dictyNews
Electronic Edition
Volume 49, number 11
April 28, 2023

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Abstracts
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A TRAF-like E3 ubiquitin ligase TrafE coordinates ESCRT and 
autophagy in endolysosomal damage response and cell-autonomous 
immunity to Mycobacterium marinum.

Lyudmil Raykov, Manon Mottet, Jahn Nitschke, Thierry Soldati


Published in eLife : https://elifesciences.org/articles/85727

Cells are perpetually challenged by pathogens, protein aggregates 
or chemicals, that induce plasma membrane or endolysosomal 
compartments damage. This severe stress is recognised and 
controlled by the endosomal sorting complex required for transport 
(ESCRT) and the autophagy machineries, which are recruited to 
damaged membranes to either repair or to remove membrane 
remnants. Yet, insight is limited about how damage is sensed and 
which effectors lead to extensive tagging of the damaged organelles 
with signals, such as K63-polyubiquitin, required for the 
recruitment of membrane repair or removal machineries. To explore 
the key factors responsible for detection and marking of damaged 
compartments, we use the professional phagocyte Dictyostelium 
discoideum. We found an evolutionary conserved E3-ligase, TrafE, 
that is robustly recruited to intracellular compartments disrupted 
after infection with Mycobacterium marinum or after sterile damage 
caused by chemical compounds. TrafE acts at the intersection of 
ESCRT and autophagy pathways and plays a key role in functional 
recruitment of the ESCRT subunits ALIX, Vps32 and Vps4 to 
damage sites. Importantly, we show that the absence of TrafE 
severely compromises the xenophagy restriction of mycobacteria 
as well as ESCRT-mediated and autophagy-mediated endolysosomal 
membrane damage repair, resulting in early cell death.


Submitted by Thierry Soldati [[log in to unmask]]
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