Abstract
Pea pod endocarp suppresses the growth of an inappropriate fungus or non-pathogen by generating a “non-host resistance response” that completely suppresses growth of the challenging fungus within 6 h. Most of the components of this resistance response including pisatin production can be elicited by an extensive number of both biotic and abiotic inducers. Thus this phytoalexin serves as an indicator to be used in evaluating the chemical properties of inducers that can initiate the resistance response. Many of the pisatin inducers are reported to interact with DNA and potentially cause DNA damage. Here we propose that EDTA (ethylenediaminetetraacetic acid) is an elicitor to evoke non-host resistance in plants. EDTA is manufactured as a chelating agent, however at low concentration it is a strong elicitor, inducing the phytoalexin pisatin, cellular DNA damage and defense-responsive genes. It is capable of activating complete resistance in peas against a pea pathogen. Since there is also an accompanying fragmentation of pea DNA and alteration in the size of pea nuclei, the potential biochemical insult as a metal chelator may not be its primary action. The potential effects of EDTA on the structure of DNA within pea chromatin may assist the transcription of plant defense genes.
Highlights
The pea endocarp system [1] has been employed to follow and understand the transcription initiation of the nonhost resistance response in plants at chromatin sites targeted by DNA-specific gene activators, one of which is a fungal DNase [2,3]
This report on EDTA is designed to examine if its effect on pisatin accumulation, DNA damage, defense gene induction and cytological changes observed in relationship to the expression of disease resistance, may be associated with a
These results suggest that the inhibition of a fungal DNase enzyme by EDTA does occur in vitro
Summary
The pea endocarp system [1] has been employed to follow and understand the transcription initiation of the nonhost resistance response in plants at chromatin sites targeted by DNA-specific gene activators, one of which is a fungal DNase [2,3]. Phaseoli (Fsph), a pathogen of bean, and causes single strand nicks in DNA in temporal association with the induction of pisatin [3] This fungal enzyme’s catalytic action is dependent on Mn2+ [3]. The induction and biosynthesis of the anti-fungal phytoalexin pisatin, as an isoflavonoid, requires the participation of multiple enzymes in this secondary pathway [11] This suggests that the sensitive regions of pea chromatin itself may often serve as the initial target of the elicitors. This report on EDTA is designed to examine if its effect on pisatin accumulation, DNA damage, defense gene induction and cytological changes observed in relationship to the expression of disease resistance, may be associated with a DNA target
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