scholarly journals 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

2017 ◽  
Vol 429 (1) ◽  
pp. 335-342 ◽  
Author(s):  
Qinfang Shen ◽  
Herong Shi ◽  
Chenxi Tian ◽  
Vikas Ghai ◽  
Jun Liu
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Blast Cell ◽  
C Elegans

scholarly journals PAG-3, a Zn-finger transcription factor, determines neuroblast fate in C. elegans

Development ◽  
2002 ◽  
Vol 129 (7) ◽  
pp. 1763-1774 ◽  
Author(s):  
Scott Cameron ◽  
Scott G. Clark ◽  
Joan B. McDermott ◽  
Eric Aamodt ◽  
H. Robert Horvitz
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Daughter Cell ◽  
Cell Lineage ◽  
Blast Cell ◽  
Cell Fates ◽  
Zinc Finger Transcription Factor ◽  
C Elegans ◽  
Mother Cells

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.

scholarly journals The transcriptional corepressor CTBP-1 acts with the SOX family transcription factor EGL-13 to maintain AIA interneuron cell identity in C. elegans

2021 ◽  
Author(s):  
Josh Saul ◽  
Takashi Hirose ◽  
Robert Horvitz
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Cell Fate ◽  
Transcriptional Corepressor ◽  
Cell Identity ◽  
C Elegans ◽  
Dna Binding Specificity ◽  
A Cell ◽  
Transcriptional Corepressors ◽  
And Function

Cell identity is characterized by a distinct combination of gene expression, cell morphology and cellular function established as progenitor cells divide and differentiate. Following establishment, cell identities can be unstable and require active and continuous maintenance throughout the remaining life of a cell. Mechanisms underlying the maintenance of cell identities are incompletely understood. Here we show that the gene ctbp-1, which encodes the transcriptional corepressor C-terminal binding protein-1 (CTBP-1), is essential for the maintenance of the identities of the two AIA interneurons in the nematode Caenorhabditis elegans. ctbp-1 is not required for the establishment of the AIA cell fate but rather functions cell-autonomously and can act in older worms to maintain proper AIA gene expression, morphology and function. From a screen for suppressors of the ctbp-1 mutant phenotype, we identified the gene egl-13, which encodes a SOX family transcription factor. We found that egl-13 regulates AIA function and aspects of AIA gene expression, but not AIA morphology. We conclude that the CTBP-1 protein maintains AIA cell identity in part by utilizing EGL-13 to repress transcriptional activity in the AIAs. More generally, we propose that transcriptional corepressors like CTBP-1 might be critical factors in the maintenance of cell identities, harnessing the DNA-binding specificity of transcription factors like EGL-13 to selectively regulate gene expression in a cell-specific manner.

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

Development ◽  
2011 ◽  
Vol 138 (6) ◽  
pp. 1033-1043 ◽  
Author(s):  
C. Tian ◽  
H. Shi ◽  
C. Colledge ◽  
M. Stern ◽  
R. Waterston ◽  
...  
Keyword(s):  
Cell Fate ◽  
Blast Cell ◽  
C Elegans ◽  
Differentiation Factors

scholarly journals Mechanism of life-long maintenance of neuron identity despite molecular fluctuations

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Joleen JH Traets ◽  
Servaas N van der Burght ◽  
Suzanne Rademakers ◽  
Gert Jansen ◽  
Jeroen S van Zon
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Experimental Evidence ◽  
Binding Site ◽  
Cell Fate ◽  
Network Architectures ◽  
Promoter Fragment ◽  
C Elegans ◽  
Long Timescales ◽  
Target Promoters

Cell fate is maintained over long timescales, yet molecular fluctuations can lead to spontaneous loss of this differentiated state. Our simulations identified a possible mechanism that explains life-long maintenance of ASE neuron fate in C. elegans by the terminal selector transcription factor CHE-1. Here, fluctuations in CHE-1 level are buffered by the reservoir of CHE-1 bound at its target promoters, which ensures continued che-1 expression by preferentially binding the che-1 promoter. We provide experimental evidence for this mechanism by showing that che-1 expression was resilient to induced transient CHE-1 depletion, while both expression of CHE-1 targets and ASE function were lost. We identified a 130 bp che-1 promoter fragment responsible for this resilience, with deletion of a homeodomain binding site in this fragment causing stochastic loss of ASE identity long after its determination. Because network architectures that support this mechanism are highly conserved in cell differentiation, it may explain stable cell fate maintenance in many systems.

scholarly journals Nanos promotes epigenetic reprograming of the germline by down-regulation of the THAP transcription factor LIN-15B

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Chih-Yung Sean Lee ◽  
Tu Lu ◽  
Geraldine Seydoux
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Transcriptional Activation ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Primordial Germ Cells ◽  
Germline Development ◽  
C Elegans ◽  
Maternal Transcripts ◽  
Underlying Mechanisms

Nanos RNA-binding proteins are required for germline development in metazoans, but the underlying mechanisms remain poorly understood. We have profiled the transcriptome of primordial germ cells (PGCs) lacking the nanos homologs nos-1 and nos-2 in C. elegans. nos-1nos-2 PGCs fail to silence hundreds of transcripts normally expressed in oocytes. We find that this misregulation is due to both delayed turnover of maternal transcripts and inappropriate transcriptional activation. The latter appears to be an indirect consequence of delayed turnover of the maternally-inherited transcription factor LIN-15B, a synMuvB class transcription factor known to antagonize PRC2 activity. PRC2 is required for chromatin reprogramming in the germline, and the transcriptome of PGCs lacking PRC2 resembles that of nos-1nos-2 PGCs. Loss of maternal LIN-15B restores fertility to nos-1nos-2 mutants. These findings suggest that Nanos promotes germ cell fate by downregulating maternal RNAs and proteins that would otherwise interfere with PRC2-dependent reprogramming of PGC chromatin.

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

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 921-932 ◽  
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.

scholarly journals Conversion of Germ Cells to Somatic Cell Types in C. elegans

2020 ◽  
Vol 8 (4) ◽  
pp. 24 ◽  
Author(s):  
Nida ul Fatima ◽  
Baris Tursun
Keyword(s):  
Transcription Factor ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Molecular Mechanisms ◽  
Essential Property ◽  
C Elegans ◽  
Differentiated Cells ◽  
A Cell

The potential of a cell to produce all types of differentiated cells in an organism is termed totipotency. Totipotency is an essential property of germ cells, which constitute the germline and pass on the parental genetic material to the progeny. The potential of germ cells to give rise to a whole organism has been the subject of intense research for decades and remains important in order to better understand the molecular mechanisms underlying totipotency. A better understanding of the principles of totipotency in germ cells could also help to generate this potential in somatic cell lineages. Strategies such as transcription factor-mediated reprogramming of differentiated cells to stem cell-like states could benefit from this knowledge. Ensuring pluripotency or even totipotency of reprogrammed stem cells are critical improvements for future regenerative medicine applications. The C. elegans germline provides a unique possibility to study molecular mechanisms that maintain totipotency and the germ cell fate with its unique property of giving rise to meiotic cells Studies that focused on these aspects led to the identification of prominent chromatin-repressing factors such as the C. elegans members of the Polycomb Repressive Complex 2 (PRC2). In this review, we summarize different factors that were recently identified, which use molecular mechanisms such as control of protein translation or chromatin repression to ensure maintenance of totipotency and the germline fate. Additionally, we focus on recently identified factors involved in preventing transcription-factor-mediated conversion of germ cells to somatic lineages. These so-called reprogramming barriers have been shown in some instances to be conserved with regard to their function as a cell fate safeguarding factor in mammals. Overall, continued studies assessing the different aspects of molecular pathways involved in maintaining the germ cell fate in C. elegans may provide more insight into cell fate safeguarding mechanisms also in other species.

scholarly journals The C. elegans RUNX transcription factor RNT-1/MAB-2 is required for asymmetrical cell division of the T blast cell

2005 ◽  
Vol 287 (2) ◽  
pp. 262-273 ◽  
Author(s):  
Hiroshi Kagoshima ◽  
Hitoshi Sawa ◽  
Shohei Mitani ◽  
Thomas R. Bürglin ◽  
Katsuya Shigesada ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Blast Cell ◽  
C Elegans ◽  
Asymmetrical Cell Division

scholarly journals Mechanism of life-long maintenance of neuron identity despite molecular fluctuations

2020 ◽  
Author(s):  
Joleen J. H. Traets ◽  
Servaas N. van der Burght ◽  
Gert Jansen ◽  
Jeroen S. van Zon
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Binding Site ◽  
Cell Fate ◽  
Network Architectures ◽  
Promoter Fragment ◽  
C Elegans ◽  
Long Timescales ◽  
Target Promoters

SummaryCell fate is maintained over long timescales, yet molecular fluctuations can lead to spontaneous loss of this differentiated state. We uncovered a mechanism that explains life-long maintenance of ASE neuron fate in C. elegans by the terminal selector transcription factor CHE-1. Fluctuations in CHE-1 level are buffered by the reservoir of CHE-1 bound at its target promoters, which ensure continued che-1 expression by preferentially binding the che-1 promoter. We validated this mechanism by showing that che-1 expression was resilient to induced transient CHE-1 depletion, while both expression of CHE-1 targets and ASE function were lost. We identified a 130 bp che-1 promoter fragment responsible for this resilience, with deletion of a homeodomain binding site in this fragment causing stochastic loss of ASE identity long after its determination. Because network architectures that support this mechanism are highly conserved in cell differentiation, it may explain stable cell fate maintenance in many systems.

Sign in / Sign up

Export Citation Format

Share Document