Autophagy differentially regulates TNF receptor Fn14 by distinct mammalian Atg8 proteins

Hila Winer, Milana Fraiberg, Adi Abada, Tali Dadosh, Bat-Chen Tamim-Yecheskel and Zvulun Elazar ()
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Hila Winer: The Weizmann Institute of Science
Milana Fraiberg: The Weizmann Institute of Science
Adi Abada: The Weizmann Institute of Science
Tali Dadosh: The Weizmann Institute of Science
Bat-Chen Tamim-Yecheskel: The Weizmann Institute of Science
Zvulun Elazar: The Weizmann Institute of Science

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract Autophagy, a conserved membrane trafficking process, sequesters cytoplasmic components into autophagosomes and targets them for lysosomal degradation. The TNF receptor Fn14 participates in multiple intracellular signaling pathways and is strongly induced upon tissue injury and solid tumorigenesis. While Fn14 is a short-lived protein, the regulation of its levels is largely obscure. Here we uncover a role for autophagy in Fn14 turnover, wherein specific core autophagy Atg8 proteins play distinct roles: Fn14 accumulates in the ERGIC in absence of GABARAP but within endosomes in the vicinity of autophagic membranes in absence of GATE-16. Moreover, GABARAP regulates overall cellular levels of Fn14, whereas GATE-16 regulates TWEAK signaling by Fn14 and thereby NF-κB activity. These findings not only implicate different Atg8 proteins in distinct roles within the mechanism of selective autophagic regulation of Fn14, but may also provide a more general view of their role in mediating autophagosome biogenesis from different membrane sources.

Date: 2018
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DOI: 10.1038/s41467-018-06275-1

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