Journal
DEVELOPMENTAL CELL
Volume 36, Issue 5, Pages 487-497Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2016.02.008
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Funding
- Japanese Society for the Promotion of Science (JSPS)
- Ministry of Education, Culture, Sports and Technology of Japan (MEXT)
- NIH [R01GM088371]
- Grants-in-Aid for Scientific Research [26640086, 14J12222] Funding Source: KAKEN
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Incorrect attachment of kinetochore microtubules is the leading cause of chromosome missegregation in cancers. The highly conserved chromosomal passenger complex (CPC), containing mitotic kinase Aurora B as a catalytic subunit, ensures faithful chromosome segregation through destabilizing incorrect microtubule attachments and promoting biorientation of chromosomes on the mitotic spindle. It is unknown whether CPC dysfunction affects chromosome segregation fidelity in cancers and, if so, how. Here, we show that heterochromatin protein 1 (HP1) is an essential CPC component required for full Aurora B activity. HP1 binding to the CPC becomes particularly important when Aurora B phos-phorylates kinetochore targets to eliminate erroneous microtubule attachments. Remarkably, a reduced proportion of HP1 bound to CPC is widespread in cancers, which causes an impairment in Aurora B activity. These results indicate that HP1 is an essential modulator for CPC function and identify a molecular basis for chromosome segregation errors in cancer cells.
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