Evidence map›Paper›PMID 42047721›Full record

ArticleTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik2026

Global perspective on the genetic architecture of susceptibility to spot form net blotch in barley.

Michele C Malvestiti, Sefunmi Alaofin, Ryan Skiba, Shengming Yang, Jason D Fiedler, Zhaohui Liu, Timothy L Friesen

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Article in TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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5 · Who and what money

Authors and funding

7 authors.

Michele C MalvestitiDepartment of Plant Pathology, North Dakota State University, Fargo, ND, USA.
Sefunmi AlaofinDepartment of Plant Pathology, North Dakota State University, Fargo, ND, USA.
Ryan SkibaCereals Crops Improvement Research Unit, USDA-ARS,, Fargo, ND, USA.
Shengming YangCereals Crops Improvement Research Unit, USDA-ARS,, Fargo, ND, USA.
Jason D FiedlerCereals Crops Improvement Research Unit, USDA-ARS,, Fargo, ND, USA.
Zhaohui LiuDepartment of Plant Pathology, North Dakota State University, Fargo, ND, USA.
Timothy L FriesenDepartment of Plant Pathology, North Dakota State University, Fargo, ND, USA. timothy.friesen@usda.gov.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key messageGlobal populations of Pyrenophora teres f. maculata have evolved to target multiple dominant barley susceptibility loci, highlighting the risk of widespread disease under local selection pressures. The necrotrophic fungal pathogen Pyrenophora teres f. maculata causes spot form net blotch (SFNB), a global disease of barley. This fungus uses effector proteins to promote infection, which act in an inverse gene-for-gene manner by targeting dominant host susceptibility genes. Currently, there is a general understanding of the genetics of resistance/susceptibility in the host; however, there are still gaps in our understanding of global pathogen virulence and how it has evolved to target the host and cause disease. Because the P. teres f. maculata-barley interaction conforms to an inverse gene-for-gene model, we crossed three different susceptible barley lines (Hockett, TR 326, and PI 392501) with the resistant line PI 67381 and mapped recombinant inbred populations to characterize the susceptibility in these lines based on their response to ten pathogen isolates collected from diverse barley growing regions on five continents. Four independent quantitative trait loci (QTL) showed associations with susceptibility and mapped to barley chromosomes (Chr) 2HS, 4HS, 4HL, and 7HL. In all three populations, the same genomic position on Chr7HL was associated with the highest susceptibility levels and was targeted by seven of the ten fungal isolates. The QTL identified on Chr2HS mapped to the same position in two populations and was also targeted by seven of the ten isolates. However, the Chr4HS and Chr4HL susceptibilities were targeted by only three and two of the global isolates, respectively. This work shows that pathogen populations under different host selection pressures can evolve to target different barley susceptibility loci.

Indexed as

AscomycotaHordeumHost-Pathogen InteractionsChromosomes, PlantCrops, AgriculturalGenetic Predisposition to DiseasePhenotypePlant DiseasesQuantitative Trait Loci

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.