cdc-25.2, a Caenorhabditis elegans ortholog of cdc25 , is required for male tail morphogenesis

2017 ◽  
Vol 482 (4) ◽  
pp. 1213-1218 ◽  
Author(s):  
Sangmi Oh ◽  
Sunghee Yoon ◽  
Esther Youn ◽  
Ichiro Kawasaki ◽  
Yhong-Hee Shim
Keyword(s):  
Caenorhabditis Elegans ◽  
Male Tail

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

2000 ◽  
Vol 113 (21) ◽  
pp. 3825-3837 ◽  
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.

scholarly journals The Caenorhabditis elegans fate-determining gene mab-9 encodes a T-box protein required to pattern the posterior hindgut

2000 ◽  
Vol 14 (5) ◽  
pp. 596-603 ◽  
Author(s):  
Alison Woollard ◽  
Jonathan Hodgkin
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Transcriptional Regulators ◽  
Male Tail ◽  
T Box ◽  
Tail Development ◽  
Blast Cells ◽  
Direct Cell

Caenorhabditis elegans mab-9 mutants are defective in hindgut and male tail development because of cell fate transformations in two posterior blast cells, B and F. We have cloned mab-9 and show that it encodes a member of the T-box family of transcriptional regulators. MAB-9 localizes to the nucleus of B and F and their descendents during development, suggesting that it acts cell autonomously in the posterior hindgut to direct cell fate. T-box genes related to brachyury have also been implicated in hindgut patterning, and our results support models for an evolutionarily ancient role for these genes in hindgut formation.

scholarly journals Regulation of body length and male tail ray pattern formation of Caenorhabditis elegans by a member of TGF-beta family

Development ◽  
1999 ◽  
Vol 126 (6) ◽  
pp. 1337-1347 ◽  
Author(s):  
K. Morita ◽  
K.L. Chow ◽  
N. Ueno
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Length ◽  
Target Genes ◽  
Dependent Manner ◽  
Tgf Beta ◽  
Wild Type ◽  
Male Tail ◽  
C Elegans ◽  
Sensory Ray ◽  
Epistasis Analysis

We have identified a new member of the TGF-beta superfamily, CET-1, from Caenorhabditis elegans, which is expressed in the ventral nerve cord and other neurons. cet-1 null mutants have shortened bodies and male tail abnormal phenotype resembling sma mutants, suggesting cet-1, sma-2, sma-3 and sma-4 share a common pathway. Overexpression experiments demonstrated that cet-1 function requires wild-type sma genes. Interestingly, CET-1 appears to affect body length in a dose-dependent manner. Heterozygotes for cet-1 displayed body lengths ranging between null mutant and wild type, and overexpression of CET-1 in wild-type worms elongated body length close to lon mutants. In male sensory ray patterning, lack of cet-1 function results in ray fusions. Epistasis analysis revealed that mab-21 lies downstream and is negatively regulated by the cet-1/sma pathway in the male tail. Our results show that cet-1 controls diverse biological processes during C. elegans development probably through different target genes.

A BMP homolog acts as a dose-dependent regulator of body size and male tail patterning in Caenorhabditis elegans

Development ◽  
1999 ◽  
Vol 126 (2) ◽  
pp. 241-250 ◽  
Author(s):  
Y. Suzuki ◽  
M.D. Yandell ◽  
P.J. Roy ◽  
S. Krishna ◽  
C. Savage-Dunn ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Expression Pattern ◽  
Genetic Interactions ◽  
Loss Of Function ◽  
Male Tail ◽  
C Elegans ◽  
Reduced Body ◽  
Smad Signaling Pathway ◽  
Dose Dependent

We cloned the dbl-1 gene, a C. elegans homolog of Drosophila decapentaplegic and vertebrate BMP genes. Loss-of-function mutations in dbl-1 cause markedly reduced body size and defective male copulatory structures. Conversely, dbl-1 overexpression causes markedly increased body size and partly complementary male tail phenotypes, indicating that DBL-1 acts as a dose-dependent regulator of these processes. Evidence from genetic interactions indicates that these effects are mediated by a Smad signaling pathway, for which DBL-1 is a previously unidentified ligand. Our study of the dbl-1 expression pattern suggests a role for neuronal cells in global size regulation as well as male tail patterning.

Association of several small heat-shock proteins with reproductive tissues in the nematode Caenorhabditis elegans

2000 ◽  
Vol 351 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Lily DING ◽  
E. Peter M. CANDIDO
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Larval Stage ◽  
Small Heat Shock Proteins ◽  
Nematode Caenorhabditis Elegans ◽  
Male Tail ◽  
Reproductive Tissues ◽  
Fourth Larval Stage ◽  
Shock Proteins

Immunohistochemical data on 10 of the 14 small heat-shock (smHSPs) proteins in fourth larval stage and adult Caenorhabditis elegans show that the tissues expressing the greatest number of smHSPs are vulva (HSP12s, HSP43 and, under stress, HSP16s) and spermatheca (HSP12s, HSP25, HSP43 and, under stress, HSP16s). HSP43 is also expressed in male tail structures, and following heat-shock HSP16s are expressed in spermatids and spermatozoa.

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