scholarly journals Transcriptional network underlying Caenorhabditis elegans vulval development

2005 ◽  
Vol 102 (14) ◽  
pp. 4972-4977 ◽  
Author(s):  
T. Inoue ◽  
M. Wang ◽  
T. O. Ririe ◽  
J. S. Fernandes ◽  
P. W. Sternberg
2005 ◽  
Vol 102 (6) ◽  
pp. 1951-1956 ◽  
Author(s):  
J. Fisher ◽  
N. Piterman ◽  
E. J. A. Hubbard ◽  
M. J. Stern ◽  
D. Harel

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4333-4342 ◽  
Author(s):  
J.C. Bettinger ◽  
S. Euling ◽  
A.E. Rougvie

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.


2006 ◽  
Vol 25 (11) ◽  
pp. 2347-2357 ◽  
Author(s):  
Attila Stetak ◽  
Erika Fröhli Hoier ◽  
Assunta Croce ◽  
Giuseppe Cassata ◽  
Pier Paolo Di Fiore ◽  
...  

PLoS Biology ◽  
2008 ◽  
Vol 6 (8) ◽  
pp. e196 ◽  
Author(s):  
Hidetoshi Komatsu ◽  
Michael Y Chao ◽  
Jonah Larkins-Ford ◽  
Mark E Corkins ◽  
Gerard A Somers ◽  
...  

1994 ◽  
Vol 5 (4) ◽  
pp. 395-411 ◽  
Author(s):  
L S Huang ◽  
P Tzou ◽  
P W Sternberg

During Caenorhabditis elegans vulval development, an inductive signal from the anchor cell stimulates three of the six vulval precursor cells (VPCs) to adopt vulval rather than nonvulval epidermal fates. Genes necessary for this induction include the lin-3 growth factor, the let-23 receptor tyrosine kinase, and let-60 ras. lin-15 is a negative regulator of this inductive pathway. In lin-15 mutant animals, all six VPCs adopt vulval fates, even in the absence of inductive signal. Previous genetic studies suggested that lin-15 is a complex locus with two independently mutable activities, A and B. We have cloned the lin-15 locus by germline transformation and find that it encodes two nonoverlapping transcripts that are transcribed in the same direction. The downstream transcript encodes the lin-15A function; the upstream transcript encodes the lin-15B function. The predicted lin-15A and lin-15B proteins are novel and hydrophilic. We have identified a molecular null allele of lin-15 and have used it to analyze the role of lin-15 in the signaling pathway. We find that lin-15 acts upstream of let-23 and in parallel to the inductive signal.


EMBO Reports ◽  
2005 ◽  
Vol 6 (12) ◽  
pp. 1169-1175 ◽  
Author(s):  
Stefano Canevascini ◽  
Mark Marti ◽  
Erika Fröhli ◽  
Alex Hajnal

2009 ◽  
Vol 20 (17) ◽  
pp. 3888-3895 ◽  
Author(s):  
Susan M. Hiatt ◽  
Holli M. Duren ◽  
Y. John Shyu ◽  
Ronald E. Ellis ◽  
Naoki Hisamoto ◽  
...  

Fos and Jun are components of activator protein-1 (AP-1) and play crucial roles in the regulation of many cellular, developmental, and physiological processes. Caenorhabditis elegans fos-1 has been shown to act in uterine and vulval development. Here, we provide evidence that C. elegans fos-1 and jun-1 control ovulation, a tightly regulated rhythmic program in animals. Knockdown of fos-1 or jun-1 blocks dilation of the distal spermathecal valve, a critical step for the entry of mature oocytes into the spermatheca for fertilization. Furthermore, fos-1 and jun-1 regulate the spermathecal-specific expression of plc-1, a gene that encodes a phospholipase C (PLC) isozyme that is rate-limiting for inositol triphosphate production and ovulation, and overexpression of PLC-1 rescues the ovulation defect in fos-1(RNAi) worms. Unlike fos-1, regulation of ovulation by jun-1 requires genetic interactions with eri-1 and lin-15B, which are involved in the RNA interference pathway and chromatin remodeling, respectively. At least two isoforms of jun-1 are coexpressed with fos-1b in the spermatheca, and different AP-1 dimers formed between these isoforms have distinct effects on the activation of a reporter gene. These findings uncover a novel role for FOS-1 and JUN-1 in the reproductive system and establish C. elegans as a model for studying AP-1 dimerization.


EMBO Reports ◽  
2002 ◽  
Vol 3 (3) ◽  
pp. 235-241 ◽  
Author(s):  
Florence Couteau ◽  
Fréderic Guerry ◽  
Fritz Müller ◽  
Francesca Palladino

2000 ◽  
Vol 11 (8) ◽  
pp. 2743-2756 ◽  
Author(s):  
Jaegal Shim ◽  
Paul W. Sternberg ◽  
Junho Lee

In the nematode Caenorhabditis elegans, there exist two μ1 medium chains of the AP-1 clathrin-associated protein complex. Mutations of unc-101, the gene that encodes one of the μ1 chains, cause pleiotropic effects ( Lee et al., 1994 ). In this report, we identified and analyzed the second μ1 chain gene, apm-1. Unlike the mammalian homologs, the two medium chains are expressed ubiquitously throughout development. RNA interference (RNAi) experiments with apm-1 showed thatapm-1 and unc-101 were redundant in embryogenesis and in vulval development. Consistent with this, a hybrid protein containing APM-1, when overexpressed, rescued the phenotype of an unc-101 mutant. However, single disruptions ofapm-1 or unc-101 have distinct phenotypes, indicating that the two medium chains may have distinct functions. RNAi of any one of the small or large chains of AP-1 complex (ς1, β1, or γ) showed a phenotype identical to that caused by the simultaneous disruption of unc-101 andapm-1, but not that by single disruption of either gene. This suggests that the two medium chains may share large and small chains in the AP-1 complexes. Thus, apm-1 andunc-101 encode two highly related μ1 chains that share redundant and distinct functions within AP-1 clathrin-associated protein complexes of the same tissue.


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