Abstract:
:Dynamic assembly and disassembly of actin filaments is a major driving force for cell movements. Border cells in the Drosophila ovary provide a simple and genetically tractable model to study the mechanisms regulating cell migration. To identify new genes that regulate cell movement in vivo, we screened lethal mutations on chromosome 3R for defects in border cell migration and identified two alleles of the gene psidin (psid). In vitro, purified Psid protein bound F-actin and inhibited the interaction of tropomyosin with F-actin. In vivo, psid mutations exhibited genetic interactions with the genes encoding tropomyosin and cofilin. Border cells overexpressing Psid together with GFP-actin exhibited altered protrusion/retraction dynamics. Psid knockdown in cultured S2 cells reduced, and Psid overexpression enhanced, lamellipodial dynamics. Knockdown of the human homolog of Psid reduced the speed and directionality of migration in wounded MCF10A breast epithelial monolayers, whereas overexpression of the protein increased migration speed and altered protrusion dynamics in EGF-stimulated cells. These results indicate that Psid is an actin regulatory protein that plays a conserved role in protrusion dynamics and cell migration.
journal_name
Genes Devjournal_title
Genes & developmentauthors
Kim JH,Cho A,Yin H,Schafer DA,Mouneimne G,Simpson KJ,Nguyen KV,Brugge JS,Montell DJdoi
10.1101/gad.2028611subject
Has Abstractpub_date
2011-04-01 00:00:00pages
730-41issue
7eissn
0890-9369issn
1549-5477pii
gad.2028611journal_volume
25pub_type
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