The mechanism of sirtuin 2–mediated exacerbation of alpha-synuclein toxicity in models of Parkinson disease

نویسندگان

  • Rita Machado de Oliveira
  • Hugo Vicente Miranda
  • Laetitia Francelle
  • Raquel Pinho
  • Éva M Szegö
  • Renato Martinho
  • Francesca Munari
  • Diana F Lázaro
  • Sébastien Moniot
  • Patrícia Guerreiro
  • Luis Fonseca-Ornelas
  • Zrinka Marijanovic
  • Pedro Antas
  • Ellen Gerhardt
  • Francisco Javier Enguita
  • Bruno Fauvet
  • Deborah Penque
  • Teresa Faria Pais
  • Qiang Tong
  • Stefan Becker
  • Sebastian Kügler
  • Hilal Ahmed Lashuel
  • Clemens Steegborn
  • Markus Zweckstetter
  • Tiago Fleming Outeiro
چکیده

Sirtuin genes have been associated with aging and are known to affect multiple cellular pathways. Sirtuin 2 was previously shown to modulate proteotoxicity associated with age-associated neurodegenerative disorders such as Alzheimer and Parkinson disease (PD). However, the precise molecular mechanisms involved remain unclear. Here, we provide mechanistic insight into the interplay between sirtuin 2 and α-synuclein, the major component of the pathognomonic protein inclusions in PD and other synucleinopathies. We found that α-synuclein is acetylated on lysines 6 and 10 and that these residues are deacetylated by sirtuin 2. Genetic manipulation of sirtuin 2 levels in vitro and in vivo modulates the levels of α-synuclein acetylation, its aggregation, and autophagy. Strikingly, mutants blocking acetylation exacerbate α-synuclein toxicity in vivo, in the substantia nigra of rats. Our study identifies α-synuclein acetylation as a key regulatory mechanism governing α-synuclein aggregation and toxicity, demonstrating the potential therapeutic value of sirtuin 2 inhibition in synucleinopathies.

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عنوان ژورنال:

دوره 15  شماره 

صفحات  -

تاریخ انتشار 2017