Amot and Yap1 regulate neuronal dendritic tree complexity and locomotor coordination in mice.

Autor: Rojek KO; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Krzemień J; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Doleżyczek H; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Boguszewski PM; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Kaczmarek L; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Konopka W; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland., Rylski M; Centre of Postgraduate Medical Education, Warsaw, Poland.; Institute of Psychiatry and Neurology, Warsaw, Poland., Jaworski J; International Institute of Molecular and Cell Biology, Warsaw, Poland., Holmgren L; Karolinska Institutet, Stockholm, Sweden., Prószyński TJ; Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Jazyk: angličtina
Zdroj: PLoS biology [PLoS Biol] 2019 May 01; Vol. 17 (5), pp. e3000253. Date of Electronic Publication: 2019 May 01 (Print Publication: 2019).
DOI: 10.1371/journal.pbio.3000253
Abstrakt: The angiomotin (Amot)-Yes-associated protein 1 (Yap1) complex plays a major role in regulating the inhibition of cell contact, cellular polarity, and cell growth in many cell types. However, the function of Amot and the Hippo pathway transcription coactivator Yap1 in the central nervous system remains unclear. We found that Amot is a critical mediator of dendritic morphogenesis in cultured hippocampal cells and Purkinje cells in the brain. Amot function in developing neurons depends on interactions with Yap1, which is also indispensable for dendrite growth and arborization in vitro. The conditional deletion of Amot and Yap1 in neurons led to a decrease in the complexity of Purkinje cell dendritic trees, abnormal cerebellar morphology, and impairments in motor coordination. Our results indicate that the function of Amot and Yap1 in dendrite growth does not rely on interactions with TEA domain (TEAD) transcription factors or the expression of Hippo pathway-dependent genes. Instead, Amot and Yap1 regulate dendrite development by affecting the phosphorylation of S6 kinase and its target S6 ribosomal protein.
Competing Interests: The authors have declared that no competing interests exist.
Databáze: MEDLINE
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