CaltechAUTHORS
  A Caltech Library Service

Mutations in mákos, a Drosophila gene encoding the Cdc27 subunit of the anaphase promoting complex, enhance centrosomal defects in polo and are suppressed by mutations in twins/aar, which encodes a regulatory subunit of PP2A

Deák, Péter and Donaldson, Mary and Glover, David M. (2003) Mutations in mákos, a Drosophila gene encoding the Cdc27 subunit of the anaphase promoting complex, enhance centrosomal defects in polo and are suppressed by mutations in twins/aar, which encodes a regulatory subunit of PP2A. Journal of Cell Science, 116 (20). pp. 4147-4158. ISSN 0021-9533. doi:10.1242/jcs.00722. https://resolver.caltech.edu/CaltechAUTHORS:20201007-150756464

[img]
Preview
PDF - Published Version
See Usage Policy.

502kB

Use this Persistent URL to link to this item: https://resolver.caltech.edu/CaltechAUTHORS:20201007-150756464

Abstract

The gene mákos (mks) encodes the Drosophila counterpart of the Cdc27 subunit of the anaphase promoting complex (APC/C). Neuroblasts from third-larval-instar mks mutants arrest mitosis in a metaphase-like state but show some separation of sister chromatids. In contrast to metaphase-checkpoint-arrested cells, such mutant neuroblasts contain elevated levels not only of cyclin B but also of cyclin A. Mutations in mks enhance the reduced ability of hypomorphic polo mutant alleles to recruit and/or maintain the centrosomal antigens γ-tubulin and CP190 at the spindle poles. Absence of the MPM2 epitope from the spindle poles in such double mutants suggests Polo kinase is not fully activated at this location. Thus, it appears that spindle pole functions of Polo kinase require the degradation of early mitotic targets of the APC/C, such as cyclin A, or other specific proteins. The metaphase-like arrest of mks mutants cannot be overcome by mutations in the spindle integrity checkpoint gene bub1, confirming this surveillance pathway has to operate through the APC/C. However, mutations in the twins/aar gene, which encodes the 55kDa regulatory subunit of PP2A, do suppress the mks metaphase arrest and so permit an alternative means of initiating anaphase. Thus the APC/C might normally be required to inactivate wild-type twins/aar gene product.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.1242/jcs.00722DOIArticle
ORCID:
AuthorORCID
Glover, David M.0000-0003-0956-0103
Additional Information:© The Company of Biologists Limited 2003. Accepted 20 June 2003. We are grateful to Cancer Research UK for supporting this work. We thank R. Giet for carrying out H1 kinase assays and for valuable discussions.
Funders:
Funding AgencyGrant Number
Cancer Research UKUNSPECIFIED
Subject Keywords:APC/C, Cdc27, Polo kinase, 55kDa regulatory subunit of PP2A, Mitosis
Issue or Number:20
DOI:10.1242/jcs.00722
Record Number:CaltechAUTHORS:20201007-150756464
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20201007-150756464
Official Citation:Mutations in mákos, a Drosophila gene encoding the Cdc27 subunit of the anaphase promoting complex, enhance centrosomal defects in polo and are suppressed by mutations in twins/aar, which encodes a regulatory subunit of PP2A Péter Deák, Mary Donaldson, David M. Glover Journal of Cell Science 2003 116: 4147-4158; doi: 10.1242/jcs.00722
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:105903
Collection:CaltechAUTHORS
Deposited By: George Porter
Deposited On:07 Oct 2020 22:40
Last Modified:16 Nov 2021 18:47

Repository Staff Only: item control page