Journal articles: 'Caenorhabditis elegans Transcription factors'

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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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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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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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Alcántar-Fernández, Jonathan, Rosa E. Navarro, Ana María Salazar-Martínez, Martha Elva Pérez-Andrade, and Juan Miranda-Ríos. "Caenorhabditis elegans respond to high-glucose diets through a network of stress-responsive transcription factors." PLOS ONE 13, no. 7 (July 10, 2018): e0199888. http://dx.doi.org/10.1371/journal.pone.0199888.

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Birkenkamp, K. U., and P. J. Coffer. "Regulation of cell survival and proliferation by the FOXO (Forkhead box, class O) subfamily of Forkhead transcription factors." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 292–97. http://dx.doi.org/10.1042/bst0310292.

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Recently, the FOXO (Forkhead box, class O) subfamily of Forkhead transcription factors has been identified as direct targets of phosphoinositide 3-kinase-mediated signal transduction. The AFX (acute-lymphocytic-leukaemia-1 fused gene from chromosome X), FKHR (Forkhead in rhabdomyosarcoma) and FKHR-L1 (FKHR-like 1) transcription factors are directly phosphorylated by protein kinase B, resulting in nuclear export and inhibition of transcription. This signalling pathway was first identified in the nematode worm Caenorhabditis elegans, where it has a role in regulation of the life span of the organism. Studies have shown that this evolutionarily conserved signalling module has a role in regulation of both cell-cycle progression and cell survival in higher eukaryotes. These effects are co-ordinated by FOXO-mediated induction of a variety of specific target genes that are only now beginning to be identified. Interestingly, FOXO transcription factors appear to be able to regulate transcription through both DNA-binding-dependent and -independent mechanisms. Our understanding of the regulation of FOXO activity, and defining specific transcriptional targets, may provide clues to the molecular mechanisms controlling cell fate decisions to divide, differentiate or die.

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Caito, Samuel W., Jennifer Newell-Caito, Megan Martell, Nicole Crawford, and Michael Aschner. "Methylmercury Induces Metabolic Alterations in Caenorhabditis elegans: Role for C/EBP Transcription Factor." Toxicological Sciences 174, no. 1 (December 18, 2019): 112–23. http://dx.doi.org/10.1093/toxsci/kfz244.

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Abstract Methylmercury (MeHg) is a well-known neurotoxicant; however, its role in metabolic diseases has been gaining wider attention. We have previously shown that MeHg causes metabolic alterations in Caenorhabditis elegans, leading to decreased nicotinamide adenine dinucleotide cofactor, mitochondrial dysfunction, and oxidative stress. We were, therefore, interested in whether MeHg also affects nutrient metabolism, particularly lipid homeostasis, which may contribute to the development of metabolic conditions such as obesity or metabolic syndrome (MS). RNA from wild-type worms exposed to MeHg was collected immediately after treatment and used for gene expression analysis by DNA microarray. MeHg differentially regulated 215 genes, 17 genes involved in lipid homeostasis, and 12 genes involved in carbohydrate homeostasis. Of particular interest was cebp-1, the worm ortholog to human C/EBP, a pro-adipogenic transcription factor implicated in MS. MeHg increased the expression of cebp-1 as well as pro-adipogenic transcription factors sbp-1 and nhr-49, triglyceride synthesis enzyme acl-6, and lipid transport proteins vit-2 and vit-6. Concurrent with the altered gene expression, MeHg increased triglyceride levels, lipid storage, and feeding behaviors. Worms expressing mutant cebp-1 were protected from MeHg-induced alterations in lipid content, feeding behaviors, and gene expression, highlighting the importance of this transcription factor in the worm’s response to MeHg. Taken together, our data demonstrate that MeHg induces biochemical, metabolic, and behavioral changes in C. elegans that can lead to metabolic dysfunction.

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Yuan, Fengling, Jiejun Zhou, Lingxiu Xu, Wenxin Jia, Lei Chun, X. Z. Shawn Xu, and Jianfeng Liu. "GABA receptors differentially regulate life span and health span in C. elegans through distinct downstream mechanisms." American Journal of Physiology-Cell Physiology 317, no. 5 (November 1, 2019): C953—C963. http://dx.doi.org/10.1152/ajpcell.00072.2019.

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GABA, a prominent inhibitory neurotransmitter, is best known to regulate neuronal functions in the nervous system. However, much less is known about the role of GABA signaling in other physiological processes. Interestingly, recent work showed that GABA signaling can regulate life span via a metabotropic GABAB receptor in Caenorhabditis elegans. However, the role of other types of GABA receptors in life span has not been clearly defined. It is also unclear whether GABA signaling regulates health span. Here, using C. elegans as a model, we systematically interrogated the role of various GABA receptors in both life span and health span. We find that mutations in four different GABA receptors extend health span by promoting resistance to stress and pathogen infection and that two such receptor mutants also show extended life span. Different GABA receptors engage distinct transcriptional factors to regulate life span and health span, and even the same receptor regulates life span and health span via different transcription factors. Our results uncover a novel, profound role of GABA signaling in aging in C. elegans, which is mediated by different GABA receptors coupled to distinct downstream effectors.

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Venz, Richard, Anastasiia Korosteleva, Elisabeth Jongsma, and Collin Y. Ewald. "Combining Auxin-Induced Degradation and RNAi Screening Identifies Novel Genes Involved in Lipid Bilayer Stress Sensing in Caenorhabditis elegans." G3: Genes|Genomes|Genetics 10, no. 11 (September 21, 2020): 3921–28. http://dx.doi.org/10.1534/g3.120.401635.

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Alteration of the lipid composition of biological membranes interferes with their function and can cause tissue damage by triggering apoptosis. Upon lipid bilayer stress, the endoplasmic reticulum mounts a stress response similar to the unfolded protein response. However, only a few genes are known to regulate lipid bilayer stress. We performed a suppressor screen that combined the auxin-inducible degradation (AID) system with conventional RNAi in C. elegans to identify members of the lipid bilayer stress response. AID-mediated degradation of the mediator MDT-15, a protein required for the upregulation of fatty acid desaturases, induced the activation of lipid bilayer stress-sensitive reporters. We screened through most C. elegans kinases and transcription factors by feeding RNAi. We discovered nine genes that suppressed the lipid bilayer stress response in C. elegans. These suppressor genes included drl-1/MAP3K3, gsk-3/GSK3, let-607/CREB3, ire-1/IRE1, and skn-1/NRF1,2,3. Our candidate suppressor genes suggest a network of transcription factors and the integration of multiple tissues for a centralized lipotoxicity response in the intestine. Thus, we demonstrated proof-of-concept for combining AID and RNAi as a new screening strategy and identified eight conserved genes that had not previously been implicated in the lipid bilayer stress response.

