Cell-recycling protein turns out to double as a flu virus fighter
Lu Y, Chen J, Xiao H, Li J, Wang H
Autophagy
Nothing in this study involves plants; it's animal-cell virology, so it won't change anything in your garden, though it shows how the same cellular machinery, like the recycling systems plant biologists also study, can take on surprise second jobs.
Cells have a recycling system that clears out worn-out parts, and one protein in that system, called ATG13, turns out to have a second job. It helps a cell sound the alarm when influenza A gets in, by tagging an alarm protein so the signal gets louder. This second job doesn't use the recycling system at all, so it's a separate defense the virus has to deal with.
Key Findings
ATG13 restricts influenza A virus replication and enhances type I interferon antiviral signalling.
ATG13 binds the signalling protein MAVS and recruits the E3 ubiquitin ligase ASB1, which adds K63-linked polyubiquitin chains at the K348 residue of MAVS.
Dual-luciferase reporter assays and pharmacological autophagy inhibition showed the antiviral role is independent of canonical autophagy.
chevron_right Technical Summary
A protein best known for helping cells recycle their own parts also helps the body fight influenza A by boosting the antiviral interferon alarm. It works through a separate route from recycling, which points to new ways of thinking about flu defenses in animal and human cells.
Abstract Preview
Original paper
ATG13 promotes K63-linked polyubiquitination of MAVS via ASB1 to restrict influenza A virus replication.
Autophagy-associated protein 13 (ATG13) plays a pivotal role in regulating the assembly of the autophagy initiation complex. However, the function and mechanism of action of ATG13 during influenza ...
open_in_new Read full abstractAbstract copyright held by the original publisher.
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