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Bonucci, Martina; Kuperwasser, Nicolas; Barbe, Serena; Koka, Vonda; de Villeneuve, Delphine; Zhang, Chi; Srivastava, Nishit; Jia, Xiaoying; Stokes, Matthew P; Bienaimé, Frank; Verkarre, Virginie; Lopez, Jean Baptiste; Jaulin, Fanny; Pontoglio, Marco; Terzi, Fabiola; Delaval, Benedicte; Piel, Matthieu; Pende, Mario
Nature communications, 06/2020, Volume: 11, Issue: 1Journal Article
mTOR activation is essential and sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) and other genetic disorders. In disease models, a sharp increase of proliferation and cyst formation correlates with a dramatic loss of oriented cell division (OCD). We find that OCD distortion is intrinsically due to S6 kinase 1 (S6K1) activation. The concomitant loss of S6K1 in Tsc1-mutant mice restores OCD but does not decrease hyperproliferation, leading to non-cystic harmonious hyper growth of kidneys. Mass spectrometry-based phosphoproteomics for S6K1 substrates revealed Afadin, a known component of cell-cell junctions required to couple intercellular adhesions and cortical cues to spindle orientation. Afadin is directly phosphorylated by S6K1 and abnormally decorates the apical surface of Tsc1-mutant cells with E-cadherin and α-catenin. Our data reveal that S6K1 hyperactivity alters centrosome positioning in mitotic cells, affecting oriented cell division and promoting kidney cysts in conditions of mTOR hyperactivity.
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