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2015 ; 17
(3
): 262-75
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Huntingtin functions as a scaffold for selective macroautophagy
#MMPMID25686248
Rui YN
; Xu Z
; Patel B
; Chen Z
; Chen D
; Tito A
; David G
; Sun Y
; Stimming EF
; Bellen HJ
; Cuervo AM
; Zhang S
Nat Cell Biol
2015[Mar]; 17
(3
): 262-75
PMID25686248
show ga
Selective macroautophagy is an important protective mechanism against diverse
cellular stresses. In contrast to the well-characterized starvation-induced
autophagy, the regulation of selective autophagy is largely unknown. Here, we
demonstrate that Huntingtin, the Huntington disease gene product, functions as a
scaffold protein for selective macroautophagy but it is dispensable for
non-selective macroautophagy. In Drosophila, Huntingtin genetically interacts
with autophagy pathway components. In mammalian cells, Huntingtin physically
interacts with the autophagy cargo receptor p62 to facilitate its association
with the integral autophagosome component LC3 and with Lys-63-linked
ubiquitin-modified substrates. Maximal activation of selective autophagy during
stress is attained by the ability of Huntingtin to bind ULK1, a kinase that
initiates autophagy, which releases ULK1 from negative regulation by mTOR. Our
data uncover an important physiological function of Huntingtin and provide a
missing link in the activation of selective macroautophagy in metazoans.
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