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Map-based cloning of plant disease resistance (R) genes is time-consuming. Here, we reported the isolation of blast R gene Pid4 using comparative transcriptomic profiling and genome-wide sequence analysis. Pid4 encodes a coiled-coil nucleotide-binding site leucine-rich repeat (CC-NBS-LRR) protein and is constitutively expressed at diverse developmental stages in the rice variety Digu. The Pid4 protein is localized in both the nucleus and cytoplasm. Introduction of Pid4 into susceptible rice cultivars confers race-specific resistance to leaf and neck blast. Amino acid sequence comparison and blast resistance spectrum tests showed that Pid4 is a novel R gene, different from the previously reported R genes located in the same gene cluster. A Pid4 Indel marker was developed to facilitate the identification of Pid4 in different rice varieties. We demonstrated that a plant R gene can be quickly isolated using transcriptomic profiling coupled with genome-wide sequence analysis.

Xanthomonas oryzae pv. oryzae is the causative agent of rice bacterial leaf blight. While the type III secretion system of X. oryzae pv. oryzae is essential for virulence, the biochemical activities and virulence mechanisms of non-transcription activator-like (non-TAL) effectors delivered by this system are largely unknown. Here, by screening for non-TAL effectors that contribute to X. oryzae pv. oryzae virulence, we revealed that Xanthomonas outer protein K (XopK) inhibits pathogen-associated molecular pattern-triggered immunity upstream of mitogen-activated protein kinase cascades. Specifically, XopK interacted with and directly ubiquitinated rice somatic embryogenic receptor kinase 2 (OsSERK2), resulting in its degradation. Accordingly, mutation of a putative ubiquitin-conjugation enzyme (E2) binding site abolished XopK-induced degradation of OsSERK2 and compromised XopK-dependent virulence. As crucial immune regulators associated with a multitude of immune receptors, SERKs have been shown to be perturbed by Pseudomonas effectors via different mechanisms. Our study revealed a distinct perturbation mechanism of SERK activity via ubiquitination achieved by Xanthomonas non-TAL effector.

Significance Crops carrying broad-spectrum resistance loci provide an effective strategy for controlling infectious disease. Despite their importance, few broad-spectrum resistance loci have been reported, and the underlying mechanisms controlling the trait remain largely unknown. This report describes the identification of a gene, called “bsr-k1,” conferring broad-spectrum resistance and demonstrates that the encoded protein regulates immunity-related genes. Loss of function of BSR-K1 in rice leads to enhanced broad-spectrum resistance to two serious rice diseases with no major penalty on yield. This report provides insights into broad-spectrum resistance and offers an efficient strategy to breeding durably resistant rice., Crops carrying broad-spectrum resistance loci provide an effective strategy for controlling infectious disease because these loci typically confer resistance to diverse races of a pathogen or even multiple species of pathogens. Despite their importance, only a few crop broad-spectrum resistance loci have been reported. Here, we report the identification and characterization of the rice bsr-k1 (broad-spectrum resistance Kitaake-1) mutant, which confers broad-spectrum resistance against Magnaporthe oryzae and Xanthomonas oryzae pv oryzae with no major penalty on key agronomic traits. Map-based cloning reveals that Bsr-k1 encodes a tetratricopeptide repeats (TPRs)-containing protein, which binds to mRNAs of multiple OsPAL (OsPAL1–7) genes and promotes their turnover. Loss of function of the Bsr-k1 gene leads to accumulation of OsPAL1–7 mRNAs in the bsr-k1 mutant. Furthermore, overexpression of OsPAL1 in wild-type rice TP309 confers resistance to M. oryzae, supporting the role of OsPAL1. Our discovery of the bsr-k1 allele constitutes a significant conceptual advancement and provides a valuable tool for breeding broad-spectrum resistant rice.

Among the phosphofructokinase B-type carbohydrate kinase (PCK) family proteins, only few proteins, like the FRUCTOKINASE-LIKE 1 and 2, have been functionally characterized in regulation of chloroplast development. Here, we report the involvement of a PCK protein PFKB1 in chloroplast development by identification of a new rice mutant, revertible early yellowing Kitaake 2 [rey(k2)]. The mutant rey(k2) shows yellow leaf phenotype, reduced photosynthetic pigments, and retarded chloroplast development during early stages of seedlings, but gradually recovered at later stages. The phenotype of rey(k2) is resulted from the disruption of the PFKB1 protein. The Pfkb1 gene is ubiquitously expressed, and its protein is mainly targeted to the chloroplast and, in some cells, to the nucleus. In addition, the PFKB1 protein possesses phosphofructokinase activity in vitro. The rey(k2) mutant affects RNA levels of chloroplast-associated genes. In particular, the nuclear-encoded RNA polymerase (NEP)-dependent genes are expressed at a sustained high level in rey(k2) even after turning green, indicating that PFKB1 is essential for suppressing the expression of NEP-dependent genes. Taken together, our study suggests that PFKB1 functions as a novel regulator indispensable for early chloroplast development, at least partly by regulating chloroplast-associated genes.