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Titolo:
Genetic analysis demonstrates a direct link between Rho signaling and nonmuscle myosin function during Drosophila morphogenesis
Autore:
Halsell, SR; Chu, BI; Kiehart, DP;
Indirizzi:
Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA Duke Univ DurhamNC USA 27710 d Ctr, Dept Cell Biol, Durham, NC 27710 USA
Titolo Testata:
GENETICS
fascicolo: 3, volume: 155, anno: 2000,
pagine: 1253 - 1265
SICI:
0016-6731(200007)155:3<1253:GADADL>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GTP-BINDING PROTEIN; CELL-SHAPE CHANGES; MYOTONIC-DYSTROPHY KINASE; HEAVY-CHAIN GENE; LIGHT-CHAIN; SACCHAROMYCES-CEREVISIAE; EPITHELIAL MORPHOGENESIS; DICTYOSTELIUM-DISCOIDEUM; CYTOPLASMIC MYOSIN; FOCAL ADHESIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
79
Recensione:
Indirizzi per estratti:
Indirizzo: Kiehart, DP Duke Univ, Med Ctr, Dept Cell Biol, Res Dr,307 Nanaline Duke Bldg, Durham,NC 27710 USA Duke Univ Res Dr,307 Nanaline Duke Bldg Durham NC USA 27710 SA
Citazione:
S.R. Halsell et al., "Genetic analysis demonstrates a direct link between Rho signaling and nonmuscle myosin function during Drosophila morphogenesis", GENETICS, 155(3), 2000, pp. 1253-1265

Abstract

A dynamic actomyosin cytoskeleton drives many morphogenetic events. Conventional nonmuscle myosin-II (myosin) is a key chemomechanical motor that drives contraction of the actin cytoskeleton. We have explored the regulation of myosin activity by performing genetic screens to identify gene products that collaborate with myosin during Drosophila morphogenesis. Specifically,we screened for second-site noncomplementors of a mutation in the zipper gene that encodes the nonmuscle myosin-II heavy chain. We determined. that asingle missense mutation in the zipper(Ebr) allele gives rise to its sensitivity to second-site noncomplementation. Mie then identify the Rho signal transduction path way as necessary for proper myosin function. First we show that a lethal P-element insertion interacts genetically with zipper. Subsequently we show that this second-site noncomplementing mutation disrupts the RhoGEF2 locus. Next, we show that two EMS-induced mutations, previously shown to interact genetically with zipper(Ebr) disrupt the RhoA locus. Further, we have identified their molecular lesions and determined that disruption of the carboxyl-terminal CaaX box gives rise to their mutant phenotype. Finally, we show that RhoA mutations themselves can be utilized in geneticscreens. Biochemical and cell analyses suggest that Rho signal transduction regulated the activity of myosin. Our studies provide direct genetic proof of the biological relevance of regulation of myosin by Rho signal transduction in an intact metazoan.

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Documento generato il 18/01/21 alle ore 14:36:15