Notes

Porcine crisis diarrhea trojan infection brings about endoplasmic reticulum anxiety and unfolded proteins reply within jejunal epithelial tissues of weaned pigs.
Chili (Capsicum annuum L.) is an important vegetable crop in Pakistan. During summer of 2019, chili leaf spot symptoms were observed on 3-month-old plants in the fields, with 30 to 40% of disease incidence, in District Faisalabad, Punjab, Pakistan. Diseased leaves were characterized by numerous tiny round spots (0.5 to 2.0 mm in diameter, average 1 mm) that were white to grey with a sunken center, surrounded with dark brown edge and chlorotic halo. The lesions gradually enlarged and coalesced into large, nearly circular, or irregularly shaped lesions that could be as long as 3 cm. Small pieces of symptomatic leaf tissues were surface sterilized in 1% sodium hypochlorite for 1 min, rinsed in sterile water, and plated on potato dextrose agar (PDA) amended with streptomycin (100 ppm). After 5 days at 25°C with a 12-hour photoperiod, same fungal colonies developed. The colonies initially appeared white and then turned olive-green. The conidiophores were brown septate and generally branched. Conidia borne singly oically and molecularly identical to A. alternata, thus fulfilling the Koch's postulates. Previously, A. alternata has been reported in Italy and India (Devappa et al. 2016; Garibaldi et al. 2019). To our knowledge, this is the first report of A. alternata causing leaf spot of C. annuum in Pakistan. This report will help the identification of leaf spot of chili and the development of management strategies for control of this disease in Pakistan.Dickeya zeae is the causative agent of rice root rot disease and causes severe harvest and economic losses. In this study, the Bacillus velezensis strain J17-4 with significant antagonist against D. zeae was used to generate DNA for sequencing. After assembly, a high-quality complete genome comprising only a circular chromosome was available. The genome sequence consists of a total of 3877 prediction coding sequences and nine types of gene clusters involved in secondary metabolite production. This genome data will provide information for understanding the underlying mechanism of strain J17-4 antagonist against D. zeae and a new useful source for comparative genomics studies between strains isolated from various habitats.Wheat powdery mildew, caused by Blumeria graminis f. sp. tritici (Bgt), is a destructive disease seriously threatening yield and quality of common wheat (Triticum aestivum L., 2n=6x=42, AABBDD). Characterization of resistance genes against powdery mildew is useful in parental selection and for developing disease resistant cultivars. Chinese wheat breeding line KN0816 has superior agronomic performance and resistance to powdery mildew at all growth stages. Genetic analysis using populations of KN0816 crossed with different susceptible parents indicated that a single dominant gene, tentatively designated PmKN0816, conferred seedling resistance to different Bgt isolates. Using a bulked segregant analysis (BSA), PmKN0816 was mapped to the Pm6 interval on chromosome arm 2BL using polymorphic markers linked to the catalogued genes Pm6, Pm52, and Pm64, and flanked by markers CISSR02g-6 and CIT02g-2 both with genetic distances of 0.7 cM. Analysis of closely linked molecular markers indicated that the marker alleles of PmKN0816 differed from those of other powdery mildew resistance genes on 2BL, including Pm6, Pm33, Pm51, Pm64, and PmQ. Based on the genetic and physical locations and response pattern to different Bgt isolates, PmKN0816 is most likely a new powdery mildew resistance gene and confers effective resistance to all the 14 tested Bgt isolates. In view of the elite agronomic performance of KN0816 combined with the resistance, PmKN0816 is expected to become a valuable resistance gene in wheat breeding. To transfer PmKN0816 to different genetic backgrounds using marker-assisted selection (MAS), closely linked markers of PmKN0816 were evaluated and four of them (CIT02g-2, CISSR02g-6, CIT02g-10, and CIT02g-17) were confirmed to be applicable for MAS in different genetic backgrounds.The Niagara fruit belt is one of the richest fruit-producing areas in Canada, contributing to 90% of Ontario's tender fruits such as peach, plum and sweet cherry. Little cherry virus 1 (LCV1) of the genus Velarivirus is a causal agent of little cherry disease which has devastated cherry crops in many regions (Eastwell and Bernardy 1998, Jelkmann and Eastwell, 2011). From 2013 to 2018, foliar symptoms indicative of viral infection such as leaf deformation, ringspot, mottling, vein clearing, and reddening were found on sweet cherry trees grown in the Niagara region. To determine if these trees were infected by a virus, small RNAs (sRNAs) were isolated from separately pooled asymptomatic and symptomatic leaves using the mirPremier microRNA isolation kit (Sigma Aldrich Canada, Oakville, ON). The sRNAs were used to create two libraries (four leaves per library) with the TruSeq Small RNA Sample Prep Kit (Illumina, San Diego, CA). selleck kinase inhibitor The sRNA libraries were separately sequenced with the MiSeq Desktop Sequencer (Illumington, California, and Oregon in the United States of America). To the best of our knowledge, this is the first report of LCV1 in any eastern region of Canada. The low incidence of LCV1 suggests that this virus is not widespread in this region. Routine monitoring and detection of LCV1 is required to prevent this devastating cherry disease from spreading in this region.Desmosomes (DSMs) together with Adherens Junctions (AJs) and Tight Junctions (TJs) constitute the apical cell junctional complex (AJC). While the importance of the apical and basolateral polarity machinery in the organization of AJs and TJs is well-established, how DSMs are positioned within the AJC is not understood. Here we use highly polarized DLD1 cells as a model to address how DSMs integrate into the AJC. We found that knockout of the desmosomal ARM protein Pkp3, but not other major DSM proteins, uncouples DSMs from AJC without blocking DSM assembly. DLD1 cells also exhibit a prominent extra-DSM pool of Pkp3, concentrated in tricellular (tC) contacts. Probing distinct apicobasal polarity pathways revealed that neither the DSM's association with AJC, nor the extra-DSM pool of Pkp3 are abolished in cells with defects in Scrib module proteins responsible for basolateral membrane development. However, a loss of the apical polarity protein, Par3 completely eliminates the extra-DSM pool of Pkp3 and disrupts AJC localization of desmosomes, dispersing these junctions along the entire length of cell-cell contacts.
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