Search

The semi-dominant mutant alleleOy1-N1989encodes a dominant-negative subunit I of Mg-Chelatase that catalyzes the first committed step of chlorophyll biosynthesis. Analyses of mutant F1 hybrids from crosses ofOy1-N1989to diverse maize lines identified a natural variant atoil yellow1as major modifier of chlorophyll content. Chlorophyll reduction increased the time to reproductive maturity, decreased stalk width, and had complex effects on plant height. We explored these effects by genome wide association studies of F1 hybrids crosses ofOy1-N1989to a maize diversity panel. The delay in reproductive maturity inOy1-N1989/+ mutants neither altered the vegetative-to-adult phase change nor total leaf number but did slow the rate of organ emergence from the whorl. In addition to the allele atoy1, analysis of tetrapyrrole, heme, and chlorophyll biosynthesis pathway genes identified multiple modifiers of mutant traits. Consistent with organ emergence, rather than a developmental delay, affecting the reproductive delay ofOy1-N1989/+ mutants, known flowering time regulators did not affect variation in the reproductive delay affected by chlorophyll loss. Plant height showed a complex relationship with chlorophyll. TheOy1-N1989/+ mutant F1 plants with a modest reduction in chlorophyll were taller than their wildtype siblings, but F1 plants with dramatically decreased chlorophyll were shorter than their wildtype siblings. Perturbations in the biosynthesis of the phytochrome chromophore increased plant height in wild-type plants but dramatically reduced plant height and chlorophyll contents ofOy1-N1989/+ mutants. The mechanism by which the interaction between chlorophyll and bilin affects height and chlorophyll remains to be explored.One sentence summaryChlorophyll reduction in maize delays reproductive maturity by altering growth and not development, and depending on the reduction can either increase or decrease plant height.

The maize protein Rp1-D21, an autoactive derivative of the Rp1-D nucleotide-binding leucine rich repeat (NLR) disease resistance protein, triggers a spontaneous hypersensitive cell death defense response (HR). ZmCER9, a member of a class of E3 ligases involved in the endoplasmic reticulum associated degradation (ERAD) protein quality control system, is a suppressor of the Rp21-D21 HR phenotype. ZmCER9, an active E3 ligase, localizes to the ER, consistent with a role in ERAD. It physically interacts with and mediates the proteasome-dependent degradation of both Rp1-D21 and another autoactive Rp1-D derivate but neither interacts with nor affects the protein levels of three non-autoactive Rp1-D derivatives. ZmCER9 also suppresses the activity and directs the degradation of autoactive NLRs from Arabidopsis and barley. We describe a novel, and possibly general, mechanism that specifically degrades activated NLRs to suppress the defense response after activation.

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 identified 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 lacking Rp1-D21. This suggests that, whereas the HR itself was cell autonomous, other aspects of the defense response initiated by Rp1-D21 were not. [Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

The partially dominant, autoactive maize dis- ease resistance gene Rp1-D21 causes hypersensitive response (HR) lesions to form spontaneously on leaves and stems in the absence of pathogen recognition. The maize nested association mapping (NAM) population consists of 25 200-line subpopulations each derived from a cross between the maize line B73 and one of 25 diverse inbred lines. By crossing a line carrying the Rp1-D21 gene with lines from three of these subpopulations and assessing the F1 progeny, we were able to map several novel loci that modify the maize HR, using both single-population quan- titative trait locus (QTL) and joint analysis of all three populations. Joint analysis detected QTL in greater number and with greater confidence and precision than did single population analysis. In particular, QTL were detected in bins 1.02, 4.04, 9.03, and 10.03. We have previously termed this technique, in which a mutant phenotype is used as a ''reporter'' for a trait of interest, Mutant-Assisted Gene Identification and Characterization (MAGIC).