Genetic loci underlying quantitative resistance to necrotrophic pathogens Sclerotinia and Diaporthe ( Phomopsis ), and c
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ORIGINAL ARTICLE
Genetic loci underlying quantitative resistance to necrotrophic pathogens Sclerotinia and Diaporthe (Phomopsis), and correlated resistance to both pathogens Cloe S. Pogoda1 · Stephan Reinert1 · Zahirul I. Talukder2 · Ziv Attia1 · Erin C. E. Collier‑zans1 · Thomas J. Gulya3 · Nolan C. Kane1 · Brent S. Hulke3 Received: 19 June 2020 / Accepted: 18 September 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Key message We provide results rooted in quantitative genetics, which combined with knowledge of candidate gene function, helps us to better understand the resistance to two major necrotrophic pathogens of sunflower. Abstract Necrotrophic pathogens can avoid or even benefit from plant defenses used against biotrophic pathogens, and thus represent a distinct challenge to plant populations in natural and agricultural systems. Sclerotinia and Phomopsis/Diaporthe are detrimental pathogens for many dicotyledonous plants, including many economically important plants. With no wellestablished methods to prevent infection in susceptible plants, host-plant resistance is currently the most effective strategy. Despite knowledge of a moderate, positive correlation in resistance to the two diseases in sunflower, detailed analysis of the genetics, in the same populations, has not been conducted. We present results of genome-wide analysis of resistance to both pathogens in a diversity panel of 218 domesticated sunflower genotypes of worldwide origin. We identified 14 Sclerotinia head rot and 7 Phomopsis stem canker unique QTLs, plus 1 co-located QTL for both traits, and observed extensive patterns of linkage disequilibrium between sites for both traits. Most QTLs contained one credible candidate gene, and gene families were common for the two disease resistance traits. These results suggest there has been strong, simultaneous selection for resistance to these two diseases and that a generalized mechanism for defense against these necrotrophic pathogens exists.
Introduction
Communicated by Volker Hahn. Cloe S. Pogoda and Stephan Reinert contributed equally. Thomas J. Gulya retired. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00122-020-03694-x) contains supplementary material, which is available to authorized users. * Brent S. Hulke [email protected] 1
Ecology and Evolutionary Biology Department, University of Colorado, 1900 Pleasant Street, 334 UCB, Boulder, CO 80309‑0334, USA
2
Department of Plant Sciences, North Dakota State University, 166 Loftsgard Hall, Fargo, ND 58108‑6050, USA
3
USDA-ARS Edward T Schafer Agricultural Research Center, 1616 Albrecht Blvd. N., Fargo, ND 58102‑2765, USA
Infection from necrotrophic pathogens represents an unique challenge, both in natural and agricultural systems (Hims 1979). Plants typically defend against biotrophic pathogens by detecting pathogen elicitors via nucleotide binding site—leucine-rich repeat (NBS-LRR) genes and related complexes, resulting in signaling cascades l
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