A link between mitotic entry and membrane growth suggests a novel model for cell size control

被引:51
作者
Anastasia, Steph D. [1 ]
Duy Linh Nguyen [1 ]
Vu Thai [1 ]
Meloy, Melissa [1 ]
MacDonough, Tracy [1 ]
Kellogg, Douglas R. [1 ]
机构
[1] Univ Calif Santa Cruz, Dept Mol Cell & Dev Biol, Santa Cruz, CA 95064 USA
基金
美国国家卫生研究院;
关键词
PROTEIN PHOSPHATASE 2A; GTP-BINDING PROTEIN; POST-GOLGI VESICLES; SACCHAROMYCES-CEREVISIAE; BUDDING YEAST; FISSION YEAST; CDC25; PROTEIN; TYROSINE PHOSPHORYLATION; MORPHOGENESIS CHECKPOINT; NEGATIVE REGULATION;
D O I
10.1083/jcb.201108108
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Addition of new membrane to the cell surface by membrane trafficking is necessary for cell growth. In this paper, we report that blocking membrane traffic causes a mitotic checkpoint arrest via Wee1-dependent inhibitory phosphorylation of Cdk1. Checkpoint signals are relayed by the Rho1 GTPase, protein kinase C (Pkc1), and a specific form of protein phosphatase 2A (PP2A(Cdc55)). Signaling via this pathway is dependent on membrane traffic and appears to increase gradually during polar bud growth. We hypothesize that delivery of vesicles to the site of bud growth generates a signal that is proportional to the extent of polarized membrane growth and that the strength of the signal is read by downstream components to determine when sufficient growth has occurred for initiation of mitosis. Growth-dependent signaling could explain how membrane growth is integrated with cell cycle progression. It could also control both cell size and morphogenesis, thereby reconciling divergent models for mitotic checkpoint function.
引用
收藏
页码:89 / 104
页数:16
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