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Chaplin, T., P. Ayton, OA Bernard, V. Saha, V. Della Valle, J. Hillion, A. Gregorini, D. Lillington, R. Berger, and BD Young. "A novel class of zinc finger/leucine zipper genes identified from the molecular cloning of the t(10;11) translocation in acute leukemia." Blood 85, no. 6 (March 15, 1995): 1435–41. http://dx.doi.org/10.1182/blood.v85.6.1435.bloodjournal8561435.

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A novel class of conserved transcription factors has been identified from the molecular cloning of AF10, the gene involved in the t(10;11)(p12;q23) translocation of acute myeloid leukemias. AF10 encodes a 109-kD protein of 1,027 amino acids and contains an N- terminal zinc finger region and a C-terminal leucine zipper. These structures have been found to be conserved in sequence and position in three other proteins, AF17, BR140, and a previously unrecognized Caenorhabditis elegans gene, provisionally named CEZF. The overall structure, level of sequence conservation, and expression pattern suggest that these genes encode a new class of transcription factors, some of which are targets for chromosomal translocation in acute leukemia.

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Wang, Chen. "Decoding Sex Differences in the Brain, One Worm at a Time." Gender and the Genome 2, no. 3 (July 2018): 76–80. http://dx.doi.org/10.1177/2470289718789306.

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Sex differences in the brain are prominent features across the animal kingdom. Understanding the anatomical and regulatory mechanisms behind these differences is critical for both explaining sexually dimorphic behaviors and developing sex-targeted treatments for neurological disorders. Clinical studies considering sex biases and basic research on animal models have provided much evidence for the existence of sex differences in the brain and, in a larger sense, sexual dimorphisms in the nervous system. However, due to the complexity of structure and dimorphic behaviors, it is yet unclear precisely how neuronal sexual dimorphisms are regulated on a molecular or cellular level. This commentary reviews available tools for investigating sexual dimorphisms using a simple model organism, the roundworm Caenorhabditis elegans ( C. elegans), which enables one to study gene regulation at single-cell resolution with a number of cutting-edge molecular and genetic technologies. I highlight the doublesex/mab-3 family of transcription factors, first discovered in invertebrates, and their roles in a potentially universal regulatory mechanism underlying neuronal sexual dimorphisms. Studies of these transcription factors using C. elegans, fruit flies, and vertebrates will promote our understanding of fundamental mechanisms behind sex differences in the brain.

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Gubert, Priscila, Bruna Puntel, Tassia Lehmen, Joshua P. Fessel, Pan Cheng, Julia Bornhorst, Lucas Siqueira Trindade, Daiana S. Avila, Michael Aschner, and Felix A. A. Soares. "Metabolic effects of manganese in the nematode Caenorhabditis elegans through DAergic pathway and transcription factors activation." NeuroToxicology 67 (July 2018): 65–72. http://dx.doi.org/10.1016/j.neuro.2018.04.008.

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Irazoqui, J. E., A. Ng, R. J. Xavier, and F. M. Ausubel. "Role for -catenin and HOX transcription factors in Caenorhabditis elegans and mammalian host epithelial-pathogen interactions." Proceedings of the National Academy of Sciences 105, no. 45 (November 3, 2008): 17469–74. http://dx.doi.org/10.1073/pnas.0809527105.

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Feng, Huiyun, John S. Reece-Hoyes, Albertha J. M. Walhout, and Ian A. Hope. "A regulatory cascade of three transcription factors in a single specific neuron, DVC, in Caenorhabditis elegans." Gene 494, no. 1 (February 2012): 73–84. http://dx.doi.org/10.1016/j.gene.2011.11.042.

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Mah, Allan K., Kristin R. Armstrong, Derek S. Chew, Jeffrey S. Chu, Domena K. Tu, Robert C. Johnsen, Nansheng Chen, Helen M. Chamberlin, and David L. Baillie. "Transcriptional Regulation of AQP-8, a Caenorhabditis elegans Aquaporin Exclusively Expressed in the Excretory System, by the POU Homeobox Transcription Factor CEH-6." Journal of Biological Chemistry 282, no. 38 (July 27, 2007): 28074–86. http://dx.doi.org/10.1074/jbc.m703305200.

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Due to the ever changing environmental conditions in soil, regulation of osmotic homeostasis in the soil-dwelling nematode Caenorhabditis elegans is critical. AQP-8 is a C. elegans aquaporin that is expressed in the excretory cell, a renal equivalent tissue, where the protein participates in maintaining water balance. To better understand the regulation of AQP-8, we undertook a promoter analysis to identify the aqp-8 cis-regulatory elements. Using progressive 5′ deletions of upstream sequence, we have mapped an essential regulatory region to roughly 300 bp upstream of the translational start site of aqp-8. Analysis of this region revealed a sequence corresponding to a known DNA functional element (octamer motif), which interacts with POU homeobox transcription factors. Phylogenetic footprinting showed that this site is perfectly conserved in four nematode species. The octamer site's function was further confirmed by deletion analyses, mutagenesis, functional studies, and electrophoretic mobility shift assays. Of the three POU homeobox proteins encoded in the C. elegans genome, CEH-6 is the only member that is expressed in the excretory cell. We show that expression of AQP-8 is regulated by CEH-6 by performing RNA interference experiments. CEH-6's mammalian ortholog, Brn1, is expressed both in the kidney and the central nervous system and binds to the same octamer consensus binding site to drive gene expression. These parallels in transcriptional control between Brn1 and CEH-6 suggest that C. elegans may well be an appropriate model for determining gene-regulatory networks in the developing vertebrate kidney.

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Van de Walle, Pieter, Celia Muñoz-Jiménez, Peter Askjaer, Liliane Schoofs, and Liesbet Temmerman. "DamID identifies targets of CEH-60/PBX that are associated with neuron development and muscle structure in Caenorhabditis elegans." PLOS ONE 15, no. 12 (December 11, 2020): e0242939. http://dx.doi.org/10.1371/journal.pone.0242939.

