Journal article
Non-host Resistance: DNA Damage Is Associated with SA Signaling for Induction of PR Genes and Contributes to the Growth Suppression of a Pea Pathogen on Pea Endocarp Tissue
Frontiers in plant science, Vol.8, pp.446-446
2017
Handle:
https://hdl.handle.net/2376/116565
PMCID: PMC5379135
PMID: 28421088
Abstract
Salicylic acid (SA) has been reported to induce plant defense responses. The transcriptions of defense genes that are responsible for a given plant's resistance to an array of plant pathogens are activated in a process called non-host resistance. Biotic signals capable of carrying out the activation of pathogenesis-related (PR) genes in pea tissue include fungal DNase and chitosan, two components released from
spores that are known to target host DNA. Recent reports indicate that SA also has a physical affinity for DNA. Here, we report that SA-induced reactive oxygen species release results in fragment alterations in pea nuclear DNA and cytologically detectable diameter and structural changes in the pea host nuclei. Additionally, we examine the subsequent SA-related increase of resistance to the true pea pathogen
f.sp.
and the accumulation of the phytoalexin pisatin. This is the first report showing that SA-induced PR gene activation may be attributed to the host pea genomic DNA damage and that at certain concentrations, SA can be temporally associated with subsequent increases in the defense response of this legume.
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Details
- Title
- Non-host Resistance: DNA Damage Is Associated with SA Signaling for Induction of PR Genes and Contributes to the Growth Suppression of a Pea Pathogen on Pea Endocarp Tissue
- Creators
- Lee A Hadwiger - Department of Plant Pathology, Washington State University, PullmanWA, USAKiwamu Tanaka - Department of Plant Pathology, Washington State University, PullmanWA, USA
- Publication Details
- Frontiers in plant science, Vol.8, pp.446-446
- Academic Unit
- Plant Pathology, Department of
- Publisher
- Switzerland
- Identifiers
- 99900548086501842
- Language
- English
- Resource Type
- Journal article