Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM), 1919 Route de Mende, 34293, Montpellier, France.
Max-Planck-Institute of Molecular Physiology, Otto-Hahn Str. 11, 44227, Dortmund, Germany.
Nat Commun. 2018 Oct 17;9(1):4308. doi: 10.1038/s41467-018-06767-0.
In many eukaryotic organisms cytokinesis is driven by a contractile actomyosin ring (CAR) that guides membrane invagination. What triggers CAR constriction at a precise time of the cell cycle is a fundamental question. In budding yeast CAR is assembled via a septin scaffold at the division site. A Hippo-like kinase cascade, the Mitotic Exit Network (MEN), promotes mitotic exit and cytokinesis, but whether and how these two processes are independently controlled by MEN is poorly understood. Here we show that a critical function of MEN is to promote displacement of the septin ring from the division site, which in turn is essential for CAR constriction. This is independent of MEN control over mitotic exit and involves recruitment of MEN components to the spindle pole body (SPB). Ubiquitination of the SPB scaffold Nud1 inhibits MEN signaling at the end of mitosis and prevents septin ring splitting, thus silencing the cytokinetic machinery.
在许多真核生物中，胞质分裂是由一个收缩的肌动球蛋白环（CAR）驱动的，该环指导膜内陷。细胞周期中 CAR 收缩的确切时间是什么触发的，这是一个基本问题。在出芽酵母中，CAR 通过在分裂位点的隔膜蛋白支架组装。Hippo 样激酶级联，即有丝分裂退出网络（MEN），促进有丝分裂退出和胞质分裂，但 MEN 是否以及如何独立控制这两个过程还知之甚少。在这里，我们表明 MEN 的一个关键功能是促进隔膜蛋白环从分裂位点的位移，这对于 CAR 收缩是必不可少的。这与 MEN 对有丝分裂退出的控制无关，并且涉及 MEN 成分向纺锤体极体（SPB）的招募。SPB 支架 Nud1 的泛素化在有丝分裂末期抑制 MEN 信号转导，并防止隔膜蛋白环分裂，从而沉默胞质分裂机制。
