The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation.
Animals
Aurora Kinase B
/ genetics
Cell Cycle Proteins
/ genetics
Drosophila
/ genetics
Drosophila Proteins
/ genetics
M Phase Cell Cycle Checkpoints
/ genetics
Mitosis
/ genetics
Neoplasms
/ metabolism
Phosphorylation
/ physiology
Protein Serine-Threonine Kinases
/ genetics
Spindle Apparatus
/ genetics
Journal
PLoS genetics
ISSN: 1553-7404
Titre abrégé: PLoS Genet
Pays: United States
ID NLM: 101239074
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
received:
03
09
2021
accepted:
14
03
2022
revised:
14
04
2022
pubmed:
5
4
2022
medline:
19
4
2022
entrez:
4
4
2022
Statut:
epublish
Résumé
The maintenance of a restricted pool of asymmetrically dividing stem cells is essential for tissue homeostasis. This process requires the control of mitotic progression that ensures the accurate chromosome segregation. In addition, this event is coupled to the asymmetric distribution of cell fate determinants in order to prevent stem cell amplification. How this coupling is regulated remains poorly described. Here, using asymmetrically dividing Drosophila neural stem cells (NSCs), we show that Polo kinase activity levels determine timely Cyclin B degradation and mitotic progression independent of the spindle assembly checkpoint (SAC). This event is mediated by the direct phosphorylation of Polo kinase by Aurora A at spindle poles and Aurora B kinases at centromeres. Furthermore, we show that Aurora A-dependent activation of Polo is the major event that promotes NSC polarization and together with the SAC prevents brain tumor growth. Altogether, our results show that an Aurora/Polo kinase module couples NSC mitotic progression and polarization for tissue homeostasis.
Identifiants
pubmed: 35377889
doi: 10.1371/journal.pgen.1010145
pii: PGENETICS-D-21-01184
pmc: PMC9009772
doi:
Substances chimiques
Cell Cycle Proteins
0
Drosophila Proteins
0
polo protein, Drosophila
EC 2.7.11.-
Aurora Kinase B
EC 2.7.11.1
Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1010145Subventions
Organisme : CIHR
Pays : Canada
Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
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