The C. elegans SoxC protein SEM-2 opposes differentiation factors to promote a proliferative blast cell fate in the postembryonic mesoderm

During Caenorhabditis elegans development, the patterns of cell divisions, cell fates and programmed cell deaths are reproducible from animal to animal. In a search for mutants with abnormal patterns of programmed cell deaths in the ventral nerve cord, we identified mutations in the gene pag-3, which encodes a zinc-finger transcription factor similar to the mammalian Gfi-1 and Drosophila Senseless proteins. In pag-3 mutants, specific neuroblasts express the pattern of divisions normally associated with their mother cells, producing with each reiteration an abnormal anterior daughter neuroblast and an extra posterior daughter cell that either terminally differentiates or undergoes programmed cell death, which accounts for the extra cell corpses seen in pag-3 mutants. In addition, some neurons do not adopt their normal fates in pag-3 mutants. The phenotype of pag-3 mutants and the expression pattern of the PAG-3 protein suggest that in some lineages pag-3 couples the determination of neuroblast cell fate to subsequent neuronal differentiation. We propose that pag-3 counterparts in other organisms determine blast cell identity and for this reason may lead to cell lineage defects and cell proliferation when mutated.

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Control of cell fate in the tail region of C. elegans by the gene egl-5

Development ◽

10.1242/dev.111.4.921 ◽

1991 ◽

Vol 111 (4) ◽

pp. 921-932 ◽

Cited By ~ 22

Author(s):

A. Chisholm

Keyword(s):

Cell Fate ◽

Normal Development ◽

Blast Cell ◽

Body Region ◽

Tail Region ◽

C Elegans ◽

Somatic Gonad ◽

Animal Phyla ◽

Anterior Body ◽

Regional Determination

The tail region of C. elegans contains a number of blast cell and neuron types that either are found only in the tail, or are different from more anterior homologues. In egl-5 mutants, the fates of many of these tail cells are abnormal or transformed to those of anterior homologues. The affected cells are related only by position and not by ancestry. egl-5 is also required for normal development of the somatic gonad and sex muscles in males. The function of egl-5 in all these tissues is cell autonomous. By genetic mapping, egl-5 lies very close to mab-5, a gene with an analogous role in the immediately anterior body region. egl-5 and mab-5 may constitute a ‘mini-cluster’ of regional determination genes, similar to those described in other animal phyla.

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The C. elegans Spalt-like protein SEM-4 functions through the SoxC transcription factor SEM-2 to promote a proliferative blast cell fate in the postembryonic mesoderm

Developmental Biology ◽

10.1016/j.ydbio.2017.06.011 ◽

2017 ◽

Vol 429 (1) ◽

pp. 335-342 ◽

Cited By ~ 1

Author(s):

Qinfang Shen ◽

Herong Shi ◽

Chenxi Tian ◽

Vikas Ghai ◽

Jun Liu

Keyword(s):

Transcription Factor ◽

Cell Fate ◽

Blast Cell ◽

C Elegans

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Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

Biochemical Society Transactions ◽

10.1042/bst20200298 ◽

2020 ◽

Vol 48 (3) ◽

pp. 1243-1253 ◽

Cited By ~ 1

Author(s):

Sukriti Kapoor ◽

Sachin Kotak

Keyword(s):

Symmetry Breaking ◽

Cell Fate ◽

Cell Cortex ◽

Axis Formation ◽

Aurora A Kinase ◽

Aurora A ◽

C Elegans ◽

Cell Embryo ◽

Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

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Faculty Opinions recommendation of TLP-1 is an asymmetric cell fate determinant that responds to Wnt signals and controls male tail tip morphogenesis in C. elegans.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1004971.57956 ◽

2002 ◽

Author(s):

Bruce Bowerman

Keyword(s):

Cell Fate ◽

Male Tail ◽

C Elegans ◽

Cell Fate Determinant ◽

Tail Tip

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Faculty Opinions recommendation of Perinuclear Anchoring of H3K9-Methylated Chromatin Stabilizes Induced Cell Fate in C. elegans Embryos.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725963375.793559128 ◽

2019 ◽

Author(s):

Jonathan Epstein

Keyword(s):

Cell Fate ◽

C Elegans

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Dauer larva quiescence alters the circuitry of microRNA pathways regulating cell fate progression in C. elegans

Development ◽

10.1242/dev.075986 ◽

2012 ◽

Vol 139 (12) ◽

pp. 2177-2186 ◽

Cited By ~ 28

Author(s):

X. Karp ◽

V. Ambros

Keyword(s):

Cell Fate ◽

C Elegans ◽

Dauer Larva

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CFP-1 interacts with HDAC1/2 complexes inC. elegansdevelopment

10.1101/451237 ◽

2018 ◽

Author(s):

Bharat Pokhrel ◽

Yannic Chen ◽

Jonathan Joseph Biro

Keyword(s):

Cell Fate ◽

Embryonic Stem ◽

Stem Cell Differentiation ◽

Embryonic Stem Cell Differentiation ◽

Dependent Manner ◽

Cell Fate Specification ◽

C Elegans ◽

Evolutionarily Conserved ◽

Epigenetic Regulator ◽

Inducible Genes

AbstractCFP-1 (CXXC finger binding protein 1) is an evolutionarily conserved protein that binds to non-methylated CpG-rich promoters in humans andC. elegans. This conserved epigenetic regulator is a part of the COMPASS complex that contains the H3K4me3 methyltransferase SET1 in mammals and SET-2 inC. elegans. Previous studies have indicated the importance ofcfp-1in embryonic stem cell differentiation and cell fate specification. However, neither the function nor the mechanism of action ofcfp-1is well understood at the organismal level. To further investigate the function of CFP-1, we have characterisedC. elegansCOMPASS mutantscfp-1(tm6369)andset-2(bn129). We found that bothcfp-1andset-2play an important role in the regulation of fertility and development of the organism. Furthermore, we found that bothcfp-1andset-2are required for H3K4 trimethylation and play a repressive role in the expression of heat shock and salt-inducible genes. Interestingly, we found thatcfp-1but notset-2genetically interacts with Histone Deacetylase (HDAC1/2) complexes to regulate fertility, suggesting a function of CFP-1 outside of the COMPASS complex. Additionally we found thatcfp-1andset-2acts on a separate pathways to regulate fertility and development ofC. elegans. Our results suggest that CFP-1 genetically interacts with HDAC1/2 complexes to regulate fertility, independent of its function within COMPASS complex. We propose that CFP-1 could cooperate with COMPASS complex and/or HDAC1/2 in a context dependent manner.

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Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽

10.1242/dev.126.5.1011 ◽

1999 ◽

Vol 126 (5) ◽

pp. 1011-1022 ◽

Cited By ~ 8

Author(s):

T.L. Gumienny ◽

E. Lambie ◽

E. Hartwieg ◽

H.R. Horvitz ◽

M.O. Hengartner

Keyword(s):

Cell Death ◽

Caenorhabditis Elegans ◽

Germ Cell ◽

Somatic Cell ◽

Cell Fate ◽

Germ Cells ◽

Mapk Pathway ◽

Apoptotic Cell ◽

C Elegans ◽

Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

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