Unique and redundant functions of C. elegans HP1 proteins in post-embryonic development

The Caenorhabditis elegans genome contains three rac-like genes, ced-10, mig-2, and rac-2. We report that ced-10, mig-2 and rac-2 act redundantly in axon pathfinding: inactivating one gene had little effect, but inactivating two or more genes perturbed both axon outgrowth and guidance. mig-2 and ced-10 also have redundant functions in some cell migrations. By contrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtle roles in this process. Rac activators are also used differentially. The UNC-73 Trio Rac GTP exchange factor affected all Rac pathways in axon pathfinding and cell migration but did not affect cell-corpse phagocytosis. CED-5 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in axon pathfinding. Thus, distinct regulatory proteins modulate Rac activation and function in different developmental processes.

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The Chromatin Remodeler LET-418/Mi2 is Required Cell Non-Autonomously for the Post-Embryonic Development of Caenorhabditis elegans

Journal of Developmental Biology ◽

10.3390/jdb7010001 ◽

2018 ◽

Vol 7 (1) ◽

pp. 1 ◽

Cited By ~ 2

Author(s):

Makhabbat Saudenova ◽

Chantal Wicky

Keyword(s):

Growth Factor ◽

Embryonic Development ◽

Progenitor Cells ◽

Growth Factor Signaling ◽

Chromatin Protein ◽

C Elegans ◽

Blast Cells ◽

A Cell ◽

Further Development ◽

Growth Factor Signaling Pathway

Chromatin condition is crucial for the cells to respond to their environment. In C. elegans, post-embryonic development is accompanied by the exit of progenitor cells from quiescence in response to food. The chromatin protein LET-418/Mi2 is required for this transition in development indicating that proper chromatin structure in cells of the freshly hatched larvae is important to respond to food. However, the identity of the tissue or cells where LET-418/Mi2 is required, as well as the developmental signals that it is modulating have not been elucidated. By restoring the activity of LET-418/Mi2 in specific tissues, we demonstrate that its activity in the intestine and the hypodermis is able to promote in a cell non-autonomous manner the exit of blast cells from quiescence and further development. Furthermore, we identify the IIS (insulin/insulin-like growth factor signaling) pathway to be one of the signaling pathways that is conveying LET-418/Mi2 cell non-autonomous effect on development.

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Overlapping and non-overlapping roles of the class-I histone deacetylase-1 corepressors, LET-418, SIN-3, and SPR-1 in Caenorhabditis elegans embryonic development

10.1101/2020.07.21.213561 ◽

2020 ◽

Author(s):

Yukihiro Kubota ◽

Yuto Ohnishi ◽

Tasuku Hamasaki ◽

Gen Yasui ◽

Natsumi Ota ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Embryonic Development ◽

Histone Deacetylases ◽

Class I ◽

Biological Processes ◽

Nucleosome Remodeling ◽

C Elegans ◽

Histone Deacetylase 1 ◽

Genome Wide ◽

Sin3 Complex

AbstractHistone deacetylases (HDACs) are divided into four classes. Class-I HDAC, HDAC-1 forms three types of complexes, namely the Nucleosome Remodeling Deacetylase complex, the Sin3 complex, and the CoREST complex, with specific corepressor component Mi2/CHD-3, Sin3, and RCOR1 in human, respectively. The functions of these HDAC-1 complexes are regulated by their corepressors, however, their exact mechanistic roles in several biological processes remain unexplored, such as in embryonic development. Here, we report that each of the corepressors, LET-418, SIN-3, and SPR-1, the homologous of Mi2, Sin3, and RCOR1, respectively, were expressed throughout Caenorhabditis elegans embryonic development and served essential roles in the process. Moreover, genetic analysis suggested that three pathways (i.e., LET-418– SIN-3–SPR-1, SIN-3–SPR-1, and LET-418) participated in embryonic development. Our terminal-phenotype observations of single mutants of each corepressor implied that LET-418, SIN-3, and SPR-1 played similar roles in promoting advancement to the middle and late embryonic stages. Genome-wide comparative-transcriptome analysis indicated that 47.5% and 42.3% of genes were commonly increased and decreased in sin-3 and spr-1 mutants, respectively. These results suggest that among the three pathways studied, the SIN-3–SPR-1 pathway mainly serves to regulate embryonic development. Comparative-Gene Ontology analysis indicated that these three pathways played overlapping and distinct roles in regulating C. elegans embryonic development.

