TATA box contains eight copies of the GATA recognition sequence within the first 300 bp, suggesting that elt-1 may be autogenously regulated. Our results suggest that the specialized role of GATA-1 in erythroid gene expression was derived after separation of the nematodes and the line that led to the vertebrates, since C. elegans lacks an erythroid lineage.

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9

Spieth, J., Y. H. Shim, K. Lea, R. Conrad, and T. Blumenthal. "elt-1, an embryonically expressed Caenorhabditis elegans gene homologous to the GATA transcription factor family." Molecular and Cellular Biology 11, no. 9 (September 1991): 4651–59. http://dx.doi.org/10.1128/mcb.11.9.4651-4659.1991.

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The short, asymmetrical DNA sequence to which the vertebrate GATA family of transcription factors binds is present in some Caenorhabditis elegans gene regulatory regions: it is required for activation of the vitellogenin genes and is also found just 5' of the TATA boxes of tra-2 and the msp genes. In vertebrates GATA-1 is specific to erythroid lineages, whereas GATA-2 and GATA-3 are present in multiple tissues. In an effort to identify the trans-acting factors that may recognize this sequence element in C. elegans, we used a degenerate oligonucleotide to clone a C. elegans homolog to this gene. We call this gene elt-1 (erythrocytelike transcription factor). It is single copy and specifies a 1.75-kb mRNA that is present predominantly, if not exclusively, in embryos. The region of elt-1 encoding two zinc fingers is remarkably similar to the DNA-binding domain of the vertebrate GATA-binding proteins. However, outside of the DNA-binding domains the amino acid sequences are quite divergent. Nevertheless, introns are located at identical or nearly identical positions in elt-1 and the mouse GATA-1 gene. In addition, elt-1 mRNA is trans-spliced to the 22-base untranslated leader, SL1. The DNA upstream of the elt-1 TATA box contains eight copies of the GATA recognition sequence within the first 300 bp, suggesting that elt-1 may be autogenously regulated. Our results suggest that the specialized role of GATA-1 in erythroid gene expression was derived after separation of the nematodes and the line that led to the vertebrates, since C. elegans lacks an erythroid lineage.

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10

Yang, Xueyan, Hong Wang, Tong Li, Ling Chen, Bisheng Zheng, and Rui Hai Liu. "Nobiletin Delays Aging and Enhances Stress Resistance of Caenorhabditis elegans." International Journal of Molecular Sciences 21, no. 1 (January 4, 2020): 341. http://dx.doi.org/10.3390/ijms21010341.

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Nobiletin (NOB), one of polymethoxyflavone existing in citrus fruits, has been reported to exhibit a multitude of biological properties, including anti-inflammation, anti-oxidation, anti-atherosclerosis, neuroprotection, and anti-tumor activity. However, little is known about the anti-aging effect of NOB. The objective of this study was to determine the effects of NOB on lifespan, stress resistance, and its associated gene expression. Using Caenorhabditis elegans, an in vivo nematode model, we found that NOB remarkably extended the lifespan; slowed aging-related functional declines; and increased the resistance against various stressors, including heat shock and ultraviolet radiation. Also, NOB reduced the effects of paraquat stressor on nematodes and scavenged reactive oxygen species (ROS). Furthermore, gene expression revealed that NOB upregulated the expression of sod-3, hsp-16.2, gst-4, skn-1, sek-1, and sir-2.1, which was suggested that anti-aging activity of NOB was mediated most likely by activation of the target genes of the transcription factors including dauer formation (DAF)-16, heat-shock transcription factor (HSF)-1, and skinhead (SKN)-1. In summary, NOB has potential application in extension of lifespan, and its associated healthspan and stress resistances.

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Dissertations / Theses on the topic "Caenorhabditis elegans Transcription factors"

1

Cheng, Albert Wu. "Characterization of irx-1 transcription factor in C. elegans male sensory ray development /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202007%20CHENG.

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2

Winkelbauer, Marlene Elizabeth. "Elucidating the role of nephronophthisis proteins utilizing Caenorhabditis elegans as a model." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/winkelbauer.pdf.

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Rupert, Peter Benjamin. "Structure determination of the SKN-1 DNA binding domain complex /." view abstract or download file of text, 1999. http://wwwlib.umi.com/cr/uoregon/fullcit?p9947981.

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Thesis (Ph. D.)--University of Oregon, 1999.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-106). Also available for download via the World Wide Web; free to University of Oregon users. Address: http://wwwlib.umi.com/cr/uoregon/fullcit?p9947981.

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4

De, Bono Mario Godwin. "Studies on the regulation and evolution of tra-1, the terminal somatic sex determining gene in Caenorhabditis elegans." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321108.

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5

White, Arron D. "The role of the C. elegans transcription factor LIN-11 in cell fate specification." Scholarly Commons, 2000. https://scholarlycommons.pacific.edu/uop_etds/533.

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Vulval differentiation in Caenorhabditis elegans is a well characterized developmental system in which three vulval precursor cells divide, generating the 22 nuclei that form the functional wild type vulva. Additionally, the combined formation of the vulva and the uterus is a model for organogenesis. Hermaphrodites homozygous for a lin-11 mutation are unable to form a functional vulva due to abnormal mitotic divisions in two of the three vulval precursor cells that contribute cells to the vulva. Laser microsurgery was used to ablate the two abnormal vulval precursor cells and other vulval precursor cells that could take on their developmental fate. These cells were believed to be responsible for the inability of hermaphrodites homozygous for a lin- 11 mutation to form a functional vulva. The results show that ablated hermaphrodites homozygous for a lin-11 mutation are rarely able to lay eggs, suggesting that there are other defects in the egg-laying apparatus in addition to the vulval precursor cells. To ensure that the ablated animals did not form a functional vulva and fail to lay eggs due to defects in the neurons regulating egg-laying, ablated lin-11 mutant animals were exposed to serotonin, imipramine or nicotine. These drugs are able to induce egglaying in wild type and ablated wild type animals. Ablated hermaphrodites homozygous for a lin-11 mutation exposed to the drug treatments were not able to lay eggs. Therefore, the abnormal secondary cells are not entirely responsible for the lack of a functional vulva and the inability to lay eggs, suggesting that either uterine cells or other vulval cells are also abnormal.

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6

Meisel, Kacey Danielle. "Characterization of lin-42/period transcriptional regulation by the Ikaros/hunchback-family transcription factor ZTF-16 in Caenorhabditis elegans." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/23130.

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The gene lin-42 is an ortholog of the mammalian period gene, a component of the circadian pathway that converts environmental stimuli into behavioral and physiological outputs over 24 hours. Mammalian period also regulates adult stem cell differentiation, although this function is poorly understood. The structure, function and expression of lin-42 are all similar to period. Therefore, we are studying lin-42 regulation and function during C. elegans larval development as a model for understanding period control of mammalian stem/progenitor cell development.

Previous work has shown that ZTF-16 is a regulator of lin-42 transcription. The lin-42 locus encodes three isoforms, and we have characterized lin-42 isoform specific regulation by ZTF-16 through phenotypic assays and analysis of transcriptional reporter strains. Our data show that ZTF-16 regulates the cyclic expression of lin-42A and lin-42B during larval development. However, ztf-16 is not expressed during the adult stage and does not regulate lin-42C, which is expressed only in adults and may be responsible for the circadian functions of lin-42. We also show that ztf-16 reduction-of-function mutations phenocopy loss-of- function phenotypes of the lin-42A/B isoforms. Finally, we have found that deletion of a putative ZTF-16 transcription factor binding site within the lin-42BC promoter abolishes tissue-specific expression patterns. Together, these data indicate that ZTF-16 is required to regulate the expression of lin-42A/B during C. elegans development, and may do this by direct binding to the lin-42BC promoter. Our findings pave the way for testing the possible regulation of period expression by HIL-family transcription factors in mammalian tissues.

