Transcriptional Down-Regulation by Abscisic Acid of Pathogenesis-Related β-1,3-Glucanase Genes in Tobacco Cell Cultures1
Author(s) -
Enea Rezzonico,
Nathalie Flury,
Frederick Meins,
Roland Beffa
Publication year - 1998
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.117.2.585
Subject(s) - abscisic acid , auxin , nicotiana tabacum , biology , pathogenesis related protein , gene expression , gene isoform , reporter gene , northern blot , microbiology and biotechnology , biochemistry , gene , cytokinin , transcription (linguistics) , linguistics , philosophy
Class I isoforms of beta-1,3-glucanases (betaGLU I) and chitinases (CHN I) are antifungal, vacuolar proteins implicated in plant defense. Tobacco (Nicotiana tabacum L.) betaGLU I and CHN I usually exhibit tightly coordinated developmental, hormonal, and pathogenesis-related regulation. Both enzymes are induced in cultured cells and tissues of cultivar Havana 425 tobacco by ethylene and are down-regulated by combinations of the growth hormones auxin and cytokinin. We report a novel pattern of betaGLU I and CHN I regulation in cultivar Havana 425 tobacco pith-cell suspensions and cultured leaf explants. Abscisic acid (ABA) at a concentration of 10 micron markedly inhibited the induction of betaGLU I but not of CHN I. RNA-blot hybridization and immunoblot analysis showed that only class I isoforms of betaGLU and CHN are induced in cell culture and that ABA inhibits steady-state betaGLU I mRNA accumulation. Comparable inhibition of beta-glucuronidase expression by ABA was observed for cells transformed with a tobacco betaGLU I gene promoter/beta-glucuronidase reporter gene fusion. Taken together, the results strongly suggest that ABA down-regulates transcription of betaGLU I genes. This raises the possibility that some of the ABA effects on plant-defense responses might involve betaGLU I.
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