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Loss of all three calreticulins, CRT1, CRT2 and CRT3, causes enhanced sensitivity to water stress in Arabidopsis

Authors
Kim, Jun HyeokNguyen Hoai NguyenNgoc Trinh NguyenHong, Suk-WhanLee, Hojoung
Issue Date
12월-2013
Publisher
SPRINGER
Keywords
Arabidopsis thaliana; Calreticulin; Cyclophilin; ER stress; t123; Water stress
Citation
PLANT CELL REPORTS, v.32, no.12, pp.1843 - 1853
Indexed
SCIE
SCOPUS
Journal Title
PLANT CELL REPORTS
Volume
32
Number
12
Start Page
1843
End Page
1853
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/101525
DOI
10.1007/s00299-013-1497-z
ISSN
0721-7714
Abstract
The calreticulin triple knockout mutant shows growth defects in response to abiotic stress. The endoplasmic reticulum (ER) is an essential organelle that is responsible for the folding and maturation of proteins. During ER stress, unfolded protein aggregates accumulate in the cell, leading to the unfolded protein response (UPR). The UPR up-regulates the expression of ER-stress-responsive genes encoding calreticulin (CRT), an ER-localized Ca2+-binding protein. To understand the function of plant CRTs, we generated a triple knockout mutant, t123, which lacks CRT1, CRT2 and CRT3 and examined the roles of calreticulins in abiotic stress tolerance. A triple knockout mutant increased sensitivity to water stress which implies that calreticulins are involved in the Arabidopsis response to water stress. We identified that the cyclophilin AtCYP21-2, which is located in the ER, was specifically enhanced in the t123 mutants. Seed germination of the atcyp21-1 mutant was retarded by water stress. Taken together, these results suggest that regulatory proteins that serve to protect plants from water stress are folded properly in part with the help of calreticulins. The AtCYP21-2 may also participate in this protein-folding process in association with calreticulins.
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