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Grove, Christian A. "A Multiparameter Network Reveals Extensive Divergence Between C. elegans bHLH Transcription Factors: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/441.

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It has become increasingly clear that transcription factors (TFs) play crucial roles in the development and day-to-day homeostasis that all biological systems experience. TFs target particular genes in a genome, at the appropriate place and time, to regulate their expression so as to elicit the most appropriate biological response from a cell or multicellular organism. TFs can often be grouped into families based on the presence of similar DNA binding domains, and these families are believed to have expanded and diverged throughout evolution by several rounds of gene duplication and mutation. The extent to which TFs within a family have functionally diverged, however, has remained unclear. We propose that systematic analysis of multiple aspects, or parameters, of TF functionality for entire families of TFs could provide clues as to how divergent paralogous TFs really are. We present here a multiparameter integrated network of the activity of the basic helix-loop-helix (bHLH) TFs from the nematode Caenorhabditis elegans. Our data, and the resulting network, indicate that several parameters of bHLH function contribute to their divergence and that many bHLH TFs and their associated parameters exhibit a wide range of connectivity in the network, some being uniquely associated to one another, whereas others are highly connected to multiple parameter associations. We find that 34 bHLH proteins dimerize to form 30 bHLH dimers, which are expressed in a wide range of tissues and cell types, particularly during the development of the nematode. These dimers bind to E-Box DNA sequences and E-Box-like sequences with specificity for nucleotides central to and flanking those E-Boxes and related sequences. Our integrated network is the first such network for a multicellular organism, describing the dimerization specificity, spatiotemporal expression patterns, and DNA binding specificities of an entire family of TFs. The network elucidates the state of bHLH TF divergence in C. elegans with respect to multiple functional parameters and suggests that each bHLH TF, despite many molecular similarities, is distinct from its family members. This functional distinction may indeed explain how TFs from a single family can acquire different biological functions despite descending from common genetic ancestry.

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8

Johnson, Ryan William. "Genetic Regulation of Caenorhabditis Elegans Post-Embryonic Development Involving the Transcription Factors EGL-38, VAB-3, and LIN-14." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1213060175.

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9

White, Arron D. "The role of the C. elegans transcription factor LIN-11 in cell fate specification : a thesis." Scholarly Commons, 2001. https://scholarlycommons.pacific.edu/uop_etds/533.

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Vulval differentiation in Caenorhabditis elegans is a well characterized developmental system in which three vulval precursor cells divide, generating the 22 nuclei that form the functional wild type vulva. Additionally, the combined formation of the vulva and the uterus is a model for organogenesis. Hermaphrodites homozygous for a lin-11 mutation are unable to form a functional vulva due to abnormal mitotic divisions in two of the three vulval precursor cells that contribute cells to the vulva. Laser microsurgery was used to ablate the two abnormal vulval precursor cells and other vulval precursor cells that could take on their developmental fate. These cells were believed to be responsible for the inability of hermaphrodites homozygous for a lin- 11 mutation to form a functional vulva. The results show that ablated hermaphrodites homozygous for a lin-11 mutation are rarely able to lay eggs, suggesting that there are other defects in the egg-laying apparatus in addition to the vulval precursor cells. To ensure that the ablated animals did not form a functional vulva and fail to lay eggs due to defects in the neurons regulating egg-laying, ablated lin-11 mutant animals were exposed to serotonin, imipramine or nicotine. These drugs are able to induce egglaying in wild type and ablated wild type animals. Ablated hermaphrodites homozygous for a lin-11 mutation exposed to the drug treatments were not able to lay eggs. Therefore, the abnormal secondary cells are not entirely responsible for the lack of a functional vulva and the inability to lay eggs, suggesting that either uterine cells or other vulval cells are also abnormal.

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10

Oh, Seung Wook. "Regulation of Life Span by DAF-16/Forkhead Transcription Factor in Caenorhabditis elegans: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/22.

