TY - JOUR
T1 - Sleeping beauty transposon-based phenotypic analysis of mice: Lack of Arpc3 results in defective trophoblast outgrowth
AU - Yae, Kojiro
AU - Keng, Wee-Keong Vincent
AU - Koike, Masato
AU - Yusa, Kosuke
AU - Kouno, Michiyoshi
AU - Uno, Yoshihiro
AU - Kondoh, Gen
AU - Gotow, Takahiro
AU - Uchiyama, Yasuo
AU - Horie, Kyoji
AU - Takeda, Junji
PY - 2006/8/1
Y1 - 2006/8/1
N2 - The Sleeping Beauty (SB) transposon system has generated many transposon-insertional mutant mouse lines, some of which have resulted in embryonic lethality when bred to homozygosity. Here we report one such insertion mapped to the mouse actin-related protein complex subunit 3 gene (Arpc3). Arpc3 is a component of the Arp2/3 complex, which plays a major role in actin nucleation with Y-shaped branching from the mother actin filament in response to migration signaling. Arpc3 transposon-inserted mutants developed only to the blastocyst stage. In vitro blastocyst culture of Arpc3 mutants exhibited severe spreading impairment of trophoblasts. This phenotype was also observed in compound heterozygotes generated using conventional gene-targeted and transposon-inserted alleles. Arpc3-deficient mutants were shown to lack actin-rich structures in the spreading trophoblast. Electron microscopic analysis demonstrated the lack of mesh-like structures at the cell periphery, suggesting a role of Arpc3 in Y-shaped branching formation. These data indicate the importance of Arpc3 in the Arp2/3 complex for trophoblast outgrowth and suggest that Arpc3 may be indispensable for implantation.
AB - The Sleeping Beauty (SB) transposon system has generated many transposon-insertional mutant mouse lines, some of which have resulted in embryonic lethality when bred to homozygosity. Here we report one such insertion mapped to the mouse actin-related protein complex subunit 3 gene (Arpc3). Arpc3 is a component of the Arp2/3 complex, which plays a major role in actin nucleation with Y-shaped branching from the mother actin filament in response to migration signaling. Arpc3 transposon-inserted mutants developed only to the blastocyst stage. In vitro blastocyst culture of Arpc3 mutants exhibited severe spreading impairment of trophoblasts. This phenotype was also observed in compound heterozygotes generated using conventional gene-targeted and transposon-inserted alleles. Arpc3-deficient mutants were shown to lack actin-rich structures in the spreading trophoblast. Electron microscopic analysis demonstrated the lack of mesh-like structures at the cell periphery, suggesting a role of Arpc3 in Y-shaped branching formation. These data indicate the importance of Arpc3 in the Arp2/3 complex for trophoblast outgrowth and suggest that Arpc3 may be indispensable for implantation.
UR - http://www.scopus.com/inward/record.url?scp=33746947884&partnerID=8YFLogxK
U2 - 10.1128/MCB.00018-06
DO - 10.1128/MCB.00018-06
M3 - Journal article
C2 - 16880528
SN - 0270-7306
VL - 26
SP - 6185
EP - 6196
JO - Molecular and Cellular Biology
JF - Molecular and Cellular Biology
IS - 16
ER -