Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development

Xiaomin Su; Chenglei Wu; Xiaoying Ye; Ming Zeng; Zhujun Zhang; Yongzhe Che; Yuan Zhang; Lin Liu; Yushuang Lin; Rongcun Yang

doi:10.1038/s41419-018-0370-y

Developmental BiologyCell Death and DiseaseFeb 21, 2018

Peer-reviewed journal article

Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development

Xiaomin Su iD, Chenglei Wu iD, Xiaoying Ye iD, Ming Zeng iD, Zhujun Zhang iD, Yongzhe Che, Yuan Zhang iD, Lin Liu iD, Yushuang Lin iD, Rongcun Yang iD

Abstract

TRIM family members have been implicated in a variety of biological processes such as differentiation and development. We here found that Trim59 plays a critical role in early embryo development from blastocyst stage to gastrula. There existed delayed development and empty yolk sacs from embryonic day (E) 8.5 in Trim59 -/- embryos. No viable Trim59 -/- embryos were observed beyond E9.5. Trim59 deficiency affected primary germ layer formation at the beginning of gastrulation. In Trim59 -/- embryos at E6.5 and E7.5, the expression of primary germ layer formation associated genes including Brachyury, lefty2, Cer1, Otx2, Wnt3 and BMP4 was reduced. Homozygous mutant embryonic epiblast was contracted and the mesoderm was absent. Trim59 could interact with actin and myosin associated proteins. Trim59 deficiency disturbed F-actin polymerization during inner cell mass differentiation. Trim59 mediated polymerization of F-actin was via WASH K63-linked ubiquitination. Thus, Trim59 may be a critical regulator for early embryo development from blastocyst stage to gastrula through modulating F-actin assembly.

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