KAT2-mediated PLK4 acetylation contributes to genomic stability by preserving centrosome number

Marjorie Fournier; László Tora

doi:10.1080/23723556.2016.1270391

KAT2-mediated PLK4 acetylation contributes to genomic stability by preserving centrosome number

Mol Cell Oncol. 2016 Dec 16;4(2):e1270391. doi: 10.1080/23723556.2016.1270391. eCollection 2017.

Authors

Marjorie Fournier¹, László Tora²

Affiliations

¹ Sir William Dunn School of Pathology, University of Oxford , Oxford, UK.
² Development and Stem Cell Department, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France; Centre National de la Recherche Scientifique, UMR7104, Illkirch, France; Institut National de la Santé et de la Recherche Médicale, U964, Illkirch, France; Université de Strasbourg, Illkirch, France.

Abstract

We have recently identified the first human lysine (K) acetyltransferase 2A and 2B (called KAT2A/2B; known also as GCN5/PCAF, respectively)-dependent acetylome and revealed a mechanism by which KAT2A/2B-mediated acetylation of serine/threonine polo-like kinase 4 (PLK4) maintains correct centrosome number in human cells, therefore contributing to the maintenance of genome stability.¹.

Keywords: Acetylation; GCN5; PCAF; cell cycle; centrosome; genome stability; inhibition; kinase activity; polo like kinase 4 (PLK4); proteomic analysis.

Grants and funding

340551/ERC_/European Research Council/International