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Research Project: Genetics of Disease Resistance and Food Quality Traits in Corn

Location: Plant Science Research

Title: Development and use of a seedling growth retardation assay to quantify and map loci underlying variation in the maize basal defense response

Author
item WANG, YANLI - North Carolina State University
item Holland, Jim - Jim
item Balint-Kurti, Peter

Submitted to: PhytoFrontiers
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/20/2021
Publication Date: 3/2/2021
Citation: Wang, Y., Holland, J.B., Balint Kurti, P.J. 2021. Development and use of a seedling growth retardation assay to quantify and map loci underlying variation in the maize basal defense response. Phytofrontiers. https://doi.org/10.1094/PHYTOFR-12-20-0038-R.
DOI: https://doi.org/10.1094/PHYTOFR-12-20-0038-R

Interpretive Summary: Plants can detect and respond to various elicitor molecules produced by microbes. This response forms the first level of the plant defense response. Here we show that we can quantify this response in maize (corn) by measuring the reduction of plant growth after exposure to the microbial elicitor. We show that different maize line respond at different levels and identify some genetic factors responsible for variation in this response.

Technical Abstract: The microbe-associated molecular pattern (MAMP) response in plants is caused by the recognition of MAMPs by plant pattern recognition receptors at the cell surface. Flg22, an epitope derived from bacterial flagellin is a commonly studied MAMP. We developed a seedling growth retardation (SGR) assay by which we could measure growth retardation in maize seedlings exposed to Flg22. We observed variation across 21 maize inbred lines. We used 161 lines from a recombinant inbred line (RIL) population derived from a cross between the lines CML228 (a high responder) and B73 (a low responder) to map QTL for this response. We found significant heritable variation in the RIL population and identified Flg22 response QTLs response on chromosomes 1, 2, and 8. We did not observe strong correlations between SGR traits and levels Flg22-induced reactive oxygen production and with other disease resistance or defense response traits we had previously measured in the same population. We discuss the implications of these findings.