QTL mapping to anthracnose leaf blight resistance in tropical maize

Romanek, Cristiane; Matiello, Rodrigo Rodrigues; Coelho, Caroline de Jesus; Schafascheck, Lilian; Silva, Danilo Fernando Guimarães; Gardingo, José Raulindo

doi:10.1590/1984-70332017v17n4a58

Cited by 1 publication

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“…The polygenic nature of ALB was further confirmed by genetic mapping of ALB resistance in a biparental recombinant inbred line (RIL) population origination from a cross between ALB-resistant L R 04-2 and ALB-susceptible L S 95-1 inbred lines. Four out of seventeen QTL, one on chromosome 9 (QTL13; Table 1 ) and three on chromosome 10 (QTL15 through 17; Table 1 and Figure 3 ) were the most stable and explained 27.7 to 54.3% of the variance in ALB severity in the RIL population [ 27 ]. However, genes underlying the QTL controlling ALB resistance remain unknown.…”

Section: Genetic Architecture Of Anthracnose Resistance In Maizementioning

confidence: 99%

Molecular Genetics of Anthracnose Resistance in Maize

Gao

Han

et al. 2022

JoF

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Maize (Zea mays), also called corn, is one of the top three staple food crops worldwide and is also utilized as feed (e.g., feed grain and silage) and a source of biofuel (e.g., bioethanol). Maize production is hampered by a myriad of factors, including although not limited to fungal diseases, which reduce grain yield and downgrade kernel quality. One such disease is anthracnose leaf blight and stalk rot (ALB and ASR) caused by the hemibiotrophic fungal pathogen Colletotrichum graminicola. The pathogen deploys a biphasic infection strategy to colonize susceptible maize genotypes, comprising latent (symptomless) biotrophic and destructive (symptomatic) necrotrophic phases. However, the resistant maize genotypes restrict the C. graminicola infection and in planta fungal proliferation during the biotrophic phase of the infection. Some studies on the inheritance of ASR resistance in the populations derived from biparental resistant and susceptible genotypes reveal that anthracnose is likely a gene-for-gene disease in which the resistant maize genotypes and C. graminicola recognize each other by their matching pairs of nucleotide-binding leucine-rich repeat resistance (NLR) proteins (whose coding genes are localized in disease QTL) and effectors (1–2 effectors/NLR) during the biotrophic phase of infection. The Z. mays genome encodes approximately 144 NLRs, two of which, RCg1 and RCg1b, located on chromosome 4, were cloned and functionally validated for their role in ASR resistance. Here, we discuss the genetic architecture of anthracnose resistance in the resistant maize genotypes, i.e., disease QTL and underlying resistance genes. In addition, this review also highlights the disease cycle of C. graminicola and molecular factors (e.g., virulence/pathogenicity factors such as effectors and secondary metabolites) that contribute to the pathogen’s virulence on maize. A detailed understanding of molecular genetics underlying the maize—C. graminicola interaction will help devise effective management strategies against ALB and ASR.

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Section: Genetic Architecture Of Anthracnose Resistance In Maizementioning

confidence: 99%