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The insulin/IGF-1 signaling pathway plays a pivotal role in life span regulation in diverse organisms. In Caenorhabditis elegans, a PI 3-kinase signaling cascade downstream of DAF-2, an ortholog of the mammalian insulin and insulin-like growth factor-1 (IGF-1) receptor, negatively regulates DAF-16/forkhead transcription factor. DAF-16 then regulates a wide variety of genes involved in longevity, stress response, metabolism and development. DAF-16 also receives signals from other pathways regulating life span and development. However, the precise mechanism by which DAF-16 directs multiple functions is poorly understood. First, in Chapter II, we demonstrate that JNK is a novel positive regulator of DAF-16 in both life span regulation and stress resistance. Our genetic analysis suggests that the JNK pathway acts in parallel with the insulin-like signaling pathway to regulate life span and both pathways converge onto DAF-16. We also show that JNK-1 directly interacts with and phosphorylates DAF-16. Moreover, in response to heat stress, JNK-1 promotes the translocation of DAF-16 into thc nucleus. Our findings define a novel interaction between the stress response pathway (JNK) and the master regulator of life span (DAF-16), and provide a mechanism by which JNK regulates longevity and stress resistance. Next, in Chapter III, we focus on the downstream targets of DAF-16. Here, we used a modified chromatin immunoprecipitation (ChIP) method to identify direct target promoters of DAF-16. We cloned 103 target sequences containing consensus DAF-16 binding sites and randomly selected 33 targets for further analysis. The expression of majority of these genes is regulated in a DAF-16-dependent manner. Moreover, inactivation of more than 50% of these genes significantly altered DAF-16-dependent functions such as longevity, fat storage and dauer diapause. Our results show that the ChIP-based cloning strategy leads to greater enrichment of DAF-16 target genes, compared to previous studies using DNA micro array or bioinformatics. We also demonstrate that DAF-16 is recruited to multiple promoters to coordinate regulation of its downstream target genes. In summary, we identified the JNK signaling pathway as a novel input into DAF-16 to adapt animals to the environmental stresses. We also revealed a large number of novel outputs of DAF-16. Taken together, these studies provide insight into the complex regulation by DAF-16 to control diverse biological functions and eventually broaden our understanding of aging.

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Books on the topic "Caenorhabditis elegans Transcription factors"

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Garroni, Michael Kenneth. Identification of cis-acting elements and trans-acting factors responsible for her-1 regulation in Caenorhabditis elegans. Ottawa: National Library of Canada, 2001.

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2

Reventar, Roddie D. Target-selected gene inactivation and gene expression patterns of ETS transcription factors in Caenorhabditis elegans. 2004.

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Book chapters on the topic "Caenorhabditis elegans Transcription factors"

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Feng, Huiyun, Hannah L. Craig, and Ian A. Hope. "Expression Pattern Analysis of Regulatory Transcription Factors in Caenorhabditis elegans." In Methods in Molecular Biology, 21–50. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-292-2_2.

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Wang, Dayong. "Role of Environmental Factors in Toxicity Induction of Environmental Toxicants or Stresses." In Exposure Toxicology in Caenorhabditis elegans, 333–57. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6129-0_12.

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3

Tajima, T., S. Nakamura, F. Ogawa, M. Hashimoto, M. Omote, and H. Nishimura. "Chemical and Genetic Approaches to Identify Caenorhabditis elegans Spermiogenesis-Related Factors." In XIIIth International Symposium on Spermatology, 179. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66292-9_25.

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von Mikecz, Anna, and Andrea Scharf. "Isochronal Visualization of Transcription and Proteasomal Proteolysis in Cell Culture or in the Model Organism, Caenorhabditis elegans." In Imaging Gene Expression, 257–73. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-526-2_19.

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5

Brdlik, Cathleen M., Wei Niu, and Michael Snyder. "Chromatin Immunoprecipitation and Multiplex Sequencing (ChIP-Seq) to Identify Global Transcription Factor Binding Sites in the Nematode Caenorhabditis Elegans." In Methods in Enzymology, 89–111. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-420120-0.00007-4.

