Mechanisms that license centrioles to duplicate in the right place and only once per cell cycle

2015 Fiscal Year Final Research Report

• Project/Area Number: 24687026
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Cell biology
• Research Institution: National Institute of Genetics
• Principal Investigator: Kitagawa Daiju 国立遺伝学研究所, 分子遺伝研究系, 教授 (80605725)
• Co-Investigator(Renkei-kenkyūsha): Shiratsuchi Gen 国立遺伝学研究所, 分子遺伝研究系, 博士研究員 (80625533)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 中心小体 / 中心体 / 細胞分裂 / 染色体分配 / 細胞がん化 / 分裂期紡錘体

Outline of Final Research Achievements

Formation of a new centriole adjacent to a pre-existing centriole occurs only once per cell cycle. Despite being crucial for genome integrity, the mechanisms controlling centriole biogenesis remain elusive. Here, we identify RBM14 as a novel suppressor of de novo assembly of centriolar protein complexes. Depletion of RBM14 in human cells induces ectopic formation of centriolar protein complexes through function of the STIL/CPAP complex. Moreover, we find that, upon RBM14 depletion, a part of the ectopic centriolar protein complexes in turn assemble into structures more akin to centrioles, presumably by incorporating cartwheel components, and cause multipolar spindle formation. We further demonstrate that such structures assemble in the cytoplasm even in the presence of pre-existing centrioles. This study sheds light on the possibility that ectopic formation of aberrant structures related to centrioles may contribute to genome instability and tumorigenesis.

Free Research Field

細胞生物学