Premium
SINAT E3 ligases regulate the stability of the ESCRT component FREE1 in response to iron deficiency in plants
Author(s) -
Xiao Zhidan,
Yang Chao,
Liu Chuanliang,
Yang Lianming,
Yang Shuhong,
Zhou Jun,
Li Faqiang,
Jiang Liwen,
Xiao Shi,
Gao Caiji,
Shen Wenjin
Publication year - 2020
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.13005
Subject(s) - escrt , ubiquitin , endosome , ubiquitin ligase , microbiology and biotechnology , biogenesis , arabidopsis , biology , vacuolar protein sorting , arabidopsis thaliana , protein degradation , nedd4 , autophagy , biochemistry , gene , mutant , apoptosis , intracellular
The endosomal sorting complex required for transport (ESCRT) machinery is an ancient, evolutionarily conserved membrane remodeling complex that is essential for multivesicular body (MVB) biogenesis in eukaryotes. FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1 (FREE1), which was previously identified as a plant‐specific ESCRT component, modulates MVB‐mediated endosomal sorting and autophagic degradation. Although the basic cellular functions of FREE1 as an ESCRT component have been described, the regulators that control FREE1 turnover remain unknown. Here, we analyzed how FREE1 homeostasis is mediated by the RING‐finger E3 ubiquitin ligases, SINA of Arabidopsis thaliana (SINATs), in response to iron deficiency. Under iron‐deficient growth conditions, SINAT1‐4 were induced and ubiquitinated FREE1, thereby promoting its degradation and relieving the repressive effect of FREE1 on iron absorption. By contrast, SINAT5, another SINAT member that lacks ubiquitin ligase activity due to the absence of the RING domain, functions as a protector protein which stabilizes FREE1. Collectively, our findings uncover a hitherto unknown mechanism of homeostatic regulation of FREE1, and demonstrate a unique regulatory SINAT–FREE1 module that subtly regulates plant response to iron deficiency stress.