CaWRKY01-10 and CaWRKY08-4 Confer Pepper's Resistance to Phytophthora capsici Infection by Directly Activating a Cluster of Defense-Related Genes.

Phytophthora blight of pepper, which is caused by the notorious oomycete pathogen Phytophthora capsici, is a serious disease in global pepper production regions. Our previous study had identified two WRKY transcription factors (TFs), CaWRKY01-10 and CaWRKY08-4, which are prominent modulators in the resistant pepper line CM334 against P. capsici infection. However, their functional mechanisms and underlying signaling networks remain unknown. Herein, we determined that CaWRKY01-10 and CaWRKY08-4 are localized in plant nuclei. Transient overexpression assays indicated that both CaWRKY01-10 and CaWRKY08-4 act as positive regulators in pepper resistance to P. capsici. Besides, the stable overexpression of CaWRKY01-10 and CaWRKY08-4 in transgenic Nicotiana benthamiana plants also significantly enhanced the resistance to P. capsici. Using comprehensive approaches including RNA-seq, CUT&RUN-qPCR, and dual-luciferase reporter assays, we revealed that overexpression of CaWRKY01-10 and CaWRKY08-4 can activate the expressions of the same four Capsicum annuum defense-related genes (one PR1, two PR4, and one pathogen-related gene) by directly binding to their promoters. However, we did not observe protein-protein interactions and transcriptional amplification/inhibition effects of their shared target genes when coexpressing these two WRKY TFs. In conclusion, these data suggest that both of the resistant line specific upregulated WRKY TFs (CaWRKY01-10 and CaWRKY08-4) can confer pepper's resistance to P. capsici infection by directly activating a cluster of defense-related genes and are potentially useful for genetic improvement against Phytophthora blight of pepper and other crops.

Integrative Transcriptome Analysis of mRNA and miRNA in Pepper's Response to Phytophthora capsici Infection.

Phytophthora blight of pepper is a notorious disease caused by the oomycete pathogen Phytophthora capsici, which poses a great threat to global pepper production. MicroRNA (miRNA) is a class of non-coding small RNAs that regulate gene expressions by altering the translation efficiency or stability of targeted mRNAs, which play important roles in the regulation of a plant's response to pathogens. Herein, time-series mRNA-seq libraries and small RNA-seq libraries were constructed using pepper roots from the resistant line CM334 and the susceptible line EC01 inoculated with P. capsici at 0, 6, 24, and 48 h post-inoculation, respectively. For mRNA-seq analysis, a total of 2159 and 2971 differentially expressed genes (DEGs) were identified in CM334 and EC01, respectively. For miRNA-seq analysis, 491 pepper miRNAs were identified, including 330 known miRNAs and 161 novel miRNAs. Among them, 69 and 88 differentially expressed miRNAs (DEMs) were identified in CM334 and EC01, respectively. Examination of DEMs and their targets revealed 22 regulatory networks, predominantly featuring up-regulated miRNAs corresponding to down-regulated target genes. Notably, these DEM-DEG regulatory networks exhibited significant overlap between CM334 and EC01, suggesting that they might contribute to pepper's basal defense against P. capsici. Furthermore, five selected DEMs (miR166, miR1171, miR395, miR530 and miRN2) and their target genes underwent qRT-PCR validation, confirming a consistent negative correlation in the expression patterns of miRNAs and their targets. This comprehensive analysis provides novel insights into the regulatory networks of miRNAs and their targets, offering valuable contributions to our understanding of pepper's defense mechanisms against P. capsici.

[Effect of uridine on mitochondrial function].

Uridine is one of the essential nutrients in organisms. To maintain normal cell growth and intracellular metabolism, the uridine must be maintained at certain concentration. Recent studies have shown that uridine can reduce inflammatory response in organisms, participate in glycolysis, and regulate intracellular protein modification, such as glycosylation and acetylation. Furthermore, it can protect cells from hypoxic injury by reducing intracellular oxidative stress, promoting high-energy compounds synthesis. Previous studies have shown that the protective effects of uridine are closely related to its effect on mitochondria. This review summarizes the effect of uridine on mitochondrial function.