endocytosis ͉ membrane trafficking ͉ protein structure

No abstract

BackgroundThe protist Plasmodiophora brassicae is a biotrophic soil-borne pathogen that causes clubroot on Brassica crops worldwide. Clubroot disease is a serious threat to the 8 M ha of canola (Brassica napus) grown annually in western Canada. While host resistance is the key to clubroot management, sources of resistance are limited.ResultsTo identify new sources of clubroot resistance (CR), we fine mapped a CR gene (Rcr1) from B. rapa ssp. chinensis to the region between 24.26 Mb and 24.50 Mb on the linkage group A03, with several closely linked markers identified. Transcriptome analysis was conducted using RNA sequencing on a segregating F1 population inoculated with P. brassicae, with 2,212 differentially expressed genes (DEGs) identified between plants carrying and not carrying Rcr1. Functional annotation of these DEGs showed that several defense-related biological processes, including signaling and metabolism of jasmonate and ethylene, defensive deposition of callose and biosynthesis of indole-containing compounds, were up-regulated significantly in plants carrying Rcr1 while genes involved in salicylic acid metabolic and signaling pathways were generally not elevated. Several DEGs involved in metabolism potentially related to clubroot symptom development, including auxin biosynthesis and cell growth/development, showed significantly lower expression in plants carrying Rcr1.ConclusionThe CR gene Rcr1 and closely linked markers will be highly useful for breeding new resistant canola cultivars. The identification of DEGs between inoculated plants carrying and not carrying Rcr1 is an important step towards understanding of specific metabolic/signaling pathways in clubroot resistance mediated by Rcr1. This information may help judicious use of CR genes with complementary resistance mechanisms for durable clubroot resistance.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1166) contains supplementary material, which is available to authorized users.

Blackleg disease, caused by the ascomycete fungal pathogen Leptosphaeria maculans, is a devastating disease of canola (Brassica napus) in Australia, Canada and Europe. The pathogen is considered a global invasive species and poses a threat to canola production in China, where only the weakly aggressive strain L. biglobosa is present. In Canada, breakdown of blackleg resistance has been shown. In order to develop a more effective disease management strategy, there is a need to elucidate host resistance and defense mechanisms underlying the B. napus-L. maculans pathosystem. This is the very first study to investigate major resistance genes (R genes) and adult plant resistance (APR) in Canadian canola germplasm. This study also analyzed the avirulence allele frequency in L. maculans populations in western Canada. R genes were detected in the majority of these B. napus germplasm, with the Rlm3 gene being predominant. The frequency of AvrLm3 allele in field fungal populations was extremely low. APR was identified in more than 50% of the germplasm. This indicated the breakdown of Rlm3 resistance, which could be due to the widespread use of this single resistance gene in Canadian B. napus germplasm and varieties. To address concerns of introducing L. maculans from Canada into China, this study further characterized R genes and APR to L. maculans in a collection of Chinese B. napus germplasm. R genes were detected in more than 40% of the germplasm tested, with Rlm3 and Rlm4 being predominant. A large portion of the Chinese germplasm showed high to moderate ii APR in field trials at three locations in MB, SK and AB in western Canada. This study highlighted the availability of fair to good resistance in the Chinese B. napus germplasm against blackleg disease and was the first study to investigate a large number of Chinese germplasm against Canadian fungal populations in different environments. RNA sequencing of resistant and susceptible host tissues and a streamlined bioinformatics pipeline identified unique genes and plant defense pathways specific to plant resistance in the B. napus-L. maculans LepR1-AvrLepR1 interaction. The sequencing data coupled with functional characterization of some unique genes, in depth histological analysis, and in situ gene activity analysis directly at the site of infection provide unprecedented spatial and temporal resolution of the plant defense response to L. maculans.

Ion channels represent the molecular entities that give rise to the cardiac action potential, the fundamental cellular electrical event in the heart. The concerted function of these channels leads to normal cyclical excitation and resultant contraction of cardiac muscle. Research into cardiac ion channel regulation and mutations that underlie disease pathogenesis has greatly enhanced our knowledge of the causes and clinical management of cardiac arrhythmia. Here we review the molecular determinants, pathogenesis, and pharmacology of congenital Long QT Syndrome. We examine mechanisms of dysfunction associated with three critical cardiac currents that comprise the majority of congenital Long QT Syndrome cases: 1) I, the slow delayed rectifier current; 2) I, the rapid delayed rectifier current; and 3) I, the voltage-dependent sodium current. Less common subtypes of congenital Long QT Syndrome affect other cardiac ionic currents that contribute to the dynamic nature of cardiac electrophysiology. Through the study of mutations that cause congenital Long QT Syndrome, the scientific community has advanced understanding of ion channel structure-function relationships, physiology, and pharmacological response to clinically employed and experimental pharmacological agents. Our understanding of congenital Long QT Syndrome continues to evolve rapidly and with great benefits: genotype-driven clinical management of the disease has improved patient care as precision medicine becomes even more a reality.