BCAT1 redox function maintains mitotic fidelity

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Abstract: The metabolic enzyme branched-chain amino acid transaminase 1 (BCAT1) drives cell proliferation in aggressive cancers such as glioblastoma. Here, we show that BCAT1 localizes to mitotic structures and has a non-metabolic function as a mitotic regulator. Furthermore, BCAT1 is required for chromosome segregation in cancer and induced pluripotent stem cells and tumor growth in human cerebral organoid and mouse syngraft models. Applying gene knockout and rescue strategies, we show that the BCAT1 CXXC redox motif is crucial for controlling cysteine sulfenylation specifically in mitotic cells, promoting Aurora kinase B localization to centromeres, and securing accurate chromosome segregation. These findings offer an explanation for the well-established role of BCAT1 in promoting cancer cell proliferation. In summary, our data establish BCAT1 as a component of the mitotic apparatus that safeguards mitotic fidelity through a moonlighting redox functionality

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
Cell reports. - 41, 3 (2022) , 111524, ISSN: 2211-1247

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2022
Urheber
Francois, Liliana
Boskovic, Pavle
Knerr, Julian
He, Wei
Sigismondo, Gianluca
Schwan, Carsten
More, Tushar H.
Schlotter, Magdalena
Krijgsveld, Jeroen
Hiller, Karsten
Grosse, Robert
Lichter, Peter
Radlwimmer, Bernhard

DOI
10.1016/j.celrep.2022.111524
URN
urn:nbn:de:bsz:25-freidok-2309634
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
25.03.2025, 13:57 MEZ

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