Late blight (LB), caused by the oomycete Phytophthora infestans, is one of the most devastating diseases of the cultivated tomato (Solanum lycopersicum) worldwide. Most commercial cultivars of tomato are susceptible to LB. Previously, three major LB resistance genes (Ph-1, Ph-2, Ph-3) were identified and incorporated into a few commercial cultivars of tomato. Reduced effectiveness and potential breakdown of the resistance genes has necessitated identification, characterization and utilization of new sources of resistance. We evaluated the response of 67 accessions of the wild tomato species, S. pimpinellifolium to LB, under multiple field and greenhouse (GH) conditions and compared them with six control genotypes. Sixteen accessions were identified with strong LB resistance in both field and GH experiments. However, 12 accessions exhibited resistance similar to a control line which was homozygous for Ph-2 + Ph-3. Genotyping accessions with molecular markers for Ph-2 and Ph-3 were not conclusive, indicating that resistance in these accessions could be due to these or other resistance genes. Strong correlations were observed between field and GH disease response and between foliar and stem infection.

Breeding for disease resistance requires efficient techniques for screening large plant populations. Late blight (LB), caused by the oomycete Phytophthora infestans, is one of the most devastating diseases of tomato (Solanum lycopersicum) worldwide, and there is a great interest in developing cultivars with resistance to this pathogen. Screening for LB resistance is commonly conducted under field or greenhouse conditions using whole plants. In a previous study, we demonstrated correspondence between field and greenhouse screening of tomato for LB resistance. Here, we report the use of a detached-leaflet assay for such screening. Seventy-two genotypes from two tomato species, varying in degree of resistance and susceptibility to LB, were evaluated in two replicated experiments for response to LB in a detached-leaflet assay, and the results were compared with those previously obtained from field and greenhouse screening of the same genotypes. There were significant (P < 0.001) positive correlations between replications (average r = 0.75) and experiments (average r = 0.72), suggesting that the detached-leaflet experiments were consistent. Further, there were significant (P < 0.001) positive correlations between responses in the detached-leaflet assay and those from field (r = 0.82) and greenhouse screenings (r = 0.84), suggesting reliability of the detached-leaflet assay. The results indicate the utility of the detached-leaflet assay for evaluating tomato for LB resistance, which may facilitate screening of large breeding populations.

Histone modifications regulate gene expression and chromosomal events, yet how histone-modifying enzymes are targeted is poorly understood. Here we report that a conserved DNA repair protein, SMRC-1, associates with MET-2, the C . elegans histone methyltransferase responsible for H3K9me1 and me2 deposition. We used molecular, genetic, and biochemical methods to investigate the biological role of SMRC-1 and to explore its relationship with MET-2. SMRC-1, like its mammalian ortholog SMARCAL1, provides protection from DNA replication stress. SMRC-1 limits accumulation of DNA damage and promotes germline and embryonic viability. MET-2 and SMRC-1 localize to mitotic and meiotic germline nuclei, and SMRC-1 promotes an increase in MET-2 abundance in mitotic germline nuclei upon replication stress. In the absence of SMRC-1, germline H3K9me2 generally decreases after multiple generations at high culture temperature. Genetic data are consistent with MET-2 and SMRC-1 functioning together to limit replication stress in the germ line and in parallel to promote other germline processes. We hypothesize that loss of SMRC-1 activity causes chronic replication stress, in part because of insufficient recruitment of MET-2 to nuclei.

Late blight (LB), caused by Phytophthora infestans, is a destructive disease of tomato (Solanum lycopersicum) worldwide. Currently, there are few commercial cultivars of tomato with resistance to LB, and the disease is mainly controlled by heavy use of fungicides. Due to the emergence of fungicide‐resistant pathogen isolates, there is a concerted effort to identify new genetic sources of resistance and breed new resistant cultivars. A recent screening identified several new tomato accessions with strong resistance to LB. Here, we report on the genetic basis of LB resistance in S. pimpinellifolium accession PI 270441, as determined by generation means analysis and analysis of response to selection, using populations derived from crosses with LB‐susceptible breeding line Fla. 8059. Heritability of LB resistance ranged from 0.76 to 0.78, and the minimum number of genes was estimated 1—few. These results suggest that transfer of LB resistance from PI 270441 to the cultivated tomato should be feasible via a traditional backcross breeding approach. Genetic mapping studies are underway to identify molecular markers associated with resistance in this accession.

Late blight (LB), caused by the oomycete Phytophthora infestans, is one of the most destructive diseases of the cultivated tomato (Solanum lycopersicum L.) and potato (Solanum tuberosum L.) worldwide. Genetic changes in the pathogen have resulted in the emergence of new genotypes, overcoming formerly effective fungicides or host resistance genes. We previously reported the identification of a LB-resistant accession (PI 270441) of the wild tomato species S. pimpinellifolium L. and the high heritability of its resistance. In the present study, an F 2 population (n = 1,209), derived from a cross between PI 270441 and a LB-susceptible tomato breeding line (Fla. 8059), was screened for response to LB infection. Extreme resistant (n = 44) and susceptible (n = 39) F 2 individuals were selected and used in a trait-based marker analysis (TBA; a.k.a selective genotyping) to identify and map quantitative trait loci (QTLs) conferring LB resistance. Reduced representation libraries (RRLs) of Fla.8059 and PI 270441 were constructed, sequenced, and mapped to the tomato genome. A total of 13,054 single-nucleotide polymorphisms (SNPs) were identified, of which, 200 were used to construct a genetic linkage map and locate QTLs. Four LB resistance QTLs were identified on chromosomes 1, 10, and 11 of PI 270441. The markers associated with these QTLs can be used to transfer LB resistance from PI 270441 into new tomato cultivars and to develop near-isogenic lines for fine mapping of the QTL.