Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development

Cell Death & Disease
Xiaomin SuRongcun Yang

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. 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 in Trim59-/- embryos. Homozygous mutant embryonic epiblasts were contracted and the mesoderm was absent. Trim59 could interact with actin- and myosin-associated proteins. Its 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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Citations

Nov 7, 2019·Stem Cells and Development·Valentina V Nenasheva, Vyacheslav Z Tarantul

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Methods Mentioned

BETA
ubiquitination
genotyping
two-hybrid
transfection
PCR
dissection
immunoprecipitation
fluorescence microscopy
confocal microscopy

Software Mentioned

ImageJ
Mascot
ProQuest
GraphPad
Prism
Excel

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