The Genetic Basis of Disease Resistance in Maize

Jamann, Tiffany M.; Nelson, Rebecca; Balint‐Kurti, Peter

doi:10.1002/9781118728475.ch3

Cited by 1 publication

(1 citation statement)

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“…A review of the genetic architecture of disease resistance in maize listed 50 publications on the mapping of maize disease resistance loci (Wisser et al, 2006). However, identifying the genes, and ultimately the genetic polymorphisms, underlying QTLs that confer QDR in maize is currently a major challenge (Jamann et al, 2013). Therefore, as an initial strategy towards cloning a QTL, transcriptomics can be employed to explore the molecular processes leading to resistance or susceptibility conferred by a QTL (Liu et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Systems genetics reveals a transcriptional network associated with susceptibility in the maize–grey leaf spot pathosystem

et al. 2017

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We used a systems genetics approach to elucidate the molecular mechanisms of the responses of maize to grey leaf spot (GLS) disease caused by Cercospora zeina, a threat to maize production globally. Expression analysis of earleaf samples in a subtropical maize recombinant inbred line population (CML444 × SC Malawi) subjected in the field to C. zeina infection allowed detection of 20 206 expression quantitative trait loci (eQTLs). Four trans-eQTL hotspots coincided with GLS disease QTLs mapped in the same field experiment. Co-expression network analysis identified three expression modules correlated with GLS disease scores. The module (GY-s) most highly correlated with susceptibility (r = 0.71; 179 genes) was enriched for the glyoxylate pathway, lipid metabolism, diterpenoid biosynthesis and responses to pathogen molecules such as chitin. The GY-s module was enriched for genes with trans-eQTLs in hotspots on chromosomes 9 and 10, which also coincided with phenotypic QTLs for susceptibility to GLS. This transcriptional network has significant overlap with the GLS susceptibility response of maize line B73, and may reflect pathogen manipulation for nutrient acquisition and/or unsuccessful defence responses, such as kauralexin production by the diterpenoid biosynthesis pathway. The co-expression module that correlated best with resistance (TQ-r; 1498 genes) was enriched for genes with trans-eQTLs in hotspots coinciding with GLS resistance QTLs on chromosome 9. Jasmonate responses were implicated in resistance to GLS through co-expression of COI1 and enrichment of genes with the Gene Ontology term 'cullin-RING ubiquitin ligase complex' in the TQ-r module. Consistent with this, JAZ repressor expression was highly correlated with the severity of GLS disease in the GY-s susceptibility network.

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Section: Introductionmentioning

confidence: 99%