Disruption of the plant-specific CFS1 gene impairs autophagosome turnover and triggers EDS1-dependent cell death.

作者: Arpaporn Sutipatanasomboon , Stefanie Herberth , Ellen G. Alwood , Heidrun Häweker , Britta Müller

DOI: 10.1038/S41598-017-08577-8

关键词:

摘要: Cell death, autophagy and endosomal sorting contribute to many physiological, developmental immunological processes in plants. They are mechanistically interconnected interdependent, but the molecular basis of their mutual regulation has only begun emerge Here, we describe identification characterization CELL DEATH RELATED ENDOSOMAL FYVE/SYLF PROTEIN 1 (CFS1). The CFS1 protein interacts with SORTING COMPLEX REQUIRED FOR TRANSPORT I (ESCRT-I) component ELCH (ELC) is localized at ESCRT-I-positive late endosomes likely through its PI3P actin binding SH3YL1 Ysc84/Lsb4p Lsb3p plant FYVE (SYLF) domain. Mutant alleles cfs1 exhibit auto-immune phenotypes including spontaneous lesions that show characteristics hypersensitive response (HR). Autoimmunity dependent on ENHANCED DISEASE SUSCEPTIBILITY (EDS1)-mediated effector-triggered immunity (ETI) independent from salicylic acid. Additionally, mutants accumulate markers ATG8 NBR1 independently EDS1. We hypothesize acts intersection autophagosomes contributes cellular homeostasis by mediating autophagosome turnover.

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