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Transcription factors govern many of the time- and tissue-specific gene expression events in living organisms. CEH-60, a homolog of the TALE transcription factor PBX in vertebrates, was recently characterized as a new regulator of intestinal lipid mobilization in Caenorhabditis elegans. Because CEH-60’s orthologs and paralogs exhibit several other functions, notably in neuron and muscle development, and because ceh-60 expression is not limited to the C. elegans intestine, we sought to identify additional functions of CEH-60 through DNA adenine methyltransferase identification (DamID). DamID identifies protein-genome interaction sites through GATC-specific methylation. We here report 872 putative CEH-60 gene targets in young adult animals, and 587 in L2 larvae, many of which are associated with neuron development or muscle structure. In light of this, we investigate morphology and function of ceh-60 expressing AWC neurons, and contraction of pharyngeal muscles. We find no clear functional consequences of loss of ceh-60 in these assays, suggesting that in AWC neurons and pharyngeal muscle, CEH-60 function is likely more subtle or redundant with other factors.

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Lee, Soyoung, and Winship Herr. "Stabilization but Not the Transcriptional Activity of Herpes Simplex Virus VP16-Induced Complexes Is Evolutionarily Conserved among HCF Family Members." Journal of Virology 75, no. 24 (December 15, 2001): 12402–11. http://dx.doi.org/10.1128/jvi.75.24.12402-12411.2001.

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ABSTRACT The human herpes simplex virus (HSV) protein VP16 induces formation of a transcriptional regulatory complex with two cellular factors—the POU homeodomain transcription factor Oct-1 and the cell proliferation factor HCF-1—to activate viral immediate-early-gene transcription. Although the cellular role of Oct-1 in transcription is relatively well understood, the cellular role of HCF-1 in cell proliferation is enigmatic. HCF-1 and the related protein HCF-2 form an HCF protein family in humans that is related to a Caenorhabditis elegans homolog called CeHCF. In this study, we show that all three proteins can promote VP16-induced-complex formation, indicating that VP16 targets a highly conserved function of HCF proteins. The resulting VP16-induced complexes, however, display different transcriptional activities. In contrast to HCF-1 and CeHCF, HCF-2 fails to support VP16 activation of transcription effectively. These results suggest that, along with HCF-1, HCF-2 could have a role, albeit probably a different role, in HSV infection. CeHCF can mimic HCF-1 for both association with viral and cellular proteins and transcriptional activation, suggesting that the function(s) of HCF-1 targeted by VP16 has been highly conserved throughout metazoan evolution.

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Maduro, Morris F. "Evolutionary Dynamics of the SKN-1 → MED → END-1,3 Regulatory Gene Cascade in Caenorhabditis Endoderm Specification." G3: Genes|Genomes|Genetics 10, no. 1 (November 18, 2019): 333–56. http://dx.doi.org/10.1534/g3.119.400724.

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Gene regulatory networks and their evolution are important in the study of animal development. In the nematode, Caenorhabditis elegans, the endoderm (gut) is generated from a single embryonic precursor, E. Gut is specified by the maternal factor SKN-1, which activates the MED → END-1,3 → ELT-2,7 cascade of GATA transcription factors. In this work, genome sequences from over two dozen species within the Caenorhabditis genus are used to identify MED and END-1,3 orthologs. Predictions are validated by comparison of gene structure, protein conservation, and putative cis-regulatory sites. All three factors occur together, but only within the Elegans supergroup, suggesting they originated at its base. The MED factors are the most diverse and exhibit an unexpectedly extensive gene amplification. In contrast, the highly conserved END-1 orthologs are unique in nearly all species and share extended regions of conservation. The END-1,3 proteins share a region upstream of their zinc finger and an unusual amino-terminal poly-serine domain exhibiting high codon bias. Compared with END-1, the END-3 proteins are otherwise less conserved as a group and are typically found as paralogous duplicates. Hence, all three factors are under different evolutionary constraints. Promoter comparisons identify motifs that suggest the SKN-1, MED, and END factors function in a similar gut specification network across the Elegans supergroup that has been conserved for tens of millions of years. A model is proposed to account for the rapid origin of this essential kernel in the gut specification network, by the upstream intercalation of duplicate genes into a simpler ancestral network.

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Joo, Hyoe-Jin, Saeram Park, Kwang-Youl Kim, Mun-Young Kim, Heekyeong Kim, Donha Park, and Young-Ki Paik. "HSF-1 is involved in regulation of ascaroside pheromone biosynthesis by heat stress in Caenorhabditis elegans." Biochemical Journal 473, no. 6 (March 10, 2016): 789–96. http://dx.doi.org/10.1042/bj20150938.

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Heat-shock transcription factor HSF-1 appears to mediate enhanced ascaroside biosynthesis under heat stress by stimulating peroxisomal gene expression. Thus HSF-1 may be one of the regulatory factors involved in biosynthesis of ascaroside pheromones.

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Chen, Pei-Jiun, Soochin Cho, Suk-Won Jin, and Ronald E. Ellis. "Specification of Germ Cell Fates by FOG-3 Has Been Conserved During Nematode Evolution." Genetics 158, no. 4 (August 1, 2001): 1513–25. http://dx.doi.org/10.1093/genetics/158.4.1513.

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Abstract Rapid changes in sexual traits are ubiquitous in evolution. To analyze this phenomenon, we are studying species of the genus Caenorhabditis. These animals use one of two different mating systems—male/hermaphroditic, like the model organism Caenorhabditis elegans, or male/female, like C. remanei. Since hermaphrodites are essentially females that produce sperm for self-fertilization, elucidating the control of cell fate in the germ line in each species could provide the key to understanding how these mating systems evolved. In C. elegans, FOG-3 is required to specify that germ cells become sperm. Thus, we cloned its homologs from both C. remanei and C. briggsae. Each species produces a single homolog of FOG-3, and RNA-mediated interference indicates that FOG-3 functions in each species to specify that germ cells develop as sperm rather than as oocytes. What factors account for the different mating systems? Northern analyses and RT-PCR data reveal that the expression of fog-3 is always correlated with spermatogenesis. Since the promoters for all three fog-3 genes contain binding sites for the transcription factor TRA-1A and are capable of driving expression of fog-3 in C. elegans hermaphrodites, we propose that alterations in the upstream sex-determination pathway, perhaps acting through TRA-1A, allow spermatogenesis in C. elegans and C. briggsae XX larvae but not in C. remanei.

