Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral-induced cellular damage
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Abstract
RNA viruses co-opt the host endomembrane system and organelles to build replication complexes for infection. How the host responds to these membrane perturbations is poorly understood. Here, we explore the autophagic response of Arabidopsis thaliana to three viruses that hijack different cellular compartments. Autophagy is significantly induced within systemically infected tissues, its disruption rendering plants highly sensitive to infection. Contrary to being an antiviral defense mechanism as previously suggested, quantitative analyses of the viral loads established autophagy as a tolerance pathway. Further analysis of one of these viruses, the Turnip Crinkle Virus (TCV) that hijack mitochondria, showed that despite perturbing mitochondrial integrity, TCV does not trigger a typical mitophagy response. Instead, TCV and Turnip yellow mosaic virus (TYMV) infection activates a distinct selective autophagy mechanism, where oligomeric metabolic enzymes moonlight as selective autophagy receptors and degrade key executors of defense and cell death such as EDS1. Altogether, our study reveals an autophagy-regulated metabolic rheostat that gauges cellular integrity during viral infection and degrades cell death executors to avoid catastrophic amplification of immune signaling.
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Results
This seems like an extensive study, but the figures have so many panels and the captions are so long, that it make it hard for the reader to quickly understand the key points. It would greatly benefit the reader if you streamline the figures and reduce redundancy within the captions (across letters in the panels and also with methods sections). Because of the different time courses, perhaps a schematic showing the overall experimental design in the first panel woud be useful for some figures.
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our study reveals an autophagy-regulated metabolic rheostat that gauges cellular integrity during viral infection and degrades cell death executors to avoid catastrophic amplification of immune signaling.
Is there a more direct way to state the findings?
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EDS1
Just a note for readers outside of the Arabidopsis field that EDS1 hasn't been defined yet in the abstract.
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