Low level DNA damage occurs as PAMPs, chitin and flg22, activates PR genes, and increases pisatin and disease resistance in pea endocarp tissue

Abstract

Background

Scientific efforts directed toward improving the defense of plants to pathogens are dependent on knowing how the defense responses are signaled. In general a given plant can resist essentially all challenging pathogens except for the true pathogens which have developed means to suppress or evade the plant's “non-host” resistance response. Thus understanding the signaling of this potent level of immunity is paramount.

Findings

The initiation of transcription of defense genes associated with non-host resistance responses in plants has been hypothesized both as the direct targeting of DNA (chromatin) and as an indirect activation of transcription factors following a PAMP (effector)/PRR (receptor) recognition. Documentation exists for both routes and this report evaluates two PAMPs in the pea endocarp system in which DNA damage has been proposed to directly initiate defense gene transcription. The induction of immune responses resulting from direct effects on chromatin has not received the attention warranted. To account for flexibility in initiating transcription of defense genes, the plant must be responsive to challenges by every organism and all biological elicitors. The PAMP/PRR hypothesis is visualized as families of pattern recognition receptor proteins localized mainly in the cell membrane that become bound with effectors thereby cascading a signal to specified transcription factors. Direct challenges from nuclear penetrating elicitors in the pea non-host resistance system are visualized as causing an unlimited diversity of structural changes to chromosomal regions in the vicinity of plant non-host defense genes and subsequently enhancing their transcription. This report further evaluates the action of candidate PAMPs; flg22 from bacteria and chitin from fungi, in signaling the non-host resistance response of peas.

Conclusions

The results indicate that these PAMPs only marginally elicit pisatin production compared with challenges containing intact fungal spore suspensions. High external conc. of the PAMPs activated both a set of PR (pathogeneses-related) genes and developed cytological-detectable disease resistance against a true pea pathogen. The failure of lower concentrations of chitinous treatments to activate cytological detectable disease resistance, PR gene induction or pisatin accumulations suggests the existence of additional signaling routes to the non-host disease resistance generated by intact fungal spores. DNA damage to the pea DNA was detected indicating direct effects from PAMPs on the chromatin occur. Only high concentration levels of these PAMPs appear to have the potential to constitute a portion of those signals generating responses in peas against the vast arsenals of microbes in nature.