Loss of function of a rice TPR-domain RNA-binding protein confers broad-spectrum disease resistance.

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.

The Xanthomonas effector XopK harbours E3 ubiquitin-ligase activity that is required for virulence.

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.

Efficient and robust estimation of single-vehicle crash severity: A mixed logit model with heterogeneity in means and variances.

This study delves into the factors that contribute to the severity of single-vehicle crashes, focusing on enhancing both computational speed and model robustness. Utilizing a mixed logit model with heterogeneity in means and variances, we offer a comprehensive understanding of the complexities surrounding crash severity. The analysis is grounded in a dataset of 39,788 crash records from the UK's STATS19 database, which includes variables such as road type, speed limits, and lighting conditions. A comparative evaluation of estimation methods, including pseudo-random, Halton, and scrambled and randomized Halton sequences, demonstrates the superior performance of the latter. Specifically, our estimation approach excels in goodness-of-fit, as measured by ρ2, and in minimizing the Akaike Information Criterion (AIC), all while optimizing computational resources like run time and memory usage. This strategic efficiency enables more thorough and credible analyses, rendering our model a robust tool for understanding crash severity. Policymakers and researchers will find this study valuable for crafting data-driven interventions aimed at reducing road crash severity.

Mitigating the impact of outliers in traffic crash analysis: A robust Bayesian regression approach with application to tunnel crash data.

Traffic crash datasets are often marred by the presence of anomalous data points, commonly referred to as outliers. These outliers can have a profound impact on the results obtained through the application of traditional methods such as logit and probit models, commonly used in the domain of traffic safety analysis, resulting in biased and unreliable estimates. To mitigate this issue, this study introduces a robust Bayesian regression approach, the robit model, which utilizes a heavy-tailed Student's t distribution to replace the link function of these thin-tailed distributions, effectively reducing the influence of outliers on the analysis. Furthermore, a sandwich algorithm based on data augmentation is proposed to enhance the estimation efficiency of posteriors. The proposed model is rigorously tested using a dataset of tunnel crashes, and the results demonstrate its efficiency, robustness, and superior performance compared to traditional methods. The study also reveals that several factors such as night and speeding have a significant impact on the injury severity of tunnel crashes. This research provides a comprehensive understanding of the outliers treatment methods in traffic safety studies and offers valuable recommendations for the development of appropriate countermeasures to effectively prevent severe injuries in tunnel crashes.

A phosphofructokinase B-type carbohydrate kinase family protein, PFKB1, is essential for chloroplast development at early seedling stage in 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.

Identification and characterization of rice blast resistance gene Pid4 by a combination of transcriptomic profiling and genome analysis.

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.