Journal
CELL REPORTS
Volume 38, Issue 4, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2021.110286
Keywords
-
Categories
Funding
- BBSRC [BB/L006324/1, BB/P007856/1]
- Leverhulme Trust project [RPG-2017-023]
- Midlands Integrative Biosciences Training Partnership
- UK-Thailand Research and Innovation Partnership Fund [623760210]
- UK Department for Business, Energy and Industrial Strategy
- Breast Cancer Now [CTR-QR14-007]
- NHS
Ask authors/readers for more resources
Selective autophagy regulates innate immune responses in Drosophila by removing the Tak1/Tab2 signaling complex, preventing constitutive activation of the IMD pathway.
Selective autophagy is a catabolic route that turns over specific cellular material for degradation by lysosomes, and whose role in the regulation of innate immunity is largely unexplored. Here, we show that the apical kinase of the Drosophila immune deficiency (IMD) pathway Tak1, as well as its co-activator Tab2, are both selective autophagy substrates that interact with the autophagy protein Atg8a. We also present a role for the Atg8a-interacting protein Sh3px1 in the downregulation of the IMD pathway, by facilitating targeting of the Tak1/Tab2 complex to the autophagy platform through its interaction with Tab2. Our findings show the Tak1/Tab2/Sh3px1 interactions with Atg8a mediate the removal of the Tak1/Tab2 signaling complex by selective autophagy. This in turn prevents constitutive activation of the IMD pathway in Drosophila. This study provides mechanistic insight on the regulation of innate immune responses by selective autophagy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available