An AP2 Transcription Factor Is Required for a Sleep-Active Neuron to Induce Sleep-like Quiescence in C. elegans

Abstract Collagen enriched cuticle forms the outermost layer of skin in nematode Caenorhabditis elegans. The nematode’s genome encodes 177 collagens, but little is known about their role in maintaining the structure or barrier function of the cuticle. In this study, we found six permeability determining (PD) collagens. Loss of any of these PD collagens- DPY-2, DPY-3, DPY-7, DPY-8, DPY-9, and DPY-10- led to enhanced susceptibility of nematodes to paraquat (PQ) and antihelminthic drugs levamisole and ivermectin. Upon exposure to paraquat, PD collagen mutants accumulated more PQ and incurred more damage and death despite the robust activation of antioxidant machinery. We find that BLMP-1, a zinc finger transcription factor, maintains the barrier function of the cuticle by regulating the expression of PD collagens. We show that the permeability barrier maintained by PD collagens acts in parallel to FOXO transcription factor DAF-16 to enhance survival of insulin-like receptor mutant, daf-2. In all, this study shows that PD collagens regulate cuticle permeability by maintaining the structure of C. elegans cuticle and thus provide protection against exogenous toxins.

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Re-evaluating the role of ELT-3 in a GATA transcription factor circuit proposed to guide aging in C. elegans

Mechanisms of Ageing and Development ◽

10.1016/j.mad.2011.09.006 ◽

2012 ◽

Vol 133 (1) ◽

pp. 50-53 ◽

Cited By ~ 15

Author(s):

Tabitha Tonsaker ◽

Ryan M. Pratt ◽

James D. McGhee

Keyword(s):

Transcription Factor ◽

C Elegans ◽

Gata Transcription Factor

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C. elegans sym-1is a downstream target of the Hunchback-like-1 developmental timing transcription factor

Cell Cycle ◽

10.4161/cc.8.24.10292 ◽

2009 ◽

Vol 8 (24) ◽

pp. 4147-4154 ◽

Cited By ~ 12

Author(s):

Ryusuke Niwa ◽

Kazumasa Hada ◽

Kouichi Moliyama ◽

Ryosuke L. Ohniwa ◽

Yi-Meng Tan ◽

...

Keyword(s):

Transcription Factor ◽

Developmental Timing ◽

C Elegans ◽

Downstream Target

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Rescue of a developmental arrest caused by a C. elegans heat-shock transcription-factor mutation by loss of ribosomal S6-kinase activity

10.1101/310086 ◽

2018 ◽

Author(s):

Peter Chisnell ◽

T. Richard Parenteau ◽

Elizabeth Tank ◽

Kaveh Ashrafi ◽

Cynthia Kenyon

Keyword(s):

Transcription Factor ◽

Transcription Factors ◽

Heat Shock ◽

Heat Shock Transcription Factor ◽

Adult Longevity ◽

Loss Of Function ◽

S6 Kinase ◽

Heat Shock Transcription Factors ◽

C Elegans ◽

Developmental Arrest

AbstractThe widely conserved heat-shock response, regulated by heat shock transcription factors, is not only essential for cellular stress resistance and adult longevity, but also for proper development. However, the genetic mechanisms by which heat-shock transcription factors regulate development are not well understood. In C. elegans, we conducted an unbiased genetic screen to identify mutations that could ameliorate the developmental arrest phenotype of a heat-shock factor mutant. Here we show that loss of the conserved translational activator rsks-1/S6-Kinase, a downstream effector of TOR kinase, can rescue the developmental-arrest phenotype of hsf-1 partial loss-of-function mutants. Unexpectedly, we show that the rescue is not likely caused by reduced translation, nor to activation of any of a variety of stress-protective genes and pathways. Our findings identify an as-yet unexplained regulatory relationship between the heat-shock transcription factor and the TOR pathway during C. elegans’ development.

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Regulation of ectodermal and excretory function by the C. elegans POU homeobox gene ceh-6

Development ◽

10.1242/dev.128.5.779 ◽

2001 ◽

Vol 128 (5) ◽

pp. 779-790 ◽

Cited By ~ 2

Author(s):

T.R. Burglin ◽

G. Ruvkun

Keyword(s):

Transcription Factor ◽

Epithelial Cells ◽

Homeobox Genes ◽

Homeobox Gene ◽

Null Mutant ◽

Reporter Construct ◽

Excretory Function ◽

C Elegans ◽

Gfp Reporter ◽

Excretory Cell

Caenorhabditis elegans has three POU homeobox genes, unc-86, ceh-6 and ceh-18. ceh-6 is the ortholog of vertebrate Brn1, Brn2, SCIP/Oct6 and Brn4 and fly Cf1a/drifter/ventral veinless. Comparison of C. elegans and C. briggsae CEH-6 shows that it is highly conserved. C. elegans has only three POU homeobox genes, while Drosophila has five that fall into four families. Immunofluorescent detection of the CEH-6 protein reveals that it is expressed in particular head and ventral cord neurons, as well as in rectal epithelial cells, and in the excretory cell, which is required for osmoregulation. A deletion of the ceh-6 locus causes 80% embryonic lethality. During morphogenesis, embryos extrude cells in the rectal region of the tail or rupture, indicative of a defect in the rectal epithelial cells that express ceh-6. Those embryos that hatch are sick and develop vacuoles, a phenotype similar to that caused by laser ablation of the excretory cell. A GFP reporter construct expressed in the excretory cell reveals inappropriate canal structures in the ceh-6 null mutant. Members of the POU-III family are expressed in tissues involved in osmoregulation and secretion in a number of species. We propose that one evolutionary conserved function of the POU-III transcription factor class could be the regulation of genes that mediate secretion/osmoregulation.

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Mitochondrial translation, dynamics, and lysosomes combine to extend lifespan

The Journal of Cell Biology ◽

10.1083/jcb.202005084 ◽

2020 ◽

Vol 219 (6) ◽

Author(s):

Levi Ali ◽

Cole M. Haynes

Keyword(s):

Transcription Factor ◽

Mitochondrial Fission ◽

Mitochondrial Translation ◽

C Elegans ◽

Mitochondrial Ribosomes

In this issue, Liu et al. (2019. J. Cell. Biol.https://doi.org/10.1083/jcb.201907067) find that the inhibition of mitochondrial ribosomes in combination with impaired mitochondrial fission or fusion increases C. elegans lifespan by activating the transcription factor HLH-30, which promotes lysosomal biogenesis.

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