| First Author | Fernández-Miranda G | Year | 2011 |
| Journal | Development | Volume | 138 |
| Issue | 13 | Pages | 2661-72 |
| PubMed ID | 21613325 | Mgi Jnum | J:173575 |
| Mgi Id | MGI:5014467 | Doi | 10.1242/dev.066381 |
| Citation | Fernandez-Miranda G, et al. (2011) Genetic disruption of aurora B uncovers an essential role for aurora C during early mammalian development. Development 138(13):2661-72 |
| abstractText | Mitosis is controlled by multiple kinases that drive cell cycle progression and prevent chromosome mis-segregation. Aurora kinase B interacts with survivin, borealin and incenp to form the chromosomal passenger complex (CPC), which is involved in the regulation of microtubule-kinetochore attachments and cytokinesis. Whereas genetic ablation of survivin, borealin or incenp results in early lethality at the morula stage, we show here that aurora B is dispensable for CPC function during early cell divisions and aurora B-null embryos are normally implanted. This is due to a crucial function of aurora C during these early embryonic cycles. Expression of aurora C decreases during late blastocyst stages resulting in post-implantation defects in aurora B-null embryos. These defects correlate with abundant prometaphase figures and apoptotic cell death of the aurora B-deficient inner cell mass. Conditional deletion of aurora B in somatic cells that do not express aurora C results in chromosomal misalignment and lack of chromosome segregation. Re-expression of wild-type, but not kinase-dead, aurora C rescues this defect, suggesting functional overlap between these two kinases. Finally, aurora B-null cells partially arrest in the presence of nocodazole, suggesting that this kinase is not essential for the spindle assembly checkpoint. |