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Evans, Kenneth J., Ni Huang, Przemyslaw Stempor, Michael A. Chesney, Thomas A. Down, and Julie Ahringer. "Stable Caenorhabditis elegans chromatin domains separate broadly expressed and developmentally regulated genes." Proceedings of the National Academy of Sciences 113, no. 45 (October 25, 2016): E7020—E7029. http://dx.doi.org/10.1073/pnas.1608162113.

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Eukaryotic genomes are organized into domains of differing structure and activity. There is evidence that the domain organization of the genome regulates its activity, yet our understanding of domain properties and the factors that influence their formation is poor. Here, we use chromatin state analyses in early embryos and third-larval stage (L3) animals to investigate genome domain organization and its regulation in Caenorhabditis elegans. At both stages we find that the genome is organized into extended chromatin domains of high or low gene activity defined by different subsets of states, and enriched for H3K36me3 or H3K27me3, respectively. The border regions between domains contain large intergenic regions and a high density of transcription factor binding, suggesting a role for transcription regulation in separating chromatin domains. Despite the differences in cell types, overall domain organization is remarkably similar in early embryos and L3 larvae, with conservation of 85% of domain border positions. Most genes in high-activity domains are expressed in the germ line and broadly across cell types, whereas low-activity domains are enriched for genes that are developmentally regulated. We find that domains are regulated by the germ-line H3K36 methyltransferase MES-4 and that border regions show striking remodeling of H3K27me1, supporting roles for H3K36 and H3K27 methylation in regulating domain structure. Our analyses of C. elegans chromatin domain structure show that genes are organized by type into domains that have differing modes of regulation.

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Grushko, Danielle, Hana Boocholez, Amir Levine, and Ehud Cohen. "Temporal requirements of SKN-1/NRF as a regulator of lifespan and proteostasis in Caenorhabditis elegans." PLOS ONE 16, no. 7 (July 1, 2021): e0243522. http://dx.doi.org/10.1371/journal.pone.0243522.

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Lowering the activity of the Insulin/IGF-1 Signaling (IIS) cascade results in elevated stress resistance, enhanced protein homeostasis (proteostasis) and extended lifespan of worms, flies and mice. In the nematode Caenorhabditis elegans (C. elegans), the longevity phenotype that stems from IIS reduction is entirely dependent upon the activities of a subset of transcription factors including the Forkhead factor DAF-16/FOXO (DAF-16), Heat Shock Factor-1 (HSF-1), SKiNhead/Nrf (SKN-1) and ParaQuat Methylviologen responsive (PQM-1). While DAF-16 determines lifespan exclusively during early adulthood and governs proteostasis in early adulthood and midlife, HSF-1 executes these functions foremost during development. Despite the central roles of SKN-1 as a regulator of lifespan and proteostasis, the temporal requirements of this transcription factor were unknown. Here we employed conditional knockdown techniques and discovered that in C. elegans, SKN-1 is primarily important for longevity and proteostasis during late larval development through early adulthood. Our findings indicate that events that occur during late larval developmental through early adulthood affect lifespan and proteostasis and suggest that subsequent to HSF-1, SKN-1 sets the conditions, partially overlapping temporally with DAF-16, that enable IIS reduction to promote longevity and proteostasis. Our findings raise the intriguing possibility that HSF-1, SKN-1 and DAF-16 function in a coordinated and sequential manner to promote healthy aging.

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DA'DARA, Akram A., and Rolf D. WALTER. "Molecular and biochemical characterization of S-adenosylmethionine decarboxylase from the free-living nematode Caenorhabditis elegans." Biochemical Journal 336, no. 3 (December 15, 1998): 545–50. http://dx.doi.org/10.1042/bj3360545.

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S-Adenosylmethionine decarboxylase (SAMDC) is a major regulatory enzyme in the polyamine biosynthesis and is considered a potentially important drug target for the chemotherapy of proliferative and parasitic diseases. To study regulatory mechanisms which are involved in the expression of SAMDC of the free-living nematode Caenorhabditis elegans, we have isolated the SAMDC gene and cDNA. Genomic Southern-blot analysis suggests that the C. elegans SAMDC is encoded by a single-copy gene which spans 3.9 kb and consists of six exons and five introns. The first two introns are located in the 5´-untranslated region (UTR). Analyses of the 5´-flanking region of the gene revealed several consensus sequences for the binding of different transcription factors such as CBP, AP2, cMyb, VPE2 and others. The C. elegans SAMDC mRNA possesses an open reading frame (ORF) which encodes a polypeptide of 368 amino acids, corresponding to a SAMDC proenzyme with a calculated molecular mass of 42141 Da. The active form of the C. elegans SAMDC is a heterotetramer, consisting of two subunits of 32 and 10 kDa derived from cleavage of the pro-enzyme. The SAMDC mRNA has an unusually long 5´-UTR of 477 nucleotides. This region has a small ORF which could encode a putative peptide of 17 residues. Moreover, the C. elegans SAMDC mRNA is trans-spliced with the 22 nucleotides spliced leader sequence at the 5´-end.

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Kalb, John M., Laura Beaster-Jones, Anthony P. Fernandez, Peter G. Okkema, Barbara Goszczynski, and James D. McGhee. "Interference Between the PHA-4 and PEB-1 Transcription Factors in Formation of the Caenorhabditis elegans Pharynx." Journal of Molecular Biology 320, no. 4 (July 2002): 697–704. http://dx.doi.org/10.1016/s0022-2836(02)00555-7.

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Higashibata, A. "Decreased expression of myogenic transcription factors and myosin heavy chains in Caenorhabditis elegans muscles developed during spaceflight." Journal of Experimental Biology 209, no. 16 (August 15, 2006): 3209–18. http://dx.doi.org/10.1242/jeb.02365.

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Higashibata, A. "Decreased expression of myogenic transcription factors and myosin heavy chains in Caenorhabditis elegans muscles developed during spaceflight." Journal of Experimental Biology 209, no. 18 (September 15, 2006): 3695. http://dx.doi.org/10.1242/jeb.02504.

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Maadani, Arash, Kristina A. Fox, Elftherios Mylonakis, and Danielle A. Garsin. "Enterococcus faecalis Mutations Affecting Virulence in the Caenorhabditis elegans Model Host." Infection and Immunity 75, no. 5 (February 16, 2007): 2634–37. http://dx.doi.org/10.1128/iai.01372-06.

