Analysis of resistance to Xylella fastidiosa within a hybrid population of Pera sweet orange × Murcott tangor

HD Coletta‐Filho, EO Pereira, AA Souza… - Plant …, 2007 - Wiley Online Library
Plant Pathology, 2007Wiley Online Library
Resistance to Xylella fastidiosa was evaluated within a population of 20 interspecific hybrids
of Pera sweet orange and Murcott tangor under greenhouse conditions. Efficiency of
inoculation, multiplication of bacteria within the plants, xylem vessel morphology, and
symptom expression were analysed. The rate of infection ranged from 40 to 100%(average
70%) for all genotypes analysed. Xylella fastidiosa populations ranged from log 0· 59 to log
2· 13 cells mg− 1 tissue for the resistant hybrids. These values were significantly different …
Resistance to Xylella fastidiosa was evaluated within a population of 20 interspecific hybrids of Pera sweet orange and Murcott tangor under greenhouse conditions. Efficiency of inoculation, multiplication of bacteria within the plants, xylem vessel morphology, and symptom expression were analysed. The rate of infection ranged from 40 to 100% (average 70%) for all genotypes analysed. Xylella fastidiosa populations ranged from log 0·59 to log 2·13 cells mg−1 tissue for the resistant hybrids. These values were significantly different (P = 0·05) from those obtained for the tolerant (no symptoms but bacteria recovered) or susceptible (symptoms and bacteria recovered) hybrids (log 3·02 to log 4·06 cells mg−1). Xylella fastidiosa was recovered from all hybrids (log 2·31 to 5·03 CFU mg−1 tissue) except the resistant ones. The first foliar symptoms appeared at least 90 days post‐inoculation, the time varying according to genotype. No correlation between xylem vessel morphology and disease expression was observed, indicating that the resistance was the result of a genetic response of the host. According to this hypothesis, a high broad‐based heritability index for resistance was obtained (0·96) at 210 days from X. fastidiosa inoculations, using bacterial quantification by real‐time PCR, which indicated that the influence of the number of bacteria was the result of genetic rather than environmental variations.
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