When corn plants come under attack from a pathogen, they sometimes respond by killing their own cells near the site of the attack, committing "cell suicide" to thwart further damage from the attacker. This cell sacrifice can cause very small, often microscopic, spots or lesions on the plant.
But up until now it's been difficult to understand how the plant regulates this "spotty" defense mechanism because the response is so quick and localized.
Researchers at North Carolina State University have identified a number of candidate genes and cellular processes that appear to control this so-called hypersensitive defense response (HR) in corn. The findings, which appear in PLOS Genetics, could help researchers build better defense responses in corn and other plants; HR is thought to occur in all higher-order plants, including all trees and crop plants, and is normally a tightly regulated response.
The 44 candidate genes appear to be involved in defense response, programmed cell death, cell wall modification and a few other responses linked to resisting attack, says Dr. Peter Balint-Kurti, the paper's corresponding author and a U.S. Department of Agriculture (USDA) professor who works in NC State's plant pathology and crop science departments.
To arrive at the finding, the NC State researchers joined researchers from Purdue University in examining more than 3,300 maize plants that contained a similar mutation: They all had exaggerated HR because one particular resistance gene, Rp1-D21, doesn't turn off.
"It's similar to a human having an auto-immune response that never stops," Balint-Kurti says. "This mutation causes a corn plant to inappropriately trigger this hypersensitive defense response, causing spots on the corn plant as well as stunted growth."
The researchers examined the entire corn gene blueprint - some 26.5 million points in the 2 to 3 billion base pair genome - to find the genes most closely associated with HR. Balint-Kurti said the top candidates made sense, as they mostly appear to be linked to defense or disease resistance.
"All of the processes associated with the top candidate genes have been previously associated with HR," Balint-Kurti said. "Hopefully this work provides an opening to really characterize this important defense response and learn more about it in other plants."
USDA plant geneticist and breeder Jim Holland co-authored the paper along with first authors Bode Olukolu and Guan Feng Wang, who are post-doctoral researchers at NC State. Vijay Vontimitta, a post-doctoral researcher at Purdue working in a group headed by Guri Johal, is also a first author.
The research was funded by USDA, the National Science Foundation, NC State and Purdue University.
Note: An abstract of the paper follows.
"Multivariate Analysis of Maize Disease Resistance Suggests a Pleiotropic Genetic Basis and Implicates a Glutathione S-transferase Gene"
Authors: Bode A. Olukolu, Guan Feng Wang, Adisu Negeri, Dahlia Nielsen, James Holland and Peter Balint-Kurti, North Carolina State University; Vijay Vontimitta, Bala Venkata, Sandeep Marla, Jiabing Ji, Emma Gachomo, Kevin Chu and Gurmukh Johal, Purdue University; Jacqueline Benson, Rebecca Nelson and Peter Bradbury, Cornell University
Published: Aug. 28, 2014, in PLOS Genetics
Abstract: Much remains unknown of molecular events controlling the plant hypersensitive defense response (HR), a rapid localized cell death that limits pathogen spread and is mediated by resistance (R-) genes. Genetic control of the HR is hard to quantify due to its microscopic and rapid nature. Natural modifiers of the ectopic HR phenotype induced by an aberrant auto-active R-gene (Rp1-D21), were mapped in a population of 3,381 recombinant inbred lines from the maize nested association mapping population. Joint linkage analysis was conducted to identify 32 additive but no epistatic quantitative trait loci (QTL) using a linkage map based on more than 7000 single nucleotide polymorphisms (SNPs). Genome-wide association (GWA) analysis of 26.5 million SNPs was conducted after adjusting for background QTL. GWA identified associated SNPs that colocalized with 44 candidate genes. Thirty-six of these genes colocalized within 23 of the 32 QTL identified by joint linkage analysis. The candidate genes included genes predicted to be in involved programmed cell death, defense response, ubiquitination, redox homeostasis, autophagy, calcium signalling, lignin biosynthesis and cell wall modification. Twelve of the candidate genes showed significant differential expression between isogenic lines differing for the presence of Rp1-D21. Low but significant correlations between HR-related traits and several previously-measured disease resistance traits suggested that the genetic control of these traits was substantially, though not entirely, independent. This study provides the first system-wide analysis of natural variation that modulates the HR response in plants.