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ABSTRACT Enterococcus faecalis transposon insertion mutants were screened for attenuated killing of the nematode model host Caenorhabditis elegans. The genes disrupted in the attenuated mutants encode a variety of factors including transcriptional regulators, transporters, and damage control and repair systems. Five of nine mutants tested were attenuated in a mouse peritonitis model.

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Jayarathne, Shasika, Latha Ramalingam, Hunter Edwards, Siva A. Vanapalli, and Naima Moustaid-Moussa. "Tart Cherry Increases Lifespan in Caenorhabditis elegans by Altering Metabolic Signaling Pathways." Nutrients 12, no. 5 (May 20, 2020): 1482. http://dx.doi.org/10.3390/nu12051482.

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Aging and healthspan are determined by both environmental and genetic factors. The insulin/insulin-like growth factor-1(IGF-1) pathway is a key mediator of aging in Caenorhabditis elegans and mammals. Specifically, DAF-2 signaling, an ortholog of human IGF, controls DAF-16/FOXO transcription factor, a master regulator of metabolism and longevity. Moreover, mitochondrial dysfunction and oxidative stress are both linked to aging. We propose that daily supplementation of tart cherry extract (TCE), rich in anthocyanins with antioxidant properties may exert dual benefits for mitochondrial function and oxidative stress, resulting in beneficial effects on aging in C. elegans. We found that TCE supplementation at 6 μg or 12 μg/mL, increased (p < 0.05) the mean lifespan of wild type N2 worms, respectively, when compared to untreated control worms. Consistent with these findings, TCE upregulated (p < 0.05) expression of longevity-related genes such as daf-16 and aak-2 (but not daf-2 or akt-1 genes) and genes related to oxidative stress such as sod-2. Further, we showed that TCE supplementation increased spare respiration in N2 worms. However, TCE did not change the mean lifespan of daf-16 and aak-2 mutant worms. In conclusion, our findings indicate that TCE confers healthspan benefits in C. elegans through enhanced mitochondrial function and reduced oxidative stress, mainly via the DAF-16 pathway.

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Natarajan, Lakshmi, Nina E. Witwer, and David M. Eisenmann. "The DivergentCaenorhabditis elegansβ-Catenin Proteins BAR-1, WRM-1 and HMP-2 Make Distinct Protein Interactions but Retain Functional Redundancyin Vivo." Genetics 159, no. 1 (September 1, 2001): 159–72. http://dx.doi.org/10.1093/genetics/159.1.159.

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Abstractβ-Catenins function both in cell adhesion as part of the cadherin/catenin complex and in Wnt signal transduction as transcription factors. Vertebrates express two related proteins, β-catenin and plakoglobin, while Drosophila has a single family member, Armadillo. Caenorhabditis elegans expresses three β-catenin-related proteins, BAR-1, HMP-2, and WRM-1, which are quite diverged in sequence from each other and other β-catenins. While BAR-1 and WRM-1 are known to act in Wnt-mediated processes, and HMP-2 acts in a complex with cadherin/α-catenin homologs, it is unclear whether all three proteins retain the other functions of β-catenin. Here we show that BAR-1, like vertebrate β-catenin, has redundant transcription activation domains in its amino- and carboxyl-terminal regions but that HMP-2 and WRM-1 also possess the ability to activate transcription. We show via yeast two-hybrid analysis that these three proteins display distinct patterns of protein interactions. Surprisingly, we find that both WRM-1 and HMP-2 can substitute for BAR-1 in C. elegans when expressed from the bar-1 promoter. Therefore, although their mutant phenotypes and protein interaction patterns strongly suggest that the functions of β-catenin in other species have been segregated among three diverged proteins in C. elegans, these proteins still retain sufficient similarity to display functional redundancy in vivo.

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Chamberlin, H. M., R. E. Palmer, A. P. Newman, P. W. Sternberg, D. L. Baillie, and J. H. Thomas. "The PAX gene egl-38 mediates developmental patterning in Caenorhabditis elegans." Development 124, no. 20 (October 15, 1997): 3919–28. http://dx.doi.org/10.1242/dev.124.20.3919.

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Mutations in the C. elegans gene egl-38 result in a discrete set of defects in developmental pattern formation. In the developing egg-laying system of egl-38 mutant hermaphrodites, the identity of four uterine cells is disrupted and they adopt the fate of their neighbor cells. Likewise, the identity of two rectal epithelial cells in the male tail is disrupted and one of these cells adopts the fate of its neighbor cell. Genetic analysis suggests that the egl-38 functions in the tail and the egg-laying system are partially separable, as different egl-38 mutations can preferentially disrupt the different functions. We have cloned egl-38 and shown that it is a member of the PAX family of genes, which encode transcription factors implicated in a variety of developmental patterning events. The predicted EGL-38 protein is most similar to the mammalian class of proteins that includes PAX2, PAX5 and PAX8. The sequence of egl-38 mutant DNA indicates that the tissue-preferential defects of egl-38 mutations result from substitutions in the DNA-binding paired domain of the EGL-38 protein. egl-38 thus provides the first molecular genetic insight into two specific patterning events that occur during C. elegans development and also provides the opportunity to investigate the in vivo functions of this class of PAX proteins with single cell resolution.

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Tao, Lian Jing, Dong Eun Seo, Benjamin Jackson, Natalia B. Ivanova, and Fabio Rinaldo Santori. "Nuclear Hormone Receptors and Their Ligands: Metabolites in Control of Transcription." Cells 9, no. 12 (December 4, 2020): 2606. http://dx.doi.org/10.3390/cells9122606.

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Nuclear hormone receptors are a family of transcription factors regulated by small molecules derived from the endogenous metabolism or diet. There are forty-eight nuclear hormone receptors in the human genome, twenty of which are still orphans. In this review, we make a brief historical journey from the first observations by Berthold in 1849 to the era of orphan receptors that began with the sequencing of the Caenorhabditis elegans genome in 1998. We discuss the evolution of nuclear hormone receptors and the putative ancestral ligands as well as how the ligand universe has expanded over time. This leads us to define four classes of metabolites—fatty acids, terpenoids, porphyrins and amino acid derivatives—that generate all known ligands for nuclear hormone receptors. We conclude by discussing the ongoing efforts to identify new classes of ligands for orphan receptors.

