Genome sequencing and comparative genomics reveal insights into pathogenicity and evolution of Fusarium zanthoxyli, the causal agent of stem canker in prickly ash.

BACKGROUND: Fusarium zanthoxyli is a destructive pathogen causing stem canker in prickly ash, an ecologically and economically important forest tree. However, the genome lack of F. zanthoxyli has hindered research on its interaction with prickly ash and the development of precise control strategies for stem canker. RESULTS: In this study, we sequenced and annotated a relatively high-quality genome of F. zanthoxyli with a size of 43.39 Mb, encoding 11,316 putative genes. Pathogenicity-related factors are predicted, comprising 495 CAZymes, 217 effectors, 156 CYP450s, and 202 enzymes associated with secondary metabolism. Besides, a comparative genomics analysis revealed Fusarium and Colletotrichum diverged from a shared ancestor approximately 141.1 ~ 88.4 million years ago (MYA). Additionally, a phylogenomic investigation of 12 different phytopathogens within Fusarium indicated that F. zanthoxyli originated approximately 34.6 ~ 26.9 MYA, and events of gene expansion and contraction within them were also unveiled. Finally, utilizing conserved domain prediction, the results revealed that among the 59 unique genes, the most enriched domains were PnbA and ULP1. Among the 783 expanded genes, the most enriched domains were PKc_like kinases and those belonging to the APH_ChoK_Like family. CONCLUSION: This study sheds light on the genetic basis of F. zanthoxyli's pathogenicity and evolution which provides valuable information for future research on its molecular interactions with prickly ash and the development of effective strategies to combat stem canker.

Exogenous priming of chitosan induces resistance in Chinese prickly ash against stem canker caused by Fusarium zanthoxyli.

Stem canker is a highly destructive disease that threatens prickly ash plantations in China. This study demonstrated the effective control of stem canker in prickly ash using chitosan priming, reducing lesion areas by 46.77 % to 75.13 % across all chitosan treatments. The mechanisms underlying chitosan-induced systemic acquired resistance (SAR) in prickly ash were further investigated. Chitosan increased H2O2 levels and enhanced peroxidase and catalase enzyme activities. A well-constructed regulatory network depicting the genes involved in the SAR and their corresponding expression levels in prickly ash plants primed with chitosan was established based on transcriptomic analysis. Additionally, 224 ZbWRKYs were identified based on the whole genome of prickly ash, and their phylogenetic evolution, conserved motifs, domains and expression patterns of ZbWRKYs were comprehensively illustrated. The expression of 12 key genes related to the SAR was significantly increased by chitosan, as determined using reverse transcription-quantitative polymerase chain reaction. Furthermore, the activities of defensive enzymes and the accumulation of lignin and flavonoids in prickly ash were significantly enhanced by chitosan treatment. Taken together, this study provides valuable insights into the chitosan-mediated activation of the immune system in prickly ash, offering a promising eco-friendly approach for forest stem canker control.

Lutein supplementation reduces plasma lipid peroxidation and C-reactive protein in healthy nonsmokers.

OBJECTIVE: The aim of this study was to determine whether lutein affected biomarkers related to cardiovascular diseases (CVD) in healthy nonsmokers. METHODS: A randomized, double-blind, placebo-controlled trial of lutein supplementation was conducted in healthy nