Acetylation of Nup62 by TIP60 ensures accurate chromosome segregation in mitosis.
Nup62
TIP60
acetylation
mitosis
spindle
Journal
Journal of molecular cell biology
ISSN: 1759-4685
Titre abrégé: J Mol Cell Biol
Pays: United States
ID NLM: 101503669
Informations de publication
Date de publication:
26 12 2022
26 12 2022
Historique:
received:
27
03
2022
revised:
14
06
2022
accepted:
29
09
2022
pubmed:
4
10
2022
medline:
16
2
2023
entrez:
3
10
2022
Statut:
ppublish
Résumé
Stable transmission of genetic information during cell division requires faithful mitotic spindle assembly and chromosome segregation. In eukaryotic cells, nuclear envelope breakdown (NEBD) is required for proper chromosome segregation. Although a list of mitotic kinases has been implicated in NEBD, how they coordinate their activity to dissolve the nuclear envelope and protein machinery such as nuclear pore complexes was unclear. Here, we identified a regulatory mechanism in which Nup62 is acetylated by TIP60 in human cell division. Nup62 is a novel substrate of TIP60, and the acetylation of Lys432 by TIP60 dissolves nucleoporin Nup62-Nup58-Nup54 complex during entry into mitosis. Importantly, this acetylation-elicited remodeling of nucleoporin complex promotes the distribution of Nup62 to the mitotic spindle, which is indispensable for orchestrating correct spindle orientation. Moreover, suppression of Nup62 perturbs accurate chromosome segregation during mitosis. These results establish a previously uncharacterized regulatory mechanism in which TIP60-elicited nucleoporin dynamics promotes chromosome segregation in mitosis.
Identifiants
pubmed: 36190325
pii: 6747133
doi: 10.1093/jmcb/mjac056
pmc: PMC9926331
pii:
doi:
Substances chimiques
Nuclear Pore Complex Proteins
0
nuclear pore protein p62
0
KAT5 protein, human
EC 2.3.1.48
Lysine Acetyltransferase 5
EC 2.3.1.48
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) (2022). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, CEMCS, CAS.
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