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ASR1, a stress‐induced tomato protein, protects yeast from osmotic stress
Author(s) -
Moretti Mariana Bermúdez,
Maskin Laura,
Gudesblat Gustavo,
García Susana Correa,
Iusem Norberto D.
Publication year - 2006
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.2006.00664.x
Subject(s) - osmotic shock , saccharomyces cerevisiae , mutant , yeast , biology , wild type , glycerol kinase , biochemistry , protein kinase a , abiotic stress , microbiology and biotechnology , osmotic concentration , osmotic pressure , kinase , gene
Asr1 , a tomato gene induced by abiotic stress, belongs to a family, composed by at least three members, involved in adaptation to dry climates. To understand the mechanism by which proteins of this family seem to protect cells from water loss in plants, we expressed Asr1 in the heterologous expression system Saccharomyces cerevisiae under the control of a galactose‐inducible promoter. In a mutant yeast strain deficient in one component of the stress‐responsive high‐osmolarity glycerol (HOG) pathway, namely the MAP kinase Hog 1, the synthesis of ASR1 protein restores growth under osmotic stress conditions such as 0.5 M NaCl and 1.2 M sorbitol. In contrast, the rescuing of this phenotype was less evident using a wild‐type strain or the upstream MAP kinase kinase (Pbs2)‐deficient strain. In both knock‐out strains impaired in glycerol synthesis because of a dysfunctional HOG pathway, but not in wild‐type, ASR1 led to the accumulation of endogenous glycerol in an osmotic stress‐independent and unrestrained manner. These data suggest that ASR1 complements yeast HOG‐deficient phenotypes by inducing downstream components of the HOG pathway. The results are discussed in terms of the function of ASR proteins in planta at the molecular and cellular level.