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Feng, Dingxia, Zhiwei Zhai, Zhiyong Shao, Yi Zhang, and Jo Anne Powell-Coffman. "Crosstalk in oxygen homeostasis networks: SKN-1/NRF inhibits the HIF-1 hypoxia-inducible factor in Caenorhabditis elegans." PLOS ONE 16, no. 7 (July 9, 2021): e0249103. http://dx.doi.org/10.1371/journal.pone.0249103.

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During development, homeostasis, and disease, organisms must balance responses that allow adaptation to low oxygen (hypoxia) with those that protect cells from oxidative stress. The evolutionarily conserved hypoxia-inducible factors are central to these processes, as they orchestrate transcriptional responses to oxygen deprivation. Here, we employ genetic strategies in C. elegans to identify stress-responsive genes and pathways that modulate the HIF-1 hypoxia-inducible factor and facilitate oxygen homeostasis. Through a genome-wide RNAi screen, we show that RNAi-mediated mitochondrial or proteasomal dysfunction increases the expression of hypoxia-responsive reporter Pnhr-57::GFP in C. elegans. Interestingly, only a subset of these effects requires hif-1. Of particular importance, we found that skn-1 RNAi increases the expression of hypoxia-responsive reporter Pnhr-57::GFP and elevates HIF-1 protein levels. The SKN-1/NRF transcription factor has been shown to promote oxidative stress resistance. We present evidence that the crosstalk between HIF-1 and SKN-1 is mediated by EGL-9, the prolyl hydroxylase that targets HIF-1 for oxygen-dependent degradation. Treatment that induces SKN-1, such as heat or gsk-3 RNAi, increases expression of a Pegl-9::GFP reporter, and this effect requires skn-1 function and a putative SKN-1 binding site in egl-9 regulatory sequences. Collectively, these data support a model in which SKN-1 promotes egl-9 transcription, thereby inhibiting HIF-1. We propose that this interaction enables animals to adapt quickly to changes in cellular oxygenation and to better survive accompanying oxidative stress.

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Schmitt-Ney, Michel. "The FOXO’s Advantages of Being a Family: Considerations on Function and Evolution." Cells 9, no. 3 (March 24, 2020): 787. http://dx.doi.org/10.3390/cells9030787.

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The nematode Caenorhabditis elegans possesses a unique (with various isoforms) FOXO transcription factor DAF-16, which is notorious for its role in aging and its regulation by the insulin-PI3K-AKT pathway. In humans, five genes (including a protein-coding pseudogene) encode for FOXO transcription factors that are targeted by the PI3K-AKT axis, such as in C. elegans. This common regulation and highly conserved DNA-binding domain are the pillars of this family. In this review, I will discuss the possible meaning of possessing a group of very similar proteins and how it can generate additional functionality to more complex organisms. I frame this discussion in relation to the much larger super family of Forkhead proteins to which they belong. FOXO members are very often co-expressed in the same cell type. The overlap of function and expression creates a certain redundancy that might be a safeguard against the accidental loss of FOXO function, which could otherwise lead to disease, particularly, cancer. This is one of the points that will be examined in this “family affair” report.

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Kai, Zoya S., Emily F. Finnegan, Stacey Huang, and Amy E. Pasquinelli. "Multiple cis-elements and trans-acting factors regulate dynamic spatio-temporal transcription of let-7 in Caenorhabditis elegans." Developmental Biology 374, no. 1 (February 2013): 223–33. http://dx.doi.org/10.1016/j.ydbio.2012.11.021.

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Chen, Zhe, Dennis J. Eastburn, and Min Han. "The Caenorhabditis elegans Nuclear Receptor Gene nhr-25 Regulates Epidermal Cell Development." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7345–58. http://dx.doi.org/10.1128/mcb.24.17.7345-7358.2004.

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ABSTRACT The development of the epidermis of Caenorhabditis elegans involves cell fusion, migration, and differentiation events. To understand the mechanisms underlying these processes, we characterized the roles of NHR-25, a member of the nuclear receptor family of transcription factors. The NHR-25 homologs Ftz-F1 in Drosophila and SF-1 in mammals are involved in various biological processes, including regulation of patterning during development, reproduction, metabolism, metamorphosis, and homeostasis. Impairment of nhr-25 activity leads to severe phenotypes in embryos and many postembryonic tissues. Further analysis has indicated that nhr-25 activity is required for the proper development, including cell-cell fusion, of several epidermal cell types, such as the epidermal syncytial, seam, and Pn.p cells. Our results also suggest that nhr-25 is likely to regulate cell-cell junctions and/or fusion. In a subset of Pn.p cells, called vulval precursor cells, nhr-25 acts collaboratively with the lin-39 Hox gene in regulating vulval cell differentiation. Additionally, our data suggest that nhr-25 may also function with another Hox gene, nob-1, during embryogenesis. Overall, our results indicate that nhr-25 plays an integral role in regulating cellular processes of epidermal cells.

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Hope, I. A. "PES-1 is expressed during early embryogenesis in Caenorhabditis elegans and has homology to the fork head family of transcription factors." Development 120, no. 3 (March 1, 1994): 505–14. http://dx.doi.org/10.1242/dev.120.3.505.

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Promoter trapping has identified a gene, pes-1, which is expressed during C. elegans embryogenesis. The beta-galactosidase expression pattern, directed by the pes-1/lacZ fusion through which this gene was cloned, has been determined precisely in terms of the embryonic cell lineage and has three components. One component is in a subset of cells of the AB founder cell lineage during early embryogenesis, suggesting pes-1 may be regulated both by cell autonomous determinants and by intercellular signals. Analysis of cDNA suggests pes-1 has two sites for initiation of transcription and the two transcripts would encode related but distinct proteins. The predicted PES-1 proteins have homology to the fork head family of transcription factors and therefore may have important regulatory roles in early embryogenesis.

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Cai, Liquan, Binh L. Phong, Alfred L. Fisher, and Zhou Wang. "Regulation of Fertility, Survival, and Cuticle Collagen Function by the Caenorhabditis elegans eaf-1 and ell-1 Genes." Journal of Biological Chemistry 286, no. 41 (August 31, 2011): 35915–21. http://dx.doi.org/10.1074/jbc.m111.270454.

