An NLR gene likely underlying RMES1 provides global sorghum resistance bolstered by RMES2
Date
2023
Journal Title
Journal ISSN
Volume Title
Abstract
Breeding for aphid host plant resistance in sorghum has been an area of interest since the emergence of Melanaphis sorghi in North America a decade ago. In order to develop durable sorghum aphid resistance, breeders must be equipped with tools (trait package) and knowledge (molecular mechanisms) of host plant resistance. In this dissertation, I characterize the current state of sorghum aphid breeding and propose a genotype to phenotype map for the major source of global resistance, Resistance to Melanaphis sorghi 1. Relying on near-isogenic lines, I demonstrate that RMES1 is applying selection pressure to sorghum aphid through reduction in fecundity that discriminates among aphid species. In global sorghum lines, RMES1 is rare whereas a second resistance source, RMES2, is common and present in historic breeding germplasm. I mapped RMES2 in Haitian breeding populations where it contributes fitness increases while lacking antagonistic pleiotropy and is selected for alongside RMES1. These results suggest breeding programs may unknowingly be deploying both sources of resistance which in combination are reducing the likelihood of M. sorghi biotype shifts to overcome RMES1. As aphid resistance may rely on phytochemical and/or induction with extended phenotypes regarding aphid populations, I used pan-genomic, transcriptomic, and metabolomic resources to describe the molecular mechanism of RMES1. Structural variation at the Chr06 locus underlies presence/absence variation of several nucleotide-binding leucine-rich repeat receptor (NLR) genes. Two of these candidate genes, SbPI276837.06G016400 and SbPI276837.06G016600, are representatives of two orthologous NLR groups which have genomic and transcriptomic evidence of underlying RMES1 resistance. The PAL branch of the salicylic acid pathway is the primary phytohormone pathway responsible for RMES1-induced resistance. Finally, metabolome reorganization mirroring transcriptome changes suggest RMES1 is inducing multiple downstream mechanisms responsible for reducing aphid fecundity. While the causal gene underlying RMES1 remains to be cloned and the eliciting aphid factor is unknown, this research suggests that gene-for-gene dynamics could lead to resistance-breaking biotype shifts and combining RMES1 with additional resistance genes e.g. RMES2, will help achieve durability.
Description
Rights Access
Subject
durability
sorghum
resistance
aphid