Abstract：
:During mitosis, kinetochores need to attach to microtubules emanating from spindle poles. Several protein complexes have been shown to mediate the kinetochore-microtubule interaction. However, with the continually growing number of newly identified kinetochore proteins, it is unclear whether all major components of the kinetochore-microtubule interface have been identified. We therefore performed a high-throughput RNAi screen to identify additional factors involved in kinetochore-microtubule attachment, and identified RAMA1 as a novel regulator of this process. Depletion of RAMA1 results in severe chromosome alignment defects and a checkpoint-dependent mitotic arrest. We show that this is due to reduced kinetochore-microtubule attachments. RAMA1 localizes to the spindle and to outer kinetochores throughout all phases of mitosis and is recruited to kinetochores by the core kinetochore-microtubule attachment factor Hec1. Interestingly, unlike Hec1, the association of RAMA1 with kinetochores is highly dynamic, suggesting that it is not a structural component of the kinetochore. Consistent with this, all other kinetochore proteins tested do not require RAMA1 for their kinetochore localization. Taken together, these results identify RAMA1 as a novel kinetochore protein and suggest that RAMA1 may have a direct role in mediating kinetochore-microtubule interactions.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Raaijmakers JA,Tanenbaum ME,Maia AF,Medema RHdoi
10.1242/jcs.051912subject
Has Abstractpub_date
2009-07-15 00:00:00pages
2436-45issue
Pt 14eissn
0021-9533issn
1477-9137pii
jcs.051912journal_volume
122pub_type
杂志文章abstract：:In situ observations of the development of hippocampal and cortical neurons indicate that final axon-dendrite identity is defined at the time of generation of the first two, oppositely positioned, neurites. Quite differently, in vitro studies demonstrated that axonal fate is defined by the stochastic selection of one ...
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abstract：:We have recently shown that leukotriene D(4) (LTD(4)) increases cell survival in intestinal epithelial cells. Here we report and explore the complementary finding that LTD(4) also enhances proliferation in these cells. This proliferative response was approximately half of that induced by epidermal growth factor (EGF) ...
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journal_title：Journal of cell science
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journal_title：Journal of cell science
pub_type： 杂志文章,评审
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journal_title：Journal of cell science
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doi：
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journal_title：Journal of cell science
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doi：
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journal_title：Journal of cell science
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doi：
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
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