| First Author | Su X | Year | 2018 |
| Journal | Cell Death Dis | Volume | 9 |
| Issue | 3 | Pages | 302 |
| PubMed ID | 29467473 | Mgi Jnum | J:272362 |
| Mgi Id | MGI:6284478 | Doi | 10.1038/s41419-018-0370-y |
| Citation | Su X, et al. (2018) Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development. Cell Death Dis 9(3):302 |
| abstractText | 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. |
