scholarly journals Genetic Analysis of the Caenorhabditis elegans MAP Kinase Gene mpk-1

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 103-117 ◽  
Author(s):  
Mark R Lackner ◽  
Stuart K Kim
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Double Mutant ◽  
Cell Fates ◽  
Gain Of Function ◽  
Kinase Gene ◽  
Epistasis Analysis ◽  
Anchor Cell ◽  
Ets Transcription Factor

Abstract The Caenorhabditis elegans mpk-1 gene encodes a MAP kinase protein that plays an important role in Ras-mediated induction of vulval cell fates. We show that mutations that eliminate mpk-1 activity result in a highly penetrant, vulvaless phenotype. A double mutant containing a gain-of-function mpk-1 mutation and a gain-of-function mek mutation (MEK phosphorylates and activates MPK-1) exhibits a multivulva phenotype. These results suggest that mpk-1 may transduce most or all of the anchor cell signal. Epistasis analysis suggests that mpk-1 acts downstream of mek-2 (encodes a MEK homolog) and upstream of lin-1 (encodes an Ets transcription factor) in the anchor cell signaling pathway. Finally, mpk-1 may act together with let-60 ras in multiple developmental processes, as mpk-1 mutants exhibit nearly the same range of developmental phenotypes as let-60 ras mutants.

scholarly journals A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans.

1994 ◽  
Vol 8 (2) ◽  
pp. 160-173 ◽  
Author(s):  
M R Lackner ◽  
K Kornfeld ◽  
L M Miller ◽  
H R Horvitz ◽  
S K Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Cell Fates

scholarly journals The lin-11 LIM domain transcription factor is necessary for morphogenesis of C. elegans uterine cells

Development ◽  
1999 ◽  
Vol 126 (23) ◽  
pp. 5319-5326 ◽  
Author(s):  
A.P. Newman ◽  
G.Z. Acton ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
P.W. Sternberg
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Egg Laying ◽  
Wild Type ◽  
Lim Domain ◽  
C Elegans ◽  
Expression Studies ◽  
Vulval Precursor Cells ◽  
Cell Induction ◽  
Anchor Cell

The Caenorhabditis elegans hermaphrodite egg-laying system comprises several tissues, including the uterus and vulva. lin-11 encodes a LIM domain transcription factor needed for certain vulval precursor cells to divide asymmetrically. Based on lin-11 expression studies and the lin-11 mutant phenotype, we find that lin-11 is also required for C. elegans uterine morphogenesis. Specifically, lin-11 is expressed in the ventral uterine intermediate precursor (pi) cells and their progeny (the utse and uv1 cells), which connect the uterus to the vulva. Like (pi) cell induction, the uterine lin-11 expression responds to the uterine anchor cell and the lin-12-encoded receptor. In wild type animals, the utse, which forms the planar process at the uterine-vulval interface, fuses with the anchor cell. We found that, in lin-11 mutants, utse differentiation was abnormal, the utse failed to fuse with the anchor cell and a functional uterine-vulval connection was not made. These findings indicate that lin-11 is essential for uterine-vulval morphogenesis.

scholarly journals ELT-1, a GATA-like transcription factor, is required for epidermal cell fates in Caenorhabditis elegans embryos.

1997 ◽  
Vol 11 (13) ◽  
pp. 1651-1661 ◽  
Author(s):  
B D Page ◽  
W Zhang ◽  
K Steward ◽  
T Blumenthal ◽  
J R Priess
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Epidermal Cell ◽  
Cell Fates

COG-2, a sox domain protein necessary for establishing a functional vulval-uterine connection in Caenorhabditis elegans

Development ◽  
1999 ◽  
Vol 126 (1) ◽  
pp. 169-179 ◽  
Author(s):  
W. Hanna-Rose ◽  
M. Han
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Caenorhabditis Elegans ◽  
Late Stage ◽  
Egg Laying ◽  
Functional Connection ◽  
Seam Cell ◽  
Anchor Cell ◽  
Domain Protein ◽  
Lineage Analysis

In screens for mutants defective in vulval morphogenesis, multiple mutants were isolated in which the uterus and the vulva fail to make a proper connection. We describe five alleles that define the gene cog-2, for connection of gonad defective. To form a functional connection between the vulva and the uterus, the anchor cell must fuse with the multinucleate uterine seam cell, derived from uterine cells that adopt a (pi) lineage. In cog-2 mutants, the anchor cell does not fuse to the uterine seam cell and, instead, remains at the apex of the vulva, blocking the connection between the vulval and uterine lumens, resulting in an egg-laying defective phenotype. According to lineage analysis and expression assays for two (pi)-cell-specific markers, induction of the (pi) fate occurs normally in cog-2 mutants. We have cloned cog-2 and shown that it encodes a Sox family transcription factor that is expressed in the (pi) lineage. Thus, it appears that COG-2 is a transcription factor that regulates a late-stage aspect of uterine seam cell differentiation that specifically affects anchor cell-uterine seam cell fusion.

