Journal
MOLECULAR PLANT-MICROBE INTERACTIONS
Volume 34, Issue 6, Pages 606-616Publisher
AMER PHYTOPATHOLOGICAL SOC
DOI: 10.1094/MPMI-04-20-0091-R
Keywords
cell death; plant responses to pathogens; resistance genes
Funding
- United States Department of Agriculture-Agricultural Research Service, North Carolina State University
- National Science Foundation Plant Genome grants [0822495, 1444503]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1444503, 0822495] Funding Source: National Science Foundation
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Mutant maize gene Rp1-D21 confers resistance to common rust and triggers a cell autonomous hypersensitive response (HR). The study found that while HR and chlorosis associated with Rp1-D21 activity were cell autonomous, other defense responses initiated by Rp1-D21 may not be.
The maize gene Rp1-D21 is a mutant form of the gene Rp1-D that confers resistance to common rust. Rp1-D21 triggers a spontaneous defense response that occurs in the absence of the pathogen and includes a programed cell death called the hypersensitive response (HR). Eleven plants heterozygous for Rp1-D21, in four different genetic backgrounds, were identi-fied that had chimeric leaves with lesioned sectors showing HR abutting green nonlesioned sectors lacking HR. The Rp1-D21 sequence derived from each of the lesioned portions of leaves was unaltered from the expected sequence whereas the Rp1-D21 sequences from nine of the nonlesioned sectors displayed various mutations, and we were unable to amplify Rp1-D21 from the other two nonlesioned sectors. In every case, the borders between the sectors were sharp, with no transition zone, suggesting that HR and chlorosis associated with Rp1-D21 activity was cell autonomous. Expression of defense response marker genes was assessed in the lesioned and nonlesioned sectors as well as in near-isogenic plants lacking and carrying Rp1-D21. Defense gene expression was somewhat elevated in nonlesioned sectors abutting sectors carrying Rp1-D21 compared with near-isogenic plants lack -ing Rp1-D21. This suggests that, whereas the HR itself was cell autonomous, other aspects of the defense response initi-ated by Rp1-D21 were not.
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