Excessive demand for translation and protein folding in the endoplasmic reticulum(ER) can cause ER stress in plants. Here, we show that CALRETICULIN 1(CRT1) and CRT2 are critical components in the accumulation of VESI...Excessive demand for translation and protein folding in the endoplasmic reticulum(ER) can cause ER stress in plants. Here, we show that CALRETICULIN 1(CRT1) and CRT2 are critical components in the accumulation of VESICLE-ASSOCIATED MEMBRANE PROTEIN 721(VAMP721) and VAMP722 during ER stress responses. We show that CRT2 interacts with VAMP722 and that CRT1/2 post-translationally maintain elevated VAMP721/722 levels under ER stress.The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes.展开更多
基金supported by grants from the National Research Foundation (2017R1D1A1B 03029802 to H.S.Y., and 2016R1D1A1B02007322 to C.K.)the Strategic Initiative for Microbiomes in Agriculture and Food, Ministry of Agriculture, Food and Rural Affairs (916007-02-1-HD020 to C.K.) Korea
文摘Excessive demand for translation and protein folding in the endoplasmic reticulum(ER) can cause ER stress in plants. Here, we show that CALRETICULIN 1(CRT1) and CRT2 are critical components in the accumulation of VESICLE-ASSOCIATED MEMBRANE PROTEIN 721(VAMP721) and VAMP722 during ER stress responses. We show that CRT2 interacts with VAMP722 and that CRT1/2 post-translationally maintain elevated VAMP721/722 levels under ER stress.The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes.
