The non-host disease resistance response in peas; alterations in phosphorylation and ubiquitination of HMG A and histones H2A/H2B

Abstract

The non-host disease resistance response of cuticle-free pea endocarp tissue against Fusarium solani f. sp. phaseoli, a bean pathogen, is a synchronous cellular response that completely inhibits the challenging fungal growth within 6 h. This tissue becomes susceptible to the true pathogen, F. solani f. sp. pisi, within 18 h. Previous research indicated that there is an early effect by both pathogens on pea chromatin possibly via the architectural transcription factor, HMG A. HMG A binds with AT-rich regions of the pea DRR206 gene (a PR gene) promoter. The total PR gene-based defense response is activated by three eliciting agents, Fsph DNase, chitosan oligomers and inhibitors of phosphatase such as calyculin A. This report monitors the presence of HMG A and histone and their phosphorylation and ubiquitination, both within the total cytoplasm and in association with isolated chromatin. Inoculation results in a diminution of both HMG A and histones H2A/H2B within 5 h, being more extensive in the susceptible interaction. The detectable phosphorylated HMG A and some accompanying nuclear proteins are diminished within 4 h after pathogen challenge. Changes in the molecular weight of the nuclear components were ELISA-monitored with anti-HMG A, anti-histone H2A/H2B and anti-ubiquitin antisera and indicated that some fungal-caused global changes in chromatin occur via ubiquitin complexing. These modifications of the pea's nuclear proteins could have major transcriptional-related roles in disease resistance since they are temporally associated with the onset of PR gene activation.