scholarly journals Caenorhabditis elegans lin-45 raf Is Essential for Larval Viability, Fertility and the Induction of Vulval Cell Fates

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 481-492
Author(s):  
Virginia Hsu ◽  
Cheri L Zobel ◽  
Eric J Lambie ◽  
Tim Schedl ◽  
Kerry Kornfeld
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Kinase ◽  
Map Kinase ◽  
Signal Transmission ◽  
Kinase Domain ◽  
Binding Domain ◽  
Protein Kinase Activity ◽  
Missense Mutations ◽  
Loss Of Function ◽  
Cell Fates

Abstract The protein kinase Raf is an important signaling protein. Raf activation is initiated by an interaction with GTP-bound Ras, and Raf functions in signal transmission by phosphorylating and activating a mitogen-activated protein (MAP) kinase kinase named MEK. We identified 13 mutations in the Caenorhabditis elegans lin-45 raf gene by screening for hermaphrodites with abnormal vulval formation or germline function. Weak, intermediate, and strong loss-of-function or null mutations were isolated. The phenotype caused by the most severe mutations demonstrates that lin-45 is essential for larval viability, fertility, and the induction of vulval cell fates. The lin-45(null) phenotype is similar to the mek-2(null) and mpk-1(null) phenotypes, indicating that LIN-45, MEK-2, and MPK-1 ERK MAP kinase function in a predominantly linear signaling pathway. The lin-45 alleles include three missense mutations that affect the Ras-binding domain, three missense mutations that affect the protein kinase domain, two missense mutations that affect the C-terminal 14-3-3 binding domain, three nonsense mutations, and one small deletion. The analysis of the missense mutations indicates that Ras binding, 14-3-3-binding, and protein kinase activity are necessary for full Raf function and suggests that a 14-3-3 protein positively regulates Raf-mediated signaling during C. elegans development.

scholarly journals Two nested gonadal inductions of the vulva in nematodes

Development ◽  
1997 ◽  
Vol 124 (1) ◽  
pp. 253-259 ◽  
Author(s):  
M.A. Felix ◽  
P.W. Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Nematode Species ◽  
Precursor Cells ◽  
Evolutionary Change ◽  
Cell Interactions ◽  
Cell Fates ◽  
Anchor Cell

How do intercellular signals that pattern cell fates vary in evolution? During nematode vulva development, precursor cells acquire one of three fates in a pattern centered around the gonadal anchor cell. Non-vulval fates are at the periphery, outer and inner vulval fates are towards the center. In Caenorhabditis elegans, the three fates are specified around the same time by an induction by the anchor cell and lateral signaling between the vulva precursor cells. We find that, in three other nematode species (Panagrolaimus, Oscheius and Rhabditella spp.) spanning two families, the centered pattern is obtained by two temporally distinct gonadal inductions. The first induction specifies vulval fates; the second induction specifies the inner vulval fates in a subset of the precursors' daughters. This evolutionary change in the spatiotemporal connectivity of cell interactions allows centering of the pattern between two precursors in Panagrolaimus.

scholarly journals Reciprocal EGFR signaling in the anchor cell ensures precise inter-organ connection during Caenorhabditis elegans vulval morphogenesis

Development ◽  
2022 ◽  
Vol 149 (1) ◽  
Author(s):  
Silvan Spiri ◽  
Simon Berger ◽  
Louisa Mereu ◽  
Andrew DeMello ◽  
Alex Hajnal
Keyword(s):  
Caenorhabditis Elegans ◽  
Egf Receptor ◽  
Adherens Junctions ◽  
Egfr Signaling ◽  
Cell Fates ◽  
Vulval Development ◽  
Sequence Of Events ◽  
Epidermal Growth ◽  
Short And Long Term ◽  
Anchor Cell

ABSTRACT During Caenorhabditis elegans vulval development, the uterine anchor cell (AC) first secretes an epidermal growth factor (EGF) to specify the vulval cell fates and then invades the underlying vulval epithelium. By doing so, the AC establishes direct contact with the invaginating primary vulF cells and attaches the developing uterus to the vulva. The signals involved and the exact sequence of events joining these two organs are not fully understood. Using a conditional let-23 EGF receptor (EGFR) allele along with novel microfluidic short- and long-term imaging methods, we discovered a specific function of the EGFR in the AC during vulval lumen morphogenesis. Tissue-specific inactivation of let-23 in the AC resulted in imprecise alignment of the AC with the primary vulval cells, delayed AC invasion and disorganized adherens junctions at the contact site forming between the AC and the dorsal vulF toroid. We propose that EGFR signaling, activated by a reciprocal EGF cue from the primary vulval cells, positions the AC at the vulval midline, guides it during invasion and assembles a cytoskeletal scaffold organizing the adherens junctions that connect the developing uterus to the dorsal vulF toroid. Thus, EGFR signaling in the AC ensures the precise alignment of the two developing organs.

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