ESTABLISHING THE GENETIC BASIS FOR RESISTANCE AND VIRULENCE IN FINGER MILLET - Magnaporthe oryzae INTERACTIONS USING GENOME-WIDE ASSOCIATION STUDIES IN EASTERN AFRICA

Abstract

Finger millet (Eleusine coracana spp. coracana) is an important food and income source for millions of smallholder farmers in eastern Africa. Most of the farmers use unimproved varieties which are vulnerable to biotic and abiotic stresses. Finger millet blast disease caused Magnaporthe oryzae, is the most important constrain to finger millet production worldwide. The development of blast-resistant finger millet varieties is widely accepted as the preferred approach towards blast management. To achieve this, knowledge of the genetic basis of resistant traits in finger millet and their corresponding avirulence genes on M. oryzae is essential. Consequently, genome-wide association studies (GWAS) were conducted with 9983 single nucleotide polymorphisms (SNPs) from 127 diverse eastern African finger millet accessions and 174300 SNPs from 187 fungal isolates which were collected from Ethiopia, Kenya, Tanzania and Uganda. These SNPs were previously identified using genotype-by-sequencing (GBS) for finger millet and Illumina whole-genome sequencing for M. oryzae isolates. To account for population structure and improve the statistical power of detection of significant peaks, Fixed and random model Circulating Probability Unification (FarmCPU) implemented in the GAPIT R programming package was used. Nineteen SNPs were significantly associated with resistance in finger millet while eight SNPs with virulence in M. oryzae. The candidate genes underpinning the blast tolerance phenotype were indicated to exhibit pathogen associated molecular patterns (PAMPs) triggered and effector-triggered immunity mechanisms. The identified genes include leucine-rich repeat receptor-like protein, serine/threonine protein kinase and receptor-like kinase which play crucial roles in plant innate immunity. The results also demonstrated the role of the plant hormones genes in immune responses to pathogen such as ethylene-responsive hormone in signaling cascades for upregulating expression of pathogenesis-responsive genes which cause the over expressions of pathogen recognition receptors. Taken together, the findings of this vi study established the platform for association mapping studies on blast disease in the region and, if the significant SNPs identified here are validated to determine blast tolerant phenotypes, it will contribute towards marker-assisted breeding and/or cloning of specific resistance or avirulence genes