SUMMARY Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola cause bacterial blight and bacterial leaf streak of rice (Oryza sativa), which constrain production of this staple crop in much of Asia and parts of Africa. Tremendous progress has been made in characterizing the diseases and breeding for resistance. X. oryzae pv. oryzae causes bacterial blight by invading the vascular tissue, while X. oryzae pv. oryzicola causes bacterial leaf streak by colonizing the parenchyma. In rice there are 29 major genes for resistance to bacterial blight, but so far only a few quantitative resistance loci for bacterial leaf streak. Over 30 races of X. oryzae pv. oryzae have been reported. Both pathogens exhibit genetic variation among isolates. Mechanisms of pathogenesis and resistance have begun to be elucidated. Members of the AvrBs3/PthA family of transcription activator‐like effectors play a major role in the virulence of X. oryzae pv. oryzae and possibly X. oryzae pv. oryzicola. Cloning of six rice resistance genes for bacterial blight and one from maize effective against bacterial leaf streak has uncovered a diversity of structure and function, some shared by genes involved in defence in animals. This article reviews research that spans a century. It also presents a perspective on challenges for sustainable control, and opportunities that interactions of X. oryzae pathovars with rice present as models for understanding fundamental aspects of bacterial pathogenesis of plants and plant disease resistance, as well as other aspects of plant and microbial biology, with implications also for animal innate immunity.

Bacterial leaf streak of rice, caused by Xanthomonas oryzae pv. oryzicola (Xoc) is an increasingly important yield constraint in this staple crop. A mesophyll colonizer, Xoc differs from X. oryzae pv. oryzae (Xoo), which invades xylem to cause bacterial blight of rice. Both produce multiple distinct TAL effectors, type III-delivered proteins that transactivate effector-specific host genes. A TAL effector finds its target(s) via a partially degenerate code whereby the modular effector amino acid sequence identifies nucleotide sequences to which the protein binds. Virulence contributions of some Xoo TAL effectors have been shown, and their relevant targets, susceptibility (S) genes, identified, but the role of TAL effectors in leaf streak is uncharacterized. We used host transcript profiling to compare leaf streak to blight and to probe functions of Xoc TAL effectors. We found that Xoc and Xoo induce almost completely different host transcriptional changes. Roughly one in three genes upregulated by the pathogens is preceded by a candidate TAL effector binding element. Experimental analysis of the 44 such genes predicted to be Xoc TAL effector targets verified nearly half, and identified most others as false predictions. None of the Xoc targets is a known bacterial blight S gene. Mutational analysis revealed that Tal2g, which activates two genes, contributes to lesion expansion and bacterial exudation. Use of designer TAL effectors discriminated a sulfate transporter gene as the S gene. Across all targets, basal expression tended to be higher than genome-average, and induction moderate. Finally, machine learning applied to real vs. falsely predicted targets yielded a classifier that recalled 92% of the real targets with 88% precision, providing a tool for better target prediction in the future. Our study expands the number of known TAL effector targets, identifies a new class of S gene, and improves our ability to predict functional targeting.

Markers corresponding to 27 plant defense genes were tested for linkage disequilibrium with quantitative resistance to late blight in a diploid potato population that had been used for mapping quantitative trait loci (QTLs) for late blight resistance. Markers were detected by using (i) hybridization probes for plant defense genes, (ii) primer pairs amplifying conserved domains of resistance (R) genes, (iii) primers for defense genes and genes encoding transcriptional regulatory factors, and (iv) primers allowing amplification of sequences flanking plant defense genes by the ligation-mediated polymerase chain reaction. Markers were initially screened by using the most resistant and susceptible individuals of the population, and those markers showing different allele frequencies between the two groups were mapped. Among the 308 segregating bands detected, 24 loci (8%) corresponding to six defense gene families were associated with resistance at chi2 > or = 13, the threshold established using the permutation test at P = 0.05. Loci corresponding to genes related to the phenylpropanoid pathway (phenylalanine ammonium lyase [PAL], chalcone isomerase [CHI], and chalcone synthase [CHS]), loci related to WRKY regulatory genes, and other -defense genes (osmotin and a Phytophthora infestans-induced cytochrome P450) were significantly associated with quantitative disease resistance. A subset of markers was tested on the mapping population of 94 individuals. Ten defense-related markers were clustered at a QTL on chromosome III, and three defense-related markers were located at a broad QTL on chromosome XII. The association of candidate genes with QTLs is a step toward understanding the molecular basis of quantitative resistance to an important plant disease.

