Submitted to: Genome
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/1/2004
Publication Date: 10/1/2004
Citation: Penning, B.W., Johal, G.S., Mcmullen, M.D. 2004. A major suppressor of cell death, slm1, modifies the expression of the maize (zea mays l.) lesion mimic mutation les23. Genome. 47:961-969. Interpretive Summary: A common plant response to attack by plant pathogens involves recognition of the pathogen's presence and initiation of a chain of events leading to a defense mechanism called "programmed cell death" whereby the plant kills its own cells to limit the disease to the initial site of infection. Although this process has great implications for plant health, little is known of the molecular mechanisms at play, particularly in crop plants such as corn. In this study, we used a model genetic system, a lesion mimic mutation, to screen for loci controlling the programmed cell death pathway. We were able to identify and genetically map a locus that profoundly affects the programmed cell death. These results provide plant cell researchers an excellent system to study the molecular basis of plant response to pathogens. In addition, these results may provide plant breeders with a novel approach to modify tolerance to pathogens for which corn has poor resistance.
Technical Abstract: Disease lesion mimics provide an excellent biological system to study the genetic basis of programmed cell death (PCD) in plants. Many lesion mimics show variation in phenotype expression in different genetic backgrounds. Our goal was to identify quantitative trait loci (QTL) modifying lesion mimic expression, thereby identifying genetic modifiers of PCD. A recessive lesion mimic, les23, in a severe-expressing line was crossed to the maize inbred line Mo20W, a lesion-suppressing line, and an F2 population was developed for QTL analysis. In addition to locating les23 to the short arm of chromosome 2, this analysis detected significant loci for modification of lesion expression. One locus with a highly significant affect was found on the long arm of chromosome 2. The Mo20W allele at this QTL significantly delayed initiation of the lesion phenotype and decreased the final lesion severity. Other smaller effect QTL affected severity of lesion expression without affecting lesion initiation date. Our results demonstrate that dramatic change in lesion phenotype can be controlled by a single, major QTL. The presumed function of the gene underlying the QTL in normal plants is to regulate an aspect of the PCD pathway in maize.