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Interplay of RFX transcription factors 1, 2 and 3 in motile ciliogenesis

Nucleic Acids Research ◽

10.1093/nar/gkaa625 ◽

2020 ◽

Vol 48 (16) ◽

pp. 9019-9036

Author(s):

Sylvain Lemeille ◽

Marie Paschaki ◽

Dominique Baas ◽

Laurette Morlé ◽

Jean-Luc Duteyrat ◽

...

Keyword(s):

Transcription Factors ◽

Transcriptional Control ◽

Ex Vivo ◽

Ependymal Cells ◽

Clear Understanding ◽

Animal Development ◽

C Elegans ◽

And Function ◽

Redundant Functions

Abstract Cilia assembly is under strict transcriptional control during animal development. In vertebrates, a hierarchy of transcription factors (TFs) are involved in controlling the specification, differentiation and function of multiciliated epithelia. RFX TFs play key functions in the control of ciliogenesis in animals. Whereas only one RFX factor regulates ciliogenesis in C. elegans, several distinct RFX factors have been implicated in this process in vertebrates. However, a clear understanding of the specific and redundant functions of different RFX factors in ciliated cells remains lacking. Using RNA-seq and ChIP-seq approaches we identified genes regulated directly and indirectly by RFX1, RFX2 and RFX3 in mouse ependymal cells. We show that these three TFs have both redundant and specific functions in ependymal cells. Whereas RFX1, RFX2 and RFX3 occupy many shared genomic loci, only RFX2 and RFX3 play a prominent and redundant function in the control of motile ciliogenesis in mice. Our results provide a valuable list of candidate ciliary genes. They also reveal stunning differences between compensatory processes operating in vivo and ex vivo.

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The C. elegans septin genes, unc-59 and unc-61, are required for normal postembryonic cytokineses and morphogenesis but have no essential function in embryogenesis

Journal of Cell Science ◽

10.1242/jcs.113.21.3825 ◽

2000 ◽

Vol 113 (21) ◽

pp. 3825-3837 ◽

Cited By ~ 4

Author(s):

T.Q. Nguyen ◽

H. Sawa ◽

H. Okano ◽

J.G. White

Keyword(s):

Caenorhabditis Elegans ◽

Embryonic Development ◽

Sensory Neurons ◽

Leading Edge ◽

The Other ◽

Male Tail ◽

Genomic Database ◽

C Elegans ◽

Essential Function ◽

Normal Embryonic Development

Septins have been shown to play important roles in cytokinesis in diverse organisms ranging from yeast to mammals. In this study, we show that both the unc-59 and unc-61 loci encode Caenorhabditis elegans septins. Genomic database searches indicate that unc-59 and unc-61 are probably the only septin genes in the C. elegans genome. UNC-59 and UNC-61 localize to the leading edge of cleavage furrows and eventually reside at the midbody. Analysis of unc-59 and unc-61 mutants revealed that each septin requires the presence of the other for localization to the cytokinetic furrow. Surprisingly, unc-59 and unc-61 mutants generally have normal embryonic development; however, defects were observed in post-embryonic development affecting the morphogenesis of the vulva, male tail, gonad, and sensory neurons. These defects can be at least partially attributed to failures in post-embryonic cytokineses although our data also suggest other possible roles for septins. unc-59 and unc-61 double mutants show similar defects to each of the single mutants.

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