title: Genetic disruption of aurora B uncovers an essential role for aurora C during early mammalian development.
abstract: 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.
authors: Cell Division and Cancer Group, Spanish National Cancer Research Center (CNIO), Madrid, Spain.
authors: Gonzalo
authors: G
authors: Fernández-Miranda
authors: Marianna
authors: M
authors: Trakala
authors: Javier
authors: J
authors: Martín
authors: Beatriz
authors: B
authors: Escobar
authors: Alejandra
authors: A
authors: González
authors: Norbert B
authors: NB
authors: Ghyselinck
authors: Sagrario
authors: S
authors: Ortega
authors: Marta
authors: M
authors: Cañamero
authors: Ignacio
authors: I
authors: Pérez de Castro
authors: Marcos
authors: M
authors: Malumbres