Genetic bases of resistance to the ricehoja blancadisease deciphered by a QTL approach

Author:

Silva Alexander,Montoya María Elker,Quintero Constanza,Cuasquer Juan,Tohme Joe,Graterol Eduardo,Cruz Maribel,Lorieux Mathias

Abstract

ABSTRACTRicehoja blanca(RHB) is one of the most serious diseases in rice growing areas in tropical Americas. Its causal agent isRice hoja blanca virus(RHBV), transmitted by the planthopperTagosodes orizicolusMüir. Genetic resistance is the most effective and environment-friendly way of controlling the disease. So far, only one major quantitative trait locus (QTL) ofOryza sativassp.japonicaorigin,qHBV4.1,that alters incidence of the virus symptoms in two Colombian cultivars has been reported. This resistance has already started to be broken, stressing the urgent need for diversifying the resistance sources. In the present study we performed a search for new QTLs ofO. sativa indicaorigin associated with RHB resistance. We used four F2:3segregating populations derived fromindicaresistant varieties crossed with a highly susceptiblejaponicapivot parent. Beside the standard method for measuring disease incidence, we developed a new method based on computer-assisted image processing to determine the affected leaf area (ALA) as a measure of symptom severity. Based on the disease severity and incidence scores in the F3families under greenhouse conditions, and SNP genotyping of the F2individuals, we identified four newindicaQTLs for RHB resistance on rice chromosomes 4, 6 and 11, namelyqHBV4.2WAS208,qHBV6.1PTB25,qHBV11.1andqHBV11.2. We also confirmed the wide-range action ofqHBV4.1. Among the five QTLs,qHBV4.1andqHBV11.1had the largest effects on incidence and severity, respectively. These results provide a more complete understanding of the genetic bases of RHBV resistance in the cultivated rice gene pool, and can be used to develop marker-aided breeding strategies to improve RHB resistance. The power of joint- and meta-analyses allowed precise mapping and candidate gene identification, providing the basis for positional cloning of the two major QTLsqHBV4.1andqHBV11.1.

Publisher

Cold Spring Harbor Laboratory

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