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Systems genetics reveals a transcriptional network associated with susceptibility in the maize–grey leaf spot pathosystem
Author(s) -
Christie Nanette,
Myburg Alexander A.,
Joubert Fourie,
Murray Shane L.,
Carstens Maryke,
Lin YaoCheng,
Meyer Jacqueline,
Crampton Bridget G.,
Christensen Shawn A.,
Ntuli Jean F.,
Wighard Sara S.,
Van de Peer Yves,
Berger Dave K.
Publication year - 2017
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.13419
Subject(s) - biology , quantitative trait locus , genetics , pathosystem , expression quantitative trait loci , population , gene , plant disease resistance , single nucleotide polymorphism , genotype , demography , sociology
Summary 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 ( CML 444 × SC Malawi) subjected in the field to C. zeina infection allowed detection of 20 206 expression quantitative trait loci ( eQTL s). Four trans ‐ eQTL hotspots coincided with GLS disease QTL s 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 ‐ eQTL s in hotspots on chromosomes 9 and 10, which also coincided with phenotypic QTL s 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 ‐ eQTL s in hotspots coinciding with GLS resistance QTL s 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.