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Biotin deficiency causes spontaneous cell death and activation of defense signaling
Author(s) -
Li Jing,
Brader Günter,
Helenius Elina,
Kariola Tarja,
Palva E. Tapio
Publication year - 2012
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2011.04871.x
Subject(s) - complementation , mutant , biotinylation , biology , arabidopsis , biochemistry , biotin , microbiology and biotechnology , signal transduction , gene , programmed cell death , gene expression , apoptosis
Summary In addition to its essential metabolic functions, biotin has been suggested to play a critical role in regulating gene expression. The first committed enzyme in biotin biosynthesis in Arabidopsis, 7‐keto‐8‐aminopelargonic acid synthase, is encoded by At5g04620 ( BIO4 ). We isolated a T‐DNA insertion mutant of BIO4 ( bio4‐1 ) with a spontaneous cell death phenotype, which was rescued both by exogenous biotin and genetic complementation. The bio4‐1 plants exhibited massive accumulation of hydrogen peroxide and constitutive up‐regulation of a number of genes that are diagnostic for defense and reactive oxygen species signaling. The cell‐death phenotype was independent of salicylic acid and jasmonate signaling. Interestingly, the observed increase in defense gene expression was not accompanied by enhanced resistance to bacterial pathogens, which may be explained by uncoupling of defense gene transcription from accumulation of the corresponding protein. Characterization of biotinylated protein profiles showed a substantial reduction of both chloroplastic biotinylated proteins and a nuclear biotinylated polypeptide in the mutant. Our results suggest that biotin deficiency results in light‐dependent spontaneous cell death and modulates defense gene expression. The isolation and molecular characterization of the bio4‐1 mutant provides a valuable tool for elucidating new functions of biotin.