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Analysis of the transcription factor CEH-60 in Caenorhabditis elegans development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE112981 | GEO | 2019/04/04

REPOSITORIES: GEO

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Analysis of the transcription factor CEH-60 in Caenorhabditis elegans development

Project description:Analysis of the transcription factor CEH-60 in Caenorhabditis elegans development

| PRJNA449674 | ENA

DamID identifies targets of CEH-60/PBX that are associated with neuron development and muscle structure in Caenorhabditis elegans.

Project description: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.

| S-EPMC7732058 | biostudies-literature

Genome-wide occupancy of the CEH-60 and UNC-62 Transcription Factors in Caenorhabditis elegans

Project description:Animals integrate metabolic, developmental, and environmental information before committing key resources to reproduction. In C. elegans, adult animals reallocate key fat stores from intestinal cells to the germline via lipoproteins to promote reproduction. I identified the evolutionarily conserved homeodomain transcription factor CEH-60/PBX as a potent regulator of lipid homeostasis, longevity, and stress response pathways. To gain a comprehensive view of CEH-60 transcriptional activity, I profiled the transcriptomes of ceh-60 mutants by mRNA-Seq and identified genome-wide CEH-60 binding sites by ChIP-Seq. These approaches revealed that several homeostatic pathways are directly controlled by the CEH-60 transcription factor. CEH-60 functions cooperatively with UNC-62/MEIS in the intestine to directly activate lipoprotein genes while simultaneously repressing genes involved in stress responses, including the innate immune and oxidative stress responses. Thus in wild-type animals, CEH-60 serves as a molecular switch that promotes reproduction (i.e., lipoproteins) while repressing stress response and longevity pathways. This study identifies a new key regulator of fat metabolism, longevity, and stress response pathways during normal C. elegans development.

2019-04-04 | GSE112979 | GEO

CEH-60/PBX regulates vitellogenesis and cuticle permeability through intestinal interaction with UNC-62/MEIS in Caenorhabditis elegans.

Project description:The onset of sexual maturity involves dramatic changes in physiology and gene expression in many animals. These include abundant yolk protein production in egg-laying species, an energetically costly process under extensive transcriptional control. Here, we used the model organism Caenorhabditis elegans to provide evidence for the spatiotemporally defined interaction of two evolutionarily conserved transcription factors, CEH-60/PBX and UNC-62/MEIS, acting as a gateway to yolk protein production. Via proteomics, bimolecular fluorescence complementation (BiFC), and biochemical and functional readouts, we show that this interaction occurs in the intestine of animals at the onset of sexual maturity and suffices to support the reproductive program. Our electron micrographs and functional assays provide evidence that intestinal PBX/MEIS cooperation drives another process that depends on lipid mobilization: the formation of an impermeable epicuticle. Without this lipid-rich protective layer, mutant animals are hypersensitive to exogenous oxidative stress and are poor partners for mating. Dedicated communication between the hypodermis and intestine in C. elegans likely supports these physiological outcomes, and we propose a fundamental role for the conserved PBX/MEIS interaction in multicellular signaling networks that rely on lipid homeostasis.

| S-EPMC6824563 | biostudies-literature

Ancestral function of Inhibitors-of-kappaB regulates Caenorhabditis elegans development

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-01 | GSE146655 | GEO

Multiple pals gene modules control a balance between immunity and development in Caenorhabditis elegans

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-04-28 | GSE229165 | GEO

High-throughput sequencing of small RNAs: Caenorhabditis elegans

Project description:This SuperSeries is composed of the SubSeries listed below.

2008-06-16 | GSE11738 | GEO

Function, targets and evolution of Caenorhabditis elegans piRNAs

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-06-18 | GSE37433 | GEO

Reduced insulin/IGF-1-like signaling restores germ cell immortality in Caenorhabditis elegans Piwi mutants

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-01 | E-GEOD-40573 | biostudies-arrayexpress

Transcription factors CEP-1/p53 and CEH-23 collaborate with AAK-2/AMPK to modulate longevity in Caenorhabditis elegans.

Project description:A decline in mitochondrial electron transport chain (ETC) function has long been implicated in aging and various diseases. Recently, moderate mitochondrial ETC dysfunction has been found to prolong lifespan in diverse organisms, suggesting a conserved and complex role of mitochondria in longevity determination. Several nuclear transcription factors have been demonstrated to mediate the lifespan extension effect associated with partial impairment of the ETC, suggesting that compensatory transcriptional response to be crucial. In this study, we showed that the transcription factors CEP-1/p53 and CEH-23 act through a similar mechanism to modulate longevity in response to defective ETC in Caenorhabditis elegans. Genomewide gene expression profiling comparison revealed a new link between these two transcription factors and AAK-2/AMP kinase (AMPK) signaling. Further functional analyses suggested that CEP-1/p53 and CEH-23 act downstream of AAK-2/AMPK signaling and CRTC-1 transcriptional coactivator to promote stress resistance and lifespan. As AAK-2, CEP-1, and CEH-23 are all highly conserved, our findings likely provide important insights for understanding the organismal adaptive response to mitochondrial dysfunction in diverse organisms and will be relevant to aging and pathologies with a mitochondrial etiology in human.

| S-EPMC5506430 | biostudies-literature

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