Abstract:
:We have recently reported that Rootletin prevents Cep68 from VHL-mediated proteasomal degradation to maintain centrosome cohesion, unveiling the first underlying mechanism of a linker protein required for maintenance of centrosome cohesion. The minichromosome maintenance (MCM) proteins 2-7 have long been noticed to localize to centrosomes, but their functions at the centrosome are presently unknown. Here, we show that MCM7 directly binds to the centrosomal linker protein Cep68 in vitro and complexes with Cep68 and VHL in vivo. Absence of MCM7 weakened the interaction between Cep68 and VHL, whereas MCM7 overexpression facilitated the Cep68-VHL association. As a result of MCM7 overexpression, Cep68 was targeted for ubiquitination and proteasomal degradation, thereby rendering centrosome splitting. We propose that Cep68 protein level needs to be fine-tuned in order to ensure that its direct interactors, such as the microcephaly protein Cep215 and PCNT, function properly.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Kong L,Yin H,Yuan Ldoi
10.1016/j.bbrc.2017.05.180subject
Has Abstractpub_date
2017-08-05 00:00:00pages
497-502issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(17)31096-3journal_volume
489pub_type
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