| First Author | Youngblood BA | Year | 2014 |
| Journal | Nucleic Acids Res | Volume | 42 |
| Issue | 13 | Pages | 8330-42 |
| PubMed ID | 24957598 | Mgi Jnum | J:218131 |
| Mgi Id | MGI:5616703 | Doi | 10.1093/nar/gku551 |
| Citation | Youngblood BA, et al. (2014) CstF-64 supports pluripotency and regulates cell cycle progression in embryonic stem cells through histone 3' end processing. Nucleic Acids Res 42(13):8330-42 |
| abstractText | Embryonic stem cells (ESCs) exhibit a unique cell cycle with a shortened G1 phase that supports their pluripotency, while apparently buffering them against pro-differentiation stimuli. In ESCs, expression of replication-dependent histones is a main component of this abbreviated G1 phase, although the details of this mechanism are not well understood. Similarly, the role of 3' end processing in regulation of ESC pluripotency and cell cycle is poorly understood. To better understand these processes, we examined mouse ESCs that lack the 3' end-processing factor CstF-64. These ESCs display slower growth, loss of pluripotency and a lengthened G1 phase, correlating with increased polyadenylation of histone mRNAs. Interestingly, these ESCs also express the tauCstF-64 paralog of CstF-64. However, tauCstF-64 only partially compensates for lost CstF-64 function, despite being recruited to the histone mRNA 3' end-processing complex. Reduction of tauCstF-64 in CstF-64-deficient ESCs results in even greater levels of histone mRNA polyadenylation, suggesting that both CstF-64 and tauCstF-64 function to inhibit polyadenylation of histone mRNAs. These results suggest that CstF-64 plays a key role in modulating the cell cycle in ESCs while simultaneously controlling histone mRNA 3' end processing. |
