slm1, a major quantitative trait locus for the suppression of les23, a disease lesion mimic in maize (Zea mays L.).

摘要

Maize plants are subjected to many stresses in the field during growth. Plant response to these stresses affect yield. If plants can be altered to have greater tolerance to stresses such as common field diseases, drought, or heat; yields would be improved. Lesion mimics are useful to study plant reactions to stress because the mutant plants show many symptoms of disease without the presence and complications of a causal organism. Many lesion mimics show variation in phenotype expression in different genetic backgrounds. In maize, lesion mimics often express more severely in early-senescence backgrounds and less severely in stay-green backgrounds. The goal of my research was to identify quantitative trait loci (QTL) that modify lesion mimic expression. A recessive lesion mimic, les23, in a severe-expressing line was crossed to Mo20W, a lesion-suppressing stay-green line. A QTL analysis was performed to detect significant loci associated with modification of lesion expression. One locus with highly significant effects was found on the long arm of chromosome 2. We have designated this QTL as slm1, suppresser of lesion mimic 1. The Mo20W allele of slm1 delayed initiation of the lesion phenotype by as much as twenty days and significantly decreased the final lesion severity. Other minor QTL affected severity of lesion expression without modifying lesion initiation date. My results demonstrate that a dramatic change in lesion phenotype can be controlled by a single, major QTL. The QTL analysis also allowed me to place les23 on the short arm of chromosome 2. The major QTL, slm1, was tested for its role in the stay-green phenotype in maize, the maturity of maize, and reduction in paraquat damage. Only marginal effects on maturity and paraquat damage were observed.