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EAF2, an androgen-regulated protein, interacts with members of the ELL (eleven-nineteen lysine-rich leukemia) transcription factor family and also acts as a tumor suppressor. Although these proteins control transcriptional elongation and perhaps modulate the effects of other transcription factors, the mechanisms of their actions remain largely unknown. To gain new insights into the biology of the EAF2 and ELL family proteins, we used Caenorhabditis elegans as a model to explore the in vivo roles of their worm orthologs. Through the use of transgenic worms, RNAi, and an eaf-1 mutant, we found that both genes are expressed in multiple cell types throughout the worm life cycle and that they play important roles in fertility, survival, and body size regulation. ELL-1 and EAF-1 likely contribute to these activities in part through modulating cuticle synthesis, given that we observed a disrupted cuticle structure in ell-1 RNAi-treated or eaf-1 mutant worms. Consistent with disruption of cuticle structure, loss of either ELL-1 or EAF-1 suppressed the rol phenotype of specific collagen mutants, possibly through the control of dpy-3, dpy-13, and sqt-3 collagen gene expression. Furthermore, we also noted the regulation of collagen expression by ELL overexpression in PC3 human prostate cancer cells. Together, these results reveal important roles for the eaf-1 and ell-1 genes in the regulation of extracellular matrix components.

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Okuyama, Tetsuya, Emi Yoshigai, Yukinobu Ikeya, and Mikio Nishizawa. "Active Hexose Correlated Compound Extends the Lifespan and Increases the Thermotolerance of Nematodes." Functional Foods in Health and Disease 3, no. 6 (June 7, 2013): 166. http://dx.doi.org/10.31989/ffhd.v3i6.55.

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Background: Active hexose correlated compound (AHCC) is the extract from cultured mycelia of Lentinula edodes, a species of Basidiomycetes mushroom. AHCC contains various polysaccharides, including partially acylated <-1,4-glucan, which is one of its major constituents. The application of AHCC has been markedly increased in complementary and alternative medicine as a functional food because AHCC improved the prognosis of postoperative hepatocellular carcinoma patients. AHCC has anti-inflammatory and antioxidant effects, such as the suppression of nitric oxide production in hepatocytes. AHCC might affect resistance to environmental stress, which is assumed to play a pivotal role in the longevity of many organisms.Objective: To investigate the effect of AHCC on longevity, we measured the lifespan of the nematode Caenorhabditis elegans, a model animal that is widely used to assess longevity. We also examined the effect of AHCC on resistance to heat stress, i.e., thermotolerance.Methods: The lifespan of C. elegans animals grown on media in the absence or presence of AHCC at 20°C was evaluated. Thermotolerance assays were performed at 35°C, the restrictive temperature of the animals. The effects of AHCC on lifespan and thermotolerance were analyzed with longevity mutants. Expression levels of stress-related genes, including heat shock genes, were measured by strand-specific reverse transcription-polymerase chain reaction after heat shock.Results: Wild-type C. elegans animals exhibited a longer mean lifespan by up to 10% in the presence of AHCC in the growth media than animals in the absence of AHCC. Furthermore, AHCC markedly increased thermotolerance at 35°C. Epistasis analyses showed that lifespan extension by AHCC at least partly required two longevity-promoting transcription factors: DAF-16 (C. elegans homolog of FOXO) and HSF-1 (C. elegans homolog of heat shock transcription factor 1). After heat shock, AHCC activated the transcription of the heat shock genes, which are the targets of HSF-1. Similarly, the expression of hsf-1 mRNA was elevated following AHCC treatment. Recently, natural antisense transcripts were shown to regulate mRNA stability at the posttranscriptional level. In nematodes, AHCC increased the natural antisense transcript of the hsf-1 gene.Conclusion: AHCC conferred lifespan extension and thermotolerance to C. elegans. Our analyses suggest that the beneficial effects of AHCC on longevity are involved in the activation of at least two transcription factors, DAF-16 and HSF-1, most likely through an antisense transcript-mediated mechanism.Keywords: longevity, heat stress resistance, HSF, FOXO, heat shock gene

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Mesbahi, Hiva, Kim B. Pho, Andrea J. Tench, Victoria L. Leon Guerrero, and Lesley T. MacNeil. "Cuticle Collagen Expression Is Regulated in Response to Environmental Stimuli by the GATA Transcription Factor ELT-3 in Caenorhabditis elegans." Genetics 215, no. 2 (March 30, 2020): 483–95. http://dx.doi.org/10.1534/genetics.120.303125.

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The nematode Caenorhabditis elegans is protected from the environment by the cuticle, an extracellular collagen-based matrix that encloses the animal. Over 170 cuticular collagens are predicted in the C. elegans genome, but the role of each individual collagen is unclear. Stage-specific specialization of the cuticle explains the need for some collagens; however, the large number of collagens suggests that specialization of the cuticle may also occur in response to other environmental triggers. Missense mutations in many collagen genes can disrupt cuticle morphology, producing a helically twisted body causing the animal to move in a stereotypical pattern described as rolling. We find that environmental factors, including diet, early developmental arrest, and population density can differentially influence the penetrance of rolling in these mutants. These effects are in part due to changes in collagen gene expression that are mediated by the GATA family transcription factor ELT-3. We propose a model by which ELT-3 regulates collagen gene expression in response to environmental stimuli to promote the assembly of a cuticle specialized to a given environment.

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Hart, Michael P. "Stress-Induced Neuron Remodeling Reveals Differential Interplay Between Neurexin and Environmental Factors in Caenorhabditis elegans." Genetics 213, no. 4 (September 26, 2019): 1415–30. http://dx.doi.org/10.1534/genetics.119.302415.

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Neurexins are neuronal adhesion molecules important for synapse maturation, function, and plasticity. Neurexins have been genetically associated with neurodevelopmental disorders, including autism spectrum disorders (ASDs) and schizophrenia, but can have variable penetrance and phenotypic severity. Heritability studies indicate that a significant percentage of risk for ASD and schizophrenia includes environmental factors, highlighting a poorly understood interplay between genetic and environmental factors. The singular Caenorhabditis elegans ortholog of human neurexins, nrx-1, controls experience-dependent morphologic remodeling of a GABAergic neuron in adult males. Here, I show remodeling of this neuron’s morphology in response to each of three environmental stressors (nutritional, heat, or genotoxic stress) when applied specifically during sexual maturation. Increased outgrowth of axon-like neurites following adolescent stress is the result of an altered morphologic plasticity in adulthood. Despite remodeling being induced by each of the three stressors, only nutritional stress affects downstream behavior and is dependent on neurexin/nrx-1. Heat or genotoxic stress in adolescence does not alter behavior despite inducing GABAergic neuron remodeling, in a neurexin/nrx-1 independent fashion. Starvation-induced remodeling is also dependent on neuroligin/nlg-1, the canonical binding partner for neurexin/nrx-1, and the transcription factors FOXO/daf-16 and HSF1/hsf-1. hsf-1 and daf-16, in addition, each have unique roles in remodeling induced by heat and UV stress. The differential molecular mechanisms underlying GABAergic neuron remodeling in response to different stressors, and the disparate effects of stressors on downstream behavior, are a paradigm for understanding how genetics, environmental exposures, and plasticity may contribute to brain dysfunction in ASDs and schizophrenia.

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Atichartpongkul, Sopapan, Mayuree Fuangthong, Paiboon Vattanaviboon, and Skorn Mongkolsuk. "Analyses of the Regulatory Mechanism and Physiological Roles of Pseudomonas aeruginosa OhrR, a Transcription Regulator and a Sensor of Organic Hydroperoxides." Journal of Bacteriology 192, no. 8 (February 5, 2010): 2093–101. http://dx.doi.org/10.1128/jb.01510-09.

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ABSTRACT ohrR encodes an organic hydroperoxide sensor and a transcriptional repressor that regulates organic hydroperoxide-inducible expression of a thiol peroxidase gene, ohr, and itself. OhrR binds directly to the operators and represses transcription of these genes. Exposure to an organic hydroperoxide leads to oxidation of OhrR and to subsequent structural changes that result in the loss of the repressor's ability to bind to the operators that allow expression of the target genes. Differential induction of ohrR and ohr by tert-butyl hydroperoxide suggests that factors such as the repressor's dissociation constants for different operators and the chemical nature of the inducer contribute to OhrR-dependent organic hydroperoxide-inducible gene expression. ohrR and ohr mutants show increased and decreased resistance to organic hydroproxides, respectively, compared to a parental strain. Moreover, the ohrR mutant had a reduced-virulence phenotype in the Pseudomonas aeruginosa-Caenorhabditis elegans pathogenicity model.

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Frank, Deborah J., and Mark B. Roth. "ncl-1 Is Required for the Regulation of Cell Size and Ribosomal RNA Synthesis in Caenorhabditis elegans." Journal of Cell Biology 140, no. 6 (March 23, 1998): 1321–29. http://dx.doi.org/10.1083/jcb.140.6.1321.

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Regulation of ribosome synthesis is an essential aspect of growth control. Thus far, little is known about the factors that control and coordinate these processes. We show here that the Caenorhabditis elegans gene ncl-1 encodes a zinc finger protein and may be a repressor of RNA polymerase I and III transcription and an inhibitor of cell growth. Loss of function mutations in ncl-1, previously shown to result in enlarged nucleoli, result in increased rates of rRNA and 5S RNA transcription and enlarged cells. Furthermore, ncl-1 adult worms are larger, have more protein, and have twice as much rRNA as wild-type worms. Localization studies show that the level of NCL-1 protein is independently regulated in different cells of the embryo. In wild-type embryos, cells with the largest nucleoli have the lowest level of NCL-1 protein. Based on these results we propose that ncl-1 is a repressor of ribosome synthesis and cell growth.

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Rafikova, Adilya, Queenie Hu, and Terrance J. Kubiseski. "The SEM-4 Transcription Factor Is Required for Regulation of the Oxidative Stress Response in Caenorhabditis elegans." G3 Genes|Genomes|Genetics 10, no. 9 (September 1, 2020): 3379–85. http://dx.doi.org/10.1534/g3.120.401316.

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Abstract Oxidative stress causes damage to cells by creating reactive oxygen species (ROS) and the overproduction of ROS have been linked to the onset of premature aging. We previously found that a brap-2 (BRCA1 associated protein 2) mutant significantly increases the expression of phase II detoxification enzymes in C. elegans. An RNAi suppression screen to identify transcription factors involved in the production of gst-4 mRNA in brap-2 worms identified SEM-4 as a potential candidate. Here, we show that knockdown of sem-4 suppresses the activation of gst-4 caused by the mutation in brap-2. We also demonstrate that sem-4 is required for survival upon exposure to oxidative stress and that SEM-4 is required for expression of the transcription factor SKN-1C. These findings identify a novel role for SEM-4 in ROS detoxification by regulating expression of SKN-1C and the phase II detoxification genes.

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Ayuda-Durán, Begoña, Susana González-Manzano, Antonio Miranda-Vizuete, Eva Sánchez-Hernández, Marta R. Romero, Montserrat Dueñas, Celestino Santos-Buelga, and Ana M. González-Paramás. "Exploring Target Genes Involved in the Effect of Quercetin on the Response to Oxidative Stress in Caenorhabditis elegans." Antioxidants 8, no. 12 (November 25, 2019): 585. http://dx.doi.org/10.3390/antiox8120585.

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Quercetin is one the most abundant flavonoids in the human diet. Although it is well known that quercetin exhibits a range of biological activities, the mechanisms behind these activities remain unresolved. The aim of this work is to progress in the knowledge of the molecular mechanisms involved in the biological effects of quercetin using Caenorhabditis elegans as a model organism. With this aim, the nematode has been used to explore the ability of this flavonoid to modulate the insulin/insulin-like growth factor 1(IGF-1) signaling pathway (IIS) and the expression of some genes related to stress response. Different methodological approaches have been used, i.e., assays in knockout mutant worms, gene expression assessment by RT-qPCR, and C. elegans transgenic strains expressing green fluorescent protein (GFP) reporters. The results showed that the improvement of the oxidative stress resistance of C. elegans induced by quercetin could be explained, at least in part, by the modulation of the insulin signaling pathway, involving genes age-1, akt-1, akt-2, daf-18, sgk-1, daf-2, and skn-1. However, this effect could be independent of the transcription factors DAF-16 and HSF-1 that regulate this pathway. Moreover, quercetin was also able to increase expression of hsp-16.2 in aged worms. This observation could be of particular interest to explain the effects of enhanced lifespan and greater resistance to stress induced by quercetin in C. elegans, since the expression of many heat shock proteins diminishes in aging worms.

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Journal articles on the topic 'Caenorhabditis elegans Transcription factors'

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