anthomonas oryzae pv. oryzae (Xoo) is the etiological agent of bacterial blight disease in rice. The disease is most severe in southeast Asia but is increasingly damaging in west African countries, and results in substantial yield loss 1. TALes from Xoo are injected by a type III secretion system into plant cells and recognize effector-binding elements (EBEs) in cognate SWEET host gene promoters, which results in induction of SWEET genes and production of sugars that enable disease susceptibility in rice 2,3. An array of central repeats, which are 34-35 amino acids long, are present in each TALe and interact with EBEs via two repeat variable di-residues (RVDs) at the 12th and 13th position of each repeat 4,5. Aberrant repeats, longer than 35 amino acids, are hypothesized to allow looping out of the repeat to accommodate alternate sequence binding for a particular TALe 6. Bacterial blight depends on TALe-mediated induction of at least one member of a family of sugar-transporter genes. Although rice has more than 20 SWEET genes, only those of clade III are reported to be induced by Xoo 7-10. Although all five of the known clade III SWEET genes in rice can function as susceptibility genes for bacterial blight, only three are known to be targeted in nature 10. More specifically, SWEET11 expression is induced by strains encoding the TALe PthXo1, SWEET13 by PthXo2 and SWEET14 by any one of several TALes, namely AvrXa7, PthXo3, TalC and TalF (originally Tal5) 7,9-15 (Table 1). Effectors of Xoo that target clade III SWEET genes are referred to as major TALes owing to their strong virulence effect. Naturally occurring resistance has arisen as the result of nucleotide polymorphisms in EBEs of SWEET promoters. EBE alleles of SWEET11 that are not recognized by PthXo1 are collectively referred to as the recessive resistance gene xa13. Rice varieties containing xa13 are resistant to strains that solely depend on PthXo1 for SWEET induction. Most indica rice varieties carry a SWEET13 allele that contains four adenines in the EBE for PthXo2, and rice lines carrying this allele are susceptible to PthXo2-dependent strains 12. A rare exception is the recessive resistance allele xa25, which contains three adenines in the EBE for SWEET13 in the indica cultivar Minghui 63, conferring resistance to strains that depend solely on PthXo2 16. A similar recessive resistance allele in japonica rice varieties is equally effective against strains relying on PthXo2 (ref. 12). Additional naturally occurring recessive EBE polymorphisms that confer resistance to strains carrying PthXo2, and the overlapping EBEs for PthXo3, TalF and AvrXa7 have subsequently been identified in the promoters of SWEET13 and SWEET14, respectively, in germplasm collections 17,18. Rice susceptibility genes are good targets for genome editing for disease resistance. TALe-mediated susceptibility is particularly modifiable. For instance, transcription-activator-like effector nuclease (TALEN)-directed mutations in SWEET14 created lines resistant to strains carrying PthXo3/Avr...

SUMMARYBacterial blight of rice is caused by the c-proteobacterium Xanthomonas oryzae pv. oryzae, which utilizes a group of type III TAL (transcription activator-like) effectors to induce host gene expression and condition host susceptibility. Five SWEET genes are functionally redundant to support bacterial disease, but only two were experimentally proven targets of natural TAL effectors. Here, we report the identification of the sucrose transporter gene OsSWEET13 as the disease-susceptibility gene for PthXo2 and the existence of cryptic recessive resistance to PthXo2-dependent X. oryzae pv. oryzae due to promoter variations of OsS-WEET13 in japonica rice. PthXo2-containing strains induce OsSWEET13 in indica rice IR24 due to the presence of an unpredicted and undescribed effector binding site not present in the alleles in japonica rice Nipponbare and Kitaake. The specificity of effector-associated gene induction and disease susceptibility is attributable to a single nucleotide polymorphism (SNP), which is also found in a polymorphic allele of OsS-WEET13 known as the recessive resistance gene xa25 from the rice cultivar Minghui 63. The mutation of OsSWEET13 with CRISPR/Cas9 technology further corroborates the requirement of OsSWEET13 expression for the state of PthXo2-dependent disease susceptibility to X. oryzae pv. oryzae. Gene profiling of a collection of 104 strains revealed OsSWEET13 induction by 42 isolates of X. oryzae pv. oryzae. Heterologous expression of OsSWEET13 in Nicotiana benthamiana leaf cells elevates sucrose concentrations in the apoplasm. The results corroborate a model whereby X. oryzae pv. oryzae enhances the release of sucrose from host cells in order to exploit the host resources.

The plant hormone abscisic acid (ABA) is involved in an array of plant processes, including the regulation of gene expression during adaptive responses to various environmental cues. Apart from its well-established role in abiotic stress adaptation, emerging evidence indicates that ABA is also prominently involved in the regulation and integration of pathogen defense responses. Here, we demonstrate that exogenously administered ABA enhances basal resistance of rice (Oryza sativa) against the brown spot-causing ascomycete Cochliobolus miyabeanus. Microscopic analysis of early infection events in control and ABAtreated plants revealed that this ABA-inducible resistance (ABA-IR) is based on restriction of fungal progression in the mesophyll. We also show that ABA-IR does not rely on boosted expression of salicylic acid-, jasmonic acid -, or callosedependent resistance mechanisms but, instead, requires a functional Ga-protein. In addition, several lines of evidence are presented suggesting that ABA steers its positive effect on brown spot resistance through antagonistic cross talk with the ethylene (ET) response pathway. Exogenous ethephon application enhances susceptibility, whereas genetic disruption of ET signaling renders plants less vulnerable to C. miyabeanus attack, thereby inducing a level of resistance similar to that observed on ABA-treated wild-type plants. Moreover, ABA treatment alleviates C. miyabeanus-induced activation of the ET reporter gene EBP89, while derepression of pathogen-triggered EBP89 transcription via RNA interference-mediated knockdown of OsMPK5, an ABA-primed mitogen-activated protein kinase gene, compromises ABA-IR. Collectively, these data favor a model whereby exogenous ABA enhances resistance against C. miyabeanus at least in part by suppressing pathogen-induced ET action in an OsMPK5-dependent manner.