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6

Okkema, P. G. "The Remarkably Diverse Family of T-Box Factors in Caenorhabditis elegans." In Current Topics in Developmental Biology, 27–54. Elsevier, 2017. http://dx.doi.org/10.1016/bs.ctdb.2016.08.005.

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Tan, Man-Wah. "Identification of host and pathogen factors involved in virulence using Caenorhabditis elegans." In Bacterial Pathogenesis Part C: Identification, Regulation, and Function of Virulence Factors, 13–28. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)58078-2.

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Conference papers on the topic "Caenorhabditis elegans Transcription factors"

1

Stenflo, J., A.-K. öhlin, Å. Lundvall, and B. Dahlback. "β-HYDROXY ASPARTIC ACID AND ft-HYDROXYASPARAGINE IN THEEGF-HOMOLOGY REGIONS OF PROTEIN C AND PROTEINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643995.

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The amino acid sequence has been determined for all of the vitamin K-dependent proteins and the gene structure is known for some of them. These findings have shown the proteins to consist of four clearly discernible domains, except protein S which has six domains. The protein domains seem to be coded on separate exons (Foster, D. C. et. al. 1985 Proc. Natl. Acad. Sci. USA 82,4673). The vitamin K-dependent γ-carboxyglutamic acid (Gla) containing domain isthe common structural denominator of the members of this protein family. In addition, all of these proteins except prothrombin contain domains that are homologous to the precursor of the epidermal growth factor (EGF). Such domains arealso found in proteins that are not vitamin K-dependent, such as the low density lipoprotein receptor, thrombomodulin, factor XII, plasminogen, the tissue type plasminogen activator, urokinase and the complement protein Clr. The vitamin K-dependent proteins can be dividedinto three groups. Factors VII, IX, X, protein C and protein Z form one group, which in addition to the Gla-region have two EGF-homology regions and one domain that is homologous to the serine proteases. Prothrombin has two 'kringle' structures and a serine protease domain and constitutes a group of its own. Protein S is also unique in that it has four EGF-homology regions and a COOH-terminal region that is homologous to the sexual hormone binding globulin (see poster by Edenbrand et. al.).Recently a posttranslationally modified amino acid, B-hydroxyaspatic acid (Hya), was identified in position 71 in the NH2-terminal EGF-homology region ofbovine protein C. The amino acid is formed by hydroxylation of aspartic acid. It has also been identified in the corresponding positions in factors VII, IX,X and protein Z (i. e. proteins which like protein C have two EGF-homology regions each). In protein S the N2-terminal of four EGF-homology regions has hydroxy lated aspartic acid .whereas the following three EGF-like domains have B-hydroxyasparagine. The nucleotide sequence codes for asparagine in the three latter positions. Neither vitamin K nor vitamin C seem to be involvedin the formation of the two hydroxylated amino acids. Recently, Hya was identified in acid hydrolysates of the complement protein Clr. Hya and Hyn have onlybeen found in domains that are homologous to the EGF precursor. In an attempt to identify the structural requirement of the hydroxylating enzyme, we have compared the sequences of EGF-homology regions that contain Hya or Hyn with the corresponding sequences that have been shown not to contain the modified amino acids. The domains that have Hya or Hyn have the consensus sequence Cx xxxx xCxC. This sequence has been found in three EGF-like domains in the EGF-precursor, in two in the LDL-receptor and in two in thrombomodulin. Furthermore, the neurogenic Notch locus in Drosophila melanogaster codes for 36 EGF-homolgy regions, 22 of which contain the consensussequence, whereas the Lin-12 locus in Caenorhabditis elegans codes for at least 11 EGF-like repeats, two of which comply with the consensus sequence. Whether any of these proteins contain Hya orHyn is not yet known with certainty.It has been hypothesized that Hya isinvolved in the Gla independent Ca2+binding of factors IX, X and protein C. In an attempt to resolve this issue, we have isolated the EGF-homology region from human protein C and been able to demonstrate that it binds Ca2+ (see poster by öhlin and Stenflo). However, we do not yet know whether Hya is directly involved in the Ca2+binding.

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