Biology subjects

Nelson, R. J.

Publications and source records attributed to Nelson, R. J..

3 recordsLinked to original sources

bioRxiv2024

Regulatory architecture of disease resistance in maize revealed by multi-omic systems genetics

Complex traits such as disease resistance have been traditionally studied using quantitative genetics. Here, we use systems genetics to integrate disease severity and multi-omic quantitate trait loci (QTL) to uncover biological networks underlying interaction with northern leaf blight (NLB), a yield-limiting disease of corn. Specifically, we integrated transcriptome, (phospho)proteome, and metabolome measurements to map molecular QTL and build predictive regulatory networks following NLB infection. These inferred networks identified a critical signaling module that was genetically validated comprised of a kinase termed NLB SUSCEPTIBLE KINASE 1, a bHLH transcription factor, and the lignin biosynthesis enzyme BROWN MIDRIB 2. Our results demonstrate the feasibility of high-throughput mapping of genetic determinants of gene- product levels and demonstrates the power of systems genetics to identify upstream regulatory genes that confer resistance to NLB that can inform future strategies for crop protection.

plant biology↗

bioRxiv2022

Uncovering the roles of lignin-related genes in disease resistance in maize using mutant and association analysis

Brown midrib (BMR) maize harbors mutations that result in lower lignin levels and higher feed digestibility, making it a desirable silage market class for ruminant nutrition. Northern leaf blight (NLB) epidemics in upstate NY highlighted the disease susceptibility of commercially grown BMR maize hybrids. We found the bm1, bm2, bm3 and bm4 mutants in a W64A genetic background to be more susceptible to foliar fungal (NLB, gray leaf spot, and anthracnose leaf blight) and bacterial (Stewarts wilt) diseases. The bm1, bm2 and bm3 mutants showed enhanced susceptibility to anthracnose stalk rot, and the bm1 and bm3 mutants were more susceptible to Gibberella ear rot. Co-localization of quantitative trait loci and correlations between stalk strength and disease traits in recombinant inbred line families suggest possible pleiotropies. The role of lignin in plant defense was explored using high-resolution, genome-wide association analysis for resistance to NLB in the Goodman diversity panel. Association analysis identified 100 single and clustered SNP associations for resistance to NLB, but did not implicate natural functional variation at bm1-bm5. Strong associations implicated a suite of diverse candidate genes, including lignin-related genes such as a {beta}-glucosidase gene cluster, hct11, knox1, knox2, zim36, lbd35, CASP-like protein 8, and xat3. The candidate genes are targets for breeding quantitative resistance to NLB in maize for use in silage and non-silage purposes. Core IdeasO_LIBrown midrib mutants (bm1-bm4) in maize, characterized as mutations with reduced lignin content, are susceptible to a range of foliar pathogens. C_LIO_LISeveral brown midrib mutants in maize show enhanced susceptibility to stalk rot and ear rot pathogens. C_LIO_LIGenome wide association analysis identified a number of diverse candidate genes associated with resistance to northern leaf blight in maize, including lignin-related genes involved in the monolignol pathway, developmental genes and transcription factors. C_LIO_LIAssociation analysis for resistance to NLB implicated a {beta}-glucosidase gene cluster, including Zmbglu24 and Zmbglu25 known for targeting monolignols and contributing to [~]15% phenotypic variation. C_LIO_LIhct11, which plays an important role in the monolignol pathway, was implicated for resistance to northern leaf blight in maize with potential for multiple stress tolerance. C_LI

genetics↗

bioRxiv2019

Maize nested introgression library provides evidence for the involvement of liguleless1 in resistance to northern leaf blight

Plant disease resistance is largely governed by complex genetic architecture. In maize, few disease resistance loci have been characterized. Near-isogenic lines (NILs) are a powerful genetic tool to dissect quantitative trait loci (QTL). We analyzed an introgression library of maize near-isogenic lines (NILs), termed a nested NIL (nNIL) library for resistance to northern leaf blight (NLB) caused by the fungal pathogen Setosphaeria turcica. The nNIL library was comprised of 412 BC5F4 NILs that originated from 18 diverse donor parents and a common recurrent parent, B73. Single nucleotide polymorphisms identified through genotyping by sequencing (GBS) were used to define introgressions and for association analysis. NILs that conferred resistance and susceptibility to NLB were comprised of introgressions that overlapped known NLB QTL. Genome-wide association analysis and stepwise regression further resolved five QTL regions, and implicated several candidate genes, including Liguleless1 (Lg1), a key determinant of leaf architecture in cereals. Two independently-derived mutant alleles of lg1 inoculated with S. turcica showed enhanced susceptibility to NLB. In the maize nested association mapping population, leaf angle was positively correlated with NLB in five recombinant inbred line (RIL) populations, and negatively correlated with NLB in four RIL populations. This study demonstrates the power of a nNIL library combined with high density SNP coverage to resolve QTLs. Furthermore, the role of lg1 in leaf architecture and in resistance to NLB has important applications in crop improvement.\n\nSignificance Statement (120 words)Understanding the genetic basis of disease resistance is important for crop improvement. We analyzed response to northern leaf blight (NLB) in a maize population consisting of 412 near-isogenic lines (NILs) derived from 18 diverse donor parents backcrossed to a recurrent parent, B73. NILs were genotyped by sequencing to detect introgressed segments. We identified NILs with greater resistance or susceptibility to NLB than B73. Genome-wide association analysis, coupled with stepwise regression, identified 5 candidate loci for NLB resistance, including the liguleless1 gene. The LIGULELESS1 transcription factor is critical in development of the leaf ligular region and influences leaf angle. We found that liguleless1 mutants are significantly more susceptible to NLB, uncovering a pleiotropic role for liguleless1 in development and disease resistance.

plant biology↗