scholarly journals Starvation activates MAP kinase through the muscarinic acetylcholine pathway in Caenorhabditis elegans pharynx

2006 ◽  
Vol 3 (4) ◽  
pp. 237-245 ◽  
Author(s):  
Young-jai You ◽  
Jeongho Kim ◽  
Melanie Cobb ◽  
Leon Avery
Keyword(s):  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Muscarinic Acetylcholine

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 MADD-3 LAMMER Kinase Interacts with a p38 MAP Kinase Pathway to Regulate the Display of the EVA-1 Guidance Receptor in Caenorhabditis elegans

PLoS Genetics ◽  
2016 ◽  
Vol 12 (4) ◽  
pp. e1006010 ◽  
Author(s):  
Serena A. D’Souza ◽  
Luckshi Rajendran ◽  
Rachel Bagg ◽  
Louis Barbier ◽  
Derek M. van Pel ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Motor Neurons ◽  
Leading Edge ◽  
P38 Map Kinase ◽  
Endosomal Trafficking ◽  
Guidance Cue ◽  
Map Kinase Pathway ◽  
Kinase Pathway

The proper display of transmembrane receptors on the leading edge of migrating cells and cell extensions is essential for their response to guidance cues. We previously discovered that MADD-4, which is an ADAMTSL secreted by motor neurons in Caenorhabditis elegans, interacts with an UNC-40/EVA-1 co-receptor complex on muscles to attract plasma membrane extensions called muscle arms. In nematodes, the muscle arm termini harbor the post-synaptic elements of the neuromuscular junction. Through a forward genetic screen for mutants with disrupted muscle arm extension, we discovered that a LAMMER kinase, which we call MADD-3, is required for the proper display of the EVA-1 receptor on the muscle’s plasma membrane. Without MADD-3, EVA-1 levels decrease concomitantly with a reduction of the late-endosomal marker RAB-7. Through a genetic suppressor screen, we found that the levels of EVA-1 and RAB-7 can be restored in madd-3 mutants by eliminating the function of a p38 MAP kinase pathway. We also found that EVA-1 and RAB-7 will accumulate in madd-3 mutants upon disrupting CUP-5, which is a mucolipin ortholog required for proper lysosome function. Together, our data suggests that the MADD-3 LAMMER kinase antagonizes the p38-mediated endosomal trafficking of EVA-1 to the lysosome. In this way, MADD-3 ensures that sufficient levels of EVA-1 are present to guide muscle arm extension towards the source of the MADD-4 guidance cue.

MAP kinase and Wnt pathways converge to downregulate an HMG-domain repressor in Caenorhabditis elegans

Nature ◽  
10.1038/21666 ◽  
1999 ◽  
Vol 399 (6738) ◽  
pp. 793-797 ◽  
Author(s):  
Marc D. Meneghini ◽  
Tohru Ishitani ◽  
J. Clayton Carter ◽  
Naoki Hisamoto ◽  
Jun Ninomiya-Tsuji ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Wnt Pathways

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.

Three genes of the MAP kinase cascade, mek-2, mpk-1/sur-1 and let-60 ras, are required for meiotic cell cycle progression in Caenorhabditis elegans

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2525-2535 ◽  
Author(s):  
D.L. Church ◽  
K.L. Guan ◽  
E.J. Lambie
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Germ Cells ◽  
Cell Cycle Progression ◽  
Extended Period ◽  
Meiotic Cell ◽  
Cycle Progression ◽  
C Elegans ◽  
Genetic Mosaic

In the germline of Caenorhabditis elegans hermaphrodites, meiotic cell cycle progression occurs in spatially restricted regions. Immediately after leaving the distal mitotic region, germ cells enter meiosis and thereafter remain in the pachytene stage of first meiotic prophase for an extended period. At the dorsoventral gonadal flexure, germ cells exit pachytene and subsequently become arrested in diakinesis. We have found that exit from pachytene is dependent on the function of three members of the MAP kinase signaling cascade. One of these genes, mek-2, is a newly identified C. elegans MEK (MAP kinase kinase). The other two genes, mpk-1/sur-1 (MAP kinase) and let-60 ras, were previously identified based on their roles in vulval induction and are shown here to act in combination with mek-2 to permit exit from pachytene. Through genetic mosaic analysis, we demonstrate that the expression of mpk-1/sur-1 is required within the germline to permit exit from pachytene.

scholarly journals Twitchin kinase interacts with MAPKAP kinase 2 in Caenorhabditis elegans striated muscle

2015 ◽  
Vol 26 (11) ◽  
pp. 2096-2111 ◽  
Author(s):  
Yohei Matsunaga ◽  
Hiroshi Qadota ◽  
Miho Furukawa ◽  
Heejoo (Helen) Choe ◽  
Guy M. Benian
Keyword(s):  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Striated Muscle ◽  
P38 Map Kinase ◽  
Dynamics Simulation ◽  
Catalytic Core ◽  
C Elegans ◽  
Map Kinase Pathway ◽  
Pulling Force

In Caenorhabditis elegans, twitchin is a giant polypeptide located in muscle A-bands. The protein kinase of twitchin is autoinhibited by 45 residues upstream (NL) and 60 residues downstream (CRD) of the kinase catalytic core. Molecular dynamics simulation on a twitchin fragment revealed that the NL is released by pulling force. However, it is unclear how the CRD is removed. To identify proteins that may remove the CRD, we performed a yeast two-hybrid screen using twitchin kinase as bait. One interactor is MAK-1, C. elegans orthologue of MAPKAP kinase 2. MAPKAP kinase 2 is phosphorylated and activated by p38 MAP kinase. We demonstrate that the CRD of twitchin is important for binding to MAK-1. mak-1 is expressed in nematode body wall muscle, and antibodies to MAK-1 localize between and around Z-disk analogues and to the edge of A-bands. Whereas unc-22 mutants are completely resistant, mak-1 mutants are partially resistant to nicotine. MAK-1 can phosphorylate twitchin NL-Kin-CRD in vitro. Genetic data suggest the involvement of two other mak-1 paralogues and two orthologues of p38 MAP kinase. These results suggest that MAK-1 is an activator of twitchin kinase and that the p38 MAP kinase pathway may be involved in the regulation of twitchin.

scholarly journals MAP Kinase Signaling Antagonizes PAR-1 Function During Polarization of the Early Caenorhabditis elegans Embryo

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 965-977 ◽  
Author(s):  
Annina C. Spilker ◽  
Alexia Rabilotta ◽  
Caroline Zbinden ◽  
Jean-Claude Labbé ◽  
Monica Gotta
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Cell Fate ◽  
Asymmetric Cell Division ◽  
Asymmetric Distribution ◽  
Kinase Signaling ◽  
C Elegans ◽  
Link Type ◽  
Map Kinase Signaling

PAR proteins (partitioning defective) are major regulators of cell polarity and asymmetric cell division. One of the par genes, par-1, encodes a Ser/Thr kinase that is conserved from yeast to mammals. In Caenorhabditis elegans, par-1 governs asymmetric cell division by ensuring the polar distribution of cell fate determinants. However the precise mechanisms by which PAR-1 regulates asymmetric cell division in C. elegans remain to be elucidated. We performed a genomewide RNAi screen and identified six genes that specifically suppress the embryonic lethal phenotype associated with mutations in par-1. One of these suppressors is mpk-1, the C. elegans homolog of the conserved mitogen activated protein (MAP) kinase ERK. Loss of function of mpk-1 restored embryonic viability, asynchronous cell divisions, the asymmetric distribution of cell fate specification markers, and the distribution of PAR-1 protein in par-1 mutant embryos, indicating that this genetic interaction is functionally relevant for embryonic development. Furthermore, disrupting the function of other components of the MAPK signaling pathway resulted in suppression of par-1 embryonic lethality. Our data therefore indicates that MAP kinase signaling antagonizes PAR-1 signaling during early C. elegans embryonic polarization.

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