ABSTRACT
Tobacco’s PR-1a gene is induced by pathogen attack or exogenous application of Salicylic Acid (SA). However, the epigenetic modifications of the most important inducible promoter of the PR-1a gene are not understood clearly.
Nucelosome mapping and chromatin immunoprecipitation assay were used to define the histone modification on the PR-1a promoter.
Here, we report the epigenetic modifications over core promoter lead to disassembly of nucleosome (spans from −102 to +55 bp,masks TATA and transcription initiation) and repressor complex in induced state. ChIP assays demonstrate repressive chromatin of dimethylation at H3K9 and H4K20 of core promoter maintain uninduced state. While, active chromatin marks di and trimethylation of H3K4, acetylation of H3K9 and H4K16 are increased and lead the induction of PR-1a following SA treatment. TSA enhances expression of PR-1a by facilitating the histone acetylation, however increased expression of negative regulator (SNI1) of AtPR1, suppresses its expression in Arabidopsis thaliana’s mutants.
Constitutive expression of AtPR1 in Histone Acetyl Transferases (HATs), LSD1, and SNI1 suggests that its inactive state is indeed maintained by a repressive complex and this strict regulation of pathogenesis related genes is conserved across species.
SUMMARY Histone methylation and acetylation regulation of tobacco PR-1a promoter are significant for disassembly of the nucleosome and repressor proteins during induction.
Competing Interest Statement
The authors have declared no competing interest.
