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.
Rp1-D21 is a maize auto-active resistance gene conferring a spontaneous hypersensitive response (HR) of variable severity depending on genetic background. We report an association mapping strategy based on the Mutant Assisted Gene Identification and Characterization approach to identify naturally occurring allelic variants associated with phenotypic variation in HR. Each member of a collection of 231 diverse inbred lines of maize constituting a high-resolution association mapping panel were crossed to a parental stock heterozygous for Rp1-D21, and the segregating F 1 generation testcrosses were evaluated for phenotypes associated with lesion severity for 2 years at two locations. A genome-wide scan for associations with HR was conducted with 47,445 SNPs using a linear mixed model that controlled for spurious associations due to population structure. Since the ability to identify candidate genes and the resolution of association mapping are highly influenced by linkage disequilibrium (LD), we examined the extent of genome-wide LD. On average, marker pairs separated by .10 kbp had an r 2 value of ,0.1. Genomic regions surrounding SNPs significantly associated with HR traits were locally saturated with additional SNP markers to establish local LD structure and precisely identify candidate genes. Six significantly associated SNPs at five loci were detected. At each locus, the associated SNP was located within or immediately adjacent to candidate causative genes predicted to play significant roles in the control of programmed cell death and especially in ubiquitin pathway-related processes.T HE hypersensitive response (HR) mechanism is a widespread and important plant defense response. Characterized by a rapid, localized cell death around the point of attempted pathogen penetration, it is a form of programmed cell death and is usually associated with an acute local resistance response and up-regulation of defense response pathways (Coll et al. 2011). HR and associated events are generally initiated by the products of resistance (R) genes, which trigger HR upon the recognition of specific pathogenderived molecules or molecular events (Bent and Mackey 2007). The HR and related responses are generally associated with resistance to biotrophic rather than necrotrophic pathogens. Among the multiple classes of R genes, those that encode proteins possessing a nucleotide-binding site (NBS) and a leucine-rich repeat (LRR) are the predominant class (Bent and Mackey 2007).The Rp1 locus on maize chromosome 10 carries multiple tandemly repeated NBS-LRR paralogs, some of which confer resistance to specific races of maize common rust conferred by the fungus Puccini sorghi (Hulbert 1997). The locus is meiotically unstable due to a high frequency of unequal crossovers between paralogs (Sudupak et al. 1993). In one such case, unequal crossing over followed by intragenic recombination resulted in the formation of the chimeric gene Rp1-D21 (Collins et al. 1999;Smith et al. 2010). In the resulting gene product, the recognition an...
Detecting phenotypically relevant variation outside the coding sequence of genes and distinguishing it from the neutral variants is not trivial partly because the mechanisms by which a subset of the DNA polymorphisms in these regions affect gene regulation are poorly understood. Here we present an approach of using dominant genetic markers with convenient phenotypes to investigate the effect of cis and trans-acting regulatory variations. In the current study, we performed a forward genetic screen for natural variants that suppress or enhance the semi-dominant mutant allele Oy1-N1989 encoding the magnesium chelatase subunit I of maize. This mutant permits rapid phenotyping of leaf color as a reporter of chlorophyll accumulation, enabling QTL mapping and GWAS approaches to identify natural variation in maize affecting chlorophyll metabolism. Using different mapping approaches, we identified the same modifier locus, very oil yellow 1 (vey1), that was linked to the reporter gene itself. Based on the analysis of OY1 transcript abundance and study of a maize gene expression dataset, vey1 is predicted to be a cis-acting regulatory sequence polymorphism that causes the differential accumulation of OY1 transcripts encoded by the mutant and wildtype alleles. Fine mapping of the vey1 genomic region using multiple independent mapping populations demonstrated the value of multiple cycles of early generation random mating to increase recombination. The vey1 allele appears to be a common polymorphism in the maize germplasm that alters the expression level of a key gene in chlorophyll biosynthesis.
We previously demonstrated that maize (Zea mays) locus very oil yellow1 (vey1) encodes a putative cis-regulatory expression polymorphism at the magnesium chelatase subunit I gene (aka oil yellow1) that strongly modifies the chlorophyll content of the semi-dominant Oy1-N1989 mutants. The vey1 allele of Mo17 inbred line reduces chlorophyll content in the mutants leading to reduced photosynthetic output. Oy1-N1989 mutants in B73 reached reproductive maturity four days later than wild-type siblings. Enhancement of Oy1-N1989 by the Mo17 allele at the vey1 QTL delayed maturity further, resulting in detection of a flowering time QTL in two bi-parental mapping populations crossed to Oy1-N1989. The near isogenic lines of B73 harboring the vey1 allele from Mo17 delayed flowering of Oy1-N1989 mutants by twelve days. Just as previously observed for chlorophyll content, vey1 had no effect on reproductive maturity in the absence of the Oy1-N1989 allele. Loss of chlorophyll biosynthesis in Oy1-N1989 mutants and enhancement by vey1 reduced CO2 assimilation. We attempted to separate the effects of photosynthesis on the induction of flowering from a possible impact of chlorophyll metabolites and retrograde signaling by manually reducing leaf area. Removal of leaves, independent of the Oy1-N1989 mutant, delayed flowering but surprisingly reduced chlorophyll contents of emerging leaves. Thus, defoliation did not completely separate the identity of the signal(s) that regulates flowering time from changes in chlorophyll content in the foliage. These findings illustrate the necessity to explore the linkage between metabolism and the mechanisms that connect it to flowering time regulation.
24We previously demonstrated that maize (Zea mays) locus very oil yellow1 (vey1) encodes a 25 putative cis-regulatory expression polymorphism at the magnesium chelatase subunit I gene (aka 26 oil yellow1) that strongly modifies the chlorophyll content of the semi-dominant Oy1-N1989 27 mutants. The vey1 allele of Mo17 inbred line reduces chlorophyll content in the mutants leading 28 to reduced photosynthetic output. Oy1-N1989 mutants in B73 reached reproductive maturity four 29 days later than wild-type siblings. Enhancement of Oy1-N1989 by the Mo17 allele at the vey1 QTL 30 delayed maturity further, resulting in detection of a flowering time QTL in two bi-parental 31 mapping populations crossed to Oy1-N1989. The near isogenic lines of B73 harboring the vey1 32 allele from Mo17 delayed flowering of Oy1-N1989 mutants by twelve days. Just as previously 33 observed for chlorophyll content, vey1 had no effect on reproductive maturity in the absence of 34 the Oy1-N1989 allele. Loss of chlorophyll biosynthesis in Oy1-N1989 mutants and enhancement 35 by vey1 reduced CO2 assimilation. We attempted to separate the effects of photosynthesis on the 36 induction of flowering from a possible impact of chlorophyll metabolites and retrograde signaling 37 by manually reducing leaf area. Removal of leaves, independent of the Oy1-N1989 mutant, 38 delayed flowering but surprisingly reduced chlorophyll contents of emerging leaves. Thus, 39 defoliation did not completely separate the identity of the signal(s) that regulates flowering time 40 from changes in chlorophyll content in the foliage. These findings illustrate the necessity to explore 41 the linkage between metabolism and the mechanisms that connect it to flowering time regulation. 42 43
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.