Most commercial cultivars of tomato, Lycopersicon esculentum Mill., are susceptible to early blight (EB), a devastating fungal ( Alternaria solani Sorauer) disease of tomato in the northern and eastern parts of the U.S. and elsewhere in the world. The disease causes plant defoliation, which reduces yield and fruit quality, and contributes to significant crop loss. Sources of resistance have been identified within related wild species of tomato. The purpose of this study was to identify and validate quantitative trait loci (QTLs) for EB resistance in backcross populations of a cross between a susceptible tomato breeding line (NC84173; maternal and recurrent parent) and a resistant Lycopersicon hirsutum Humb. and Bonpl. accession (PI126445). Sixteen hundred BC(1) plants were grown to maturity in a field in 1998. Plants that were self-incompatible, indeterminant in growth habit, and/or extremely late in maturity, were discarded in order to eliminate confounding effects of these factors on disease evaluation, QTL mapping, and future breeding research. The remaining 145 plants (referred to as the BC(1) population) were genotyped for 141 restriction fragment length polymorphism (RFLP) markers and 23 resistance gene analogs (RGAs), and a genetic linkage map was constructed. BC(1) plants were evaluated for disease symptoms throughout the season, and the area under the disease progress curve (AUDPC) and the final percent defoliation (disease severity) were determined for each plant. BC(1) plants were self-pollinated and produced BC(1)S(1) seed. The BC(1)S(1) population, consisting of 145 BC(1)S(1) families, was grown and evaluated for disease symptoms in replicated field trials in two subsequent years (1999 and 2000) and AUDPC and/or final percent defoliation were determined for each family in each year. Two QTL mapping approaches, simple interval mapping (SIM) and composite interval mapping (CIM), were used to identify QTLs for EB resistance in the BC(1) and BC(1)S(1) populations. QTL results were highly consistent across generations, years and mapping approaches. Approximately ten significant QTLs (LOD >/= 2.4, P 57% of the total phenotypic variation. All QTLs had the positive alleles from the disease-resistant parent. The good agreement between results of the BC(1) and 2 years of the BC(1)S(1) generations indicated the stability of the identified QTLs and their potential usefulness for improving tomato EB resistance using marker-assisted selection (MAS). Further inspections using SIM and CIM indicated that six of the ten QTLs had independent additive effects and together could account for up to 56.4% of the total phenotypic variation. These complementary QTLs, which were identified in two generations and 3 years, should be the most useful QTLs for MAS and improvement of tomato EB resistance using PI126445 as a gene resource. Furthermore, the chromosomal locations of 10 of the 23...

A molecular linkage map of tomato was constructed based on a BC1 population (N = 145) of a cross between Lycopersicon esculentum Mill. line NC84173 (maternal and recurrent parent) and Lycopersicon hirsutum Humb. and Bonpl. accession PI126445. NC84173 is an advanced breeding line that is resistant to several tomato diseases, not including early blight (EB) and late blight (LB). PI126445 is a self-incompatible accession that is resistant to many tomato diseases, including EB and LB. The map included 142 restriction fragment length polymorphism (RFLP) markers and 29 resistance gene analogs (RGAs). RGA loci were identified by PCR amplification of genomic DNA from the BC1 population, using ten pairs of degenerate oligonucleotide primers designed based on conserved leucine-rich repeat (LRR), nucleotide binding site (NBS), and serine (threonine) protein kinase (PtoKin) domains of known resistance genes (R genes). The PCR-amplified DNAs were separated by denaturing polyacrylamide gel electrophoresis (PAGE), which allowed separation of heterogeneous products and identification and mapping of individual RGA loci. The map spanned 1469 cM of the 12 tomato chromosomes with an average marker distance of 8.6 cM. The RGA loci were mapped to 9 of the 12 tomato chromosomes. Locations of some RGAs coincided with locations of several known tomato R genes or quantitative resistance loci (QRLs), including Cf-1, Cf-4, Cf-9, Cf-ECP2, rx-1, and Cm1.1 (chromosome 1); Tm-1 (chromosome 2); Asc (chrromosme 3); Pto, Fen, and Prf (chromosome 5); 01-1, Mi, Ty-1, Cm6.1, Cf-2, CF-5, Bw-5, and Bw-1 (chromosome 6); I-1, 1-3, and Ph-1 (chromosome 7); Tm-2a and Fr1 (chromosome 9); and Lv (chromosome 12). These co-localizations indicate that the RGA loci were either linked to or part of the known R genes. Furthermore, similar to that for many R gene families, several RGA loci were found in clusters, suggesting their potential evolutionary relationship with R genes. Comparisons of the present map with other molecular linkage maps of tomato, including the high density L. esculentum x Lycopersicon pennellii map, indicated that the lengths of the maps and linear order of RFLP markers were in good agreement, though certain chromosomal regions were less consistent than others in terms of the frequency of recombination. The present map provides a basis for identification and mapping of genes and QTLs for disease resistance and other desirable traits in PI126445 and other L. hirsutum accessions, and will be useful for marker-assisted selection and map-based gene cloning in tomato.