RESUMO
Leveillula taurica is a major pathogen of tomato and several other crops that can cause substantial yield losses in favorable conditions for the fungus. Quinone outside inhibitor fungicides (QoIs) are routinely used for the control of the pathogen in tomato fields across California, but their recurrent use could lead to the emergence of resistance against these compounds. Here, we partially cloned the cytochrome b gene from L. taurica (Lt cytb) and searched within populations of the fungus collected from tomato fields across California for mutations that confer resistance to QoIs. A total of 21 single nucleotide polymorphisms (SNPs) were identified within a 704 bp fragment of the Lt cytb gene analyzed, of which five were non-synonymous substitutions. Among the most frequent SNPs encountered within field populations of the pathogen was the G143A substitution that confers high levels of resistance against QoIs in several fungi. The other four amino acid substitutions were novel mutations, whose effect on QoI resistance is currently unknown. Sequencing of the Lt cytb gene from individual single-cell conidia of the fungus further revealed that most SNPs, including the one leading to the G143A substitution, were present in a heteroplasmic state, indicating the co-existence of multiple mitotypes in single cells. Analysis of the field samples showed that the G143A substitution is predominantly heteroplasmic also within field populations of L. taurica in California, suggesting that QoI resistance in this fungus is likely to be quantitative rather than qualitative.
RESUMO
Fusarium wilt of tomato, caused by the soilborne fungus Fusarium oxysporum f. sp. lycopersici, is an increasingly important disease of tomato. This paper reports the high-quality draft genome assembly of F. oxysporum f. sp. lycopersici isolate D11 (race 3), which consists of 39 scaffolds with 57,281,978 bp (GC content, 47.5%), an N 50 of 4,408,267 bp, a mean read coverage of 99.8×, and 17,682 predicted genes.
RESUMO
KEY MESSAGE: Screening of wild tomato accessions revealed a source of resistance to Pseudomonas syringe pv. tomato race 1 from Solanum habrochaites and facilitated mapping of QTLs controlling disease resistance. Pseudomonas syringae pv. tomato (Pst) causes bacterial speck of tomato, which is one of the most persistent bacterial diseases in tomato worldwide. Existing Pst populations have overcome genetic resistance mediated by the tomato genes Pto and Prf. The objective of this study was to identify sources of resistance to race 1 strains and map quantitative trait loci (QTLs) controlling resistance in the wild tomato Solanum habrochaites LA1777. Pst strains A9 and 407 are closely related to current field strains and genome sequencing revealed the lack of the avrPto effector as well as select mutations in the avrPtoB effector, which are recognized by Pto and Prf. Strains A9 and 407 were used to screen 278 tomato accessions, identifying five exhibiting resistance: S. peruvianum LA3799, S. peruvianum var. dentatum PI128655, S. chilense LA2765, S. habrochaites LA2869, and S. habrochaites LA1777. An existing set of 93 introgression lines developed from S. habrochaites LA1777 was screened for resistance to strain A9 in a replicated greenhouse trial. Four QTLs were identified using composite interval mapping and mapped to different chromosomes. bsRr1-1 was located on chromosome 1, bsRr1-2 on chromosome 2, and bsRr1-12a and bsRr1-12b on chromosome 12. The QTLs detected explained 10.5-12.5% of the phenotypic variation. Promising lines were also subjected to bacterial growth curves to verify resistance and were analyzed for general horticultural attributes under greenhouse conditions. These findings will provide useful information for future high-resolution mapping of each QTL and integration into marker-assisted breeding programs.
