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PMID:16954378
| Citation |
Lu, ZH, Books, JT and Ley, TJ (2006) Cold shock domain family members YB-1 and MSY4 share essential functions during murine embryogenesis. Mol. Cell. Biol. 26:8410-7 |
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| Abstract |
Three cold shock domain (CSD) family members (YB-1, MSY2, and MSY4) exist in vertebrate species ranging from frogs to humans. YB-1 is expressed throughout embryogenesis and is ubiquitously expressed in adult animals; it protects cells from senescence during periods of proliferative stress. YB-1-deficient embryos die unexpectedly late in embryogenesis (embryonic day 18.5 [E18.5] to postnatal day 1) with a runting phenotype. We have now determined that MSY4, but not MSY2, is also expressed during embryogenesis; its abundance declines substantially from E9.5 to E17.5 and is undetectable on postnatal day 1(adult mice express MSY4 in testes only). Whole-mount analysis revealed similar patterns of YB-1 and MSY4 RNA expression in E11.5 embryos. To determine whether MSY4 delays the death of YB-1-deficient embryos, we created and analyzed MSY4-deficient mice and then generated YB-1 and MSY4 double-knockout embryos. MSY4 is dispensable for normal development and survival, but the testes of adult mice have excessive spermatocyte apoptosis and seminiferous tubule degeneration. Embryos doubly deficient for YB-1 and MSY4 are severely runted and die much earlier (E8.5 to E11.5) than YB-1-deficient embryos, suggesting that MSY4 indeed shares critical cellular functions with YB-1 in the embryonic tissues where they are coexpressed. |
| Links |
PubMed PMC1636768 Online version:10.1128/MCB.01196-06 |
| Keywords |
Animals; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; DNA-Binding Proteins/physiology; Embryonic Development; Female; Male; Mice; Mice, Knockout; Protein Structure, Tertiary; RNA, Messenger/metabolism; Seminiferous Tubules/physiopathology; Spermatocytes/physiology; Tissue Distribution |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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