These authors contributed equally to this work.
Biotin deficiency causes spontaneous cell death and activation of defense signaling
Article first published online: 16 JAN 2012
© 2011 The Authors. The Plant Journal © 2011 Blackwell Publishing Ltd
The Plant Journal
Volume 70, Issue 2, pages 315–326, April 2012
How to Cite
Li, J., Brader, G., Helenius, E., Kariola, T. and Palva, E. T. (2012), Biotin deficiency causes spontaneous cell death and activation of defense signaling. The Plant Journal, 70: 315–326. doi: 10.1111/j.1365-313X.2011.04871.x
- Issue published online: 3 APR 2012
- Article first published online: 16 JAN 2012
- Accepted manuscript online: 29 NOV 2011 10:49AM EST
- Received 3 September 2011; revised 25 November 2011; accepted 28 November 2011; published online 16 January 2012.
- biotin biosynthesis;
- cell death;
- hydrogen peroxide;
- defense gene expression;
- signal transduction
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.