scholarly journals The forkhead transcription factor LET-381 functions to pattern the C. elegans postembryonic mesoderm

2009 ◽  
Vol 331 (2) ◽  
pp. 514
Author(s):  
Nirav M. Amin ◽  
Herong Shi ◽  
Jun Liu
Keyword(s):  
Transcription Factor ◽  
Forkhead Transcription Factor ◽  
C Elegans

scholarly journals Asymmetric Arginine Dimethylation Determines Life Span in C. elegans by Regulating Forkhead Transcription Factor DAF-16

2011 ◽  
Vol 13 (5) ◽  
pp. 505-516 ◽  
Author(s):  
Yuta Takahashi ◽  
Hiroaki Daitoku ◽  
Keiko Hirota ◽  
Hiroko Tamiya ◽  
Atsuko Yokoyama ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Life Span ◽  
Forkhead Transcription Factor ◽  
C Elegans

Evolutionary conservation of redundancy between a diverged pair of forkhead transcription factor homologues

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4825-4835 ◽  
Author(s):  
L. Molin ◽  
A. Mounsey ◽  
S. Aslam ◽  
P. Bauer ◽  
J. Young ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Expression Patterns ◽  
Evolutionary Conservation ◽  
Early Embryo ◽  
Genetic Redundancy ◽  
Evolutionary Time ◽  
Forkhead Transcription Factor ◽  
C Elegans ◽  
Transitory Effect

The Caenorhabditis elegans gene pes-1 encodes a transcription factor of the forkhead family and is expressed in specific cells of the early embryo. Despite these observations suggesting pes-1 to have an important regulatory role in embryogenesis, inactivation of pes-1 caused no apparent phenotype. This lack of phenotype is a consequence of genetic redundancy. Whereas a weak, transitory effect was observed upon disruption of just T14G12.4 (renamed fkh-2) gene function, simultaneous disruption of the activity of both fkh-2 and pes-1 resulted in a penetrant lethal phenotype. Sequence comparison suggests these two forkhead genes are not closely related and the functional association of fkh-2 and pes-1 was only explored because of the similarity of their expression patterns. Conservation of the fkh-2/pes-1 genetic redundancy between C. elegans and the related species C. briggsae was demonstrated. Interestingly the redundancy in C. briggsae is not as complete as in C. elegans and this could be explained by alterations of pes-1 specific to the C. briggsae ancestry. With overlapping function retained on an evolutionary time-scale, genetic redundancy may be extensive and expression pattern data could, as here, have a crucial role in characterization of developmental processes.

scholarly journals Lineage-specific control of convergent differentiation by a Forkhead repressor

Development ◽  
2021 ◽  
Author(s):  
Karolina Mizeracka ◽  
Julia M. Rogers ◽  
Jonathan D. Rumley ◽  
Shai Shaham ◽  
Martha L. Bulyk ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Human Homolog ◽  
Cell Type ◽  
Forkhead Transcription Factor ◽  
C Elegans ◽  
A Cell ◽  
Identical Cell ◽  
Cell Type Specific ◽  
Activate Cell ◽  
Specific Control

During convergent differentiation, multiple developmental lineages produce a highly similar or identical cell type. However, few molecular players that drive convergent differentiation are known. Here, we show that the C. elegans Forkhead transcription factor UNC-130 is required in only one of three convergent lineages that produce the same glial cell type. UNC-130 acts transiently as a repressor in progenitors and newly-born terminal cells to allow the proper specification of cells related by lineage rather than by cell type or function. Specification defects correlate with UNC-130:DNA binding, and UNC-130 can be functionally replaced by its human homolog, the neural crest lineage determinant FoxD3. We propose that, in contrast to terminal selectors that activate cell-type specific transcriptional programs in terminally differentiating cells, UNC-130 acts early and specifically in one convergent lineage to produce a cell type that also arises from molecularly distinct progenitors in other lineages.

scholarly journals Specific collagens maintain the cuticle permeability barrier in Caenorhabditis elegans

Genetics ◽  
2021 ◽  
Author(s):  
Anjali Sandhu ◽  
Divakar Badal ◽  
Riya Sheokand ◽  
Shalini Tyagi ◽  
Varsha Singh
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Barrier Function ◽  
Permeability Barrier ◽  
Nematode Caenorhabditis Elegans ◽  
Zinc Finger Transcription Factor ◽  
Outermost Layer ◽  
C Elegans ◽  
Receptor Mutant ◽  
Antioxidant Machinery

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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