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A stable intense resistance called "nonhost resistance" generates a complete multiple-gene resistance against plant pathogenic species that are not pathogens of pea such as the bean pathogen, Fusarium solani f. sp. phaseoli (Fsph). Chitosan is a natural nonhost resistance response gene activator of defense responses in peas. Chitosan may share with cancer-treatment compounds, netropsin and some anti-cancer drugs, a DNA minor groove target in plant host tissue. The chitosan heptamer and netropsin have the appropriate size and charge to reside in the DNA minor groove. The localization of a percentage of administered radio-labeled chitosan in the nucleus of plant tissue in vivo indicates its potential to transport to site(s) within the nuclear chromatin (1,2). Other minor groove-localizing compounds administered to pea tissue activate the same secondary plant pathway that terminates in the production of the anti-fungal isoflavonoid, pisatin an indicator of the generated resistance response. Some DNA minor groove compounds also induce defense genes designated as "pathogenesis-related" (PR) genes. Hypothetically, DNA targeting components alter host DNA in a manner enabling the transcription of defense genes previously silenced or minimally expressed. Defense-response-elicitors can directly (a) target host DNA at the site of transcription or (b) act by a series of cascading events beginning at the cell membrane and indirectly influence transcription. A single defense response, pisatin induction, induced by chitosan and compounds with known DNA minor groove attachment potential was followed herein. A hypothesis is formulated suggesting that this DNA target may be accountable for a portion of the defense response generated in nonhost resistance.

Over the last decades, medical research has utilized DNA altering procedures in cancer treatments with the objective of killing cells or suppressing cell proliferation. Simultaneous research related to enhancing disease resistance in plants reported that alterations in DNA can enhance defense responses. These two opposite perspectives have in common their effects on the center for gene transcription, the nuclear chromatin. A review of selected research from both anticancer- and plant defense-related research provides examples of some specific DNA altering actions: DNA helical distortion, DNA intercalation, DNA base substitution, DNA single cleavage by DNases, DNA alkylation/methylation, and DNA binding/exclusion. The actions of the pertinent agents are compared, and their proposed modes of action are described in this study. Many of the DNA specific agents affecting resistance responses in plants, e.g., the model system using pea endocarp tissue, are indeed anticancer agents. The tumor cell death or growth suppression in cancer cells following high level treatments may be accompanied with chromatin distortions. Likewise, in plants, DNA-specific agents activate enhanced expression of many genes including defense genes, probably due to the chromatin alterations resulting from the agents. Here, we propose a hypothesis that DNA damage and chromatin structural changes are central mechanisms in initiating defense gene transcription during the nonhost resistance response in plants.

Phytoalexins are antimicrobial substance synthesized in plants upon pathogen infection. Pisatin ( Pisum sativum phytoalexin) is the major phytoalexin in pea, while it is also a valuable indicator of plant defense response. Pisatin can be quantitated in various methods from classical organic chemistry to Mass-spectrometry analysis. Here we describe a procedure with high reproducibility and simplicity that can easily handle large numbers of treatments. The method only requires a spectrophotometer as laboratory equipment, does not require any special analytical instruments ( e.g ., HPLC, mass spectrometers, etc .) to measure the phytoalexin molecule quantitatively, i.e ., most scientific laboratories can perform the experiment., (Copyright © 2017 The Authors; exclusive licensee Bio-protocol LLC.)

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 Fusarium solani 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. solani f.sp. pisi 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.

Of the multiplicity of plant pathogens in nature, only a few are virulent on a given plant species. Conversely, plants develop a rapid "nonhost" resistance response to the majority of the pathogens. The anatomy of the nonhost resistance of pea endocarp tissue against a pathogen of bean, Fusarium solani f.sp. phaseoli (Fsph) and the susceptibility of pea to F. solani f sp. pisi (Fspi) has been described cytologically, biochemically and molecular-biologically. Cytological changes have been followed by electron microscope and stain differentiation under white and UV light. The induction of changes in transcription, protein synthesis, expression of pathogenesis-related (PR) genes, and increases in metabolic pathways culminating in low molecular weight, antifungal compounds are described biochemically. Molecular changes initiated by fungal signals to host organelles, primarily to chromatin within host nuclei, are identified according to source of the signal and the mechanisms utilized in activating defense genes. The functions of some PR genes are defined. A hypothesis based on this data is developed to explain both why fungal growth is suppressed in nonhost resistance and why growth can continue in a susceptible reaction.