Hsp70 and Hsp40 inhibit an inter-domain interaction necessary for transcriptional activity in the androgen receptor

Bahareh Eftekharzadeh(Institute for Research in Biomedicine), Varuna C. Banduseela(University of Michigan), Giulio Chiesa(Institute for Research in Biomedicine), Paula Martínez-Cristóbal(Institute for Research in Biomedicine), Jennifer N. Rauch(University of California, San Francisco), Samir R. Nath(University of Michigan), Daniel M. C. Schwarz(University of California, San Francisco), Hao Shao(University of California, San Francisco), Marta Marin‐Argany(Institute for Research in Biomedicine), Claudio Di Sanza(Institute for Research in Biomedicine), E. Giorgetti(University of Michigan), Zhigang Yu(University of Michigan), Roberta Pierattelli(University of Florence), Isabella C. Felli(University of Florence), Isabelle Brun‐Heath(Institute for Research in Biomedicine), Jesús García(Institute for Research in Biomedicine), Ángel R. Nebreda(Institució Catalana de Recerca i Estudis Avançats), Jason E. Gestwicki(University of California, San Francisco), Andrew P. Lieberman(University of Michigan), Xavier Salvatella(Institució Catalana de Recerca i Estudis Avançats)
Nature Communications
August 8, 2019
Cited by 85Open Access
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Abstract

Molecular chaperones such as Hsp40 and Hsp70 hold the androgen receptor (AR) in an inactive conformation. They are released in the presence of androgens, enabling transactivation and causing the receptor to become aggregation-prone. Here we show that these molecular chaperones recognize a region of the AR N-terminal domain (NTD), including a FQNLF motif, that interacts with the AR ligand-binding domain (LBD) upon activation. This suggests that competition between molecular chaperones and the LBD for the FQNLF motif regulates AR activation. We also show that, while the free NTD oligomerizes, binding to Hsp70 increases its solubility. Stabilizing the NTD-Hsp70 interaction with small molecules reduces AR aggregation and promotes its degradation in cellular and mouse models of the neuromuscular disorder spinal bulbar muscular atrophy. These results help resolve the mechanisms by which molecular chaperones regulate the balance between AR aggregation, activation and quality control.


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