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<p>Pierce’s disease (PD) is a serious malady of grapevines caused by the bacterium <i>Xylella fastidiosa</i>. Identification of unique resistant sources is crucial for breeding programs. In this report, we describe the results of genetic mapping and quantitative trait locus (QTL) analyses for the resistance to PD in the accession b42-26. A total of 323 seedlings from a F1 mapping population were used to construct a framework genetic map with simple sequence repeat markers. Of the 1,069 markers tested for accession b42-26, 883 amplified successfully, with 217 showing polymorphism. Evaluations for PD resistance were carried out by a greenhouse-based ELISA screen. Genetic mapping and QTL analyses were carried out with JOINMAP and MAPQTL. An additional 66 seedlings from six pseudo backcross populations were also evaluated for PD and marker tested to confirm the results. The genetic analysis of b42-26 revealed a high level of homozygosity with only a quarter of the markers showing polymorphism. Chromosome 19 was completely monomorphic for all tested markers. Several chromosomes exhibited significant deviation from the expected segregation ratio, namely chromosome 1, 4, 6, and 7. Additionally, all the markers on chromosomes 10, 11, 12, and 18 were distorted in their segregation. One main (chromosome 8) and three minor QTLs were detected on chromosomes 10, 14 and 17, accounting for a total 16.3% phenotypic variation, cumulatively. The main QTL on chromosome 8 was named Pierce’s disease resistance 2 (q-<i>PdR2</i>) and was further evaluated in backcross populations. Disease evaluation showed that pBC1 and pBC2 lines with the q-<i>PdR2</i> locus alone had better resistance than those without it. This work provides genetic insights for the PD resistant accession b42-26, a <i>Vitis girdiana/arizonica</i> genotype collected from the Baja California Sur peninsula. Isolation led to inbreeding that created high level of homozygosity and segregation distortion. Pierce’s disease resistance in b42-26 is multigenetic.</p>

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Identification of Pierce’s Disease Resistance in a V. girdiana Hybrid from Baja California Sur, Mexico

  • 期刊论文

  • 发表日期：

    2026年1月6日

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  • Summaira Riaz,
  • Alan Tenscher,
  • Michael A. Walker

摘要

Pierce’s disease (PD) is a serious malady of grapevines caused by the bacterium Xylella fastidiosa. Identification of unique resistant sources is crucial for breeding programs. In this report, we describe the results of genetic mapping and quantitative trait locus (QTL) analyses for the resistance to PD in the accession b42-26. A total of 323 seedlings from a F1 mapping population were used to construct a framework genetic map with simple sequence repeat markers. Of the 1,069 markers tested for accession b42-26, 883 amplified successfully, with 217 showing polymorphism. Evaluations for PD resistance were carried out by a greenhouse-based ELISA screen. Genetic mapping and QTL analyses were carried out with JOINMAP and MAPQTL. An additional 66 seedlings from six pseudo backcross populations were also evaluated for PD and marker tested to confirm the results. The genetic analysis of b42-26 revealed a high level of homozygosity with only a quarter of the markers showing polymorphism. Chromosome 19 was completely monomorphic for all tested markers. Several chromosomes exhibited significant deviation from the expected segregation ratio, namely chromosome 1, 4, 6, and 7. Additionally, all the markers on chromosomes 10, 11, 12, and 18 were distorted in their segregation. One main (chromosome 8) and three minor QTLs were detected on chromosomes 10, 14 and 17, accounting for a total 16.3% phenotypic variation, cumulatively. The main QTL on chromosome 8 was named Pierce’s disease resistance 2 (q-PdR2) and was further evaluated in backcross populations. Disease evaluation showed that pBC1 and pBC2 lines with the q-PdR2 locus alone had better resistance than those without it. This work provides genetic insights for the PD resistant accession b42-26, a Vitis girdiana/arizonica genotype collected from the Baja California Sur peninsula. Isolation led to inbreeding that created high level of homozygosity and segregation distortion. Pierce’s disease resistance in b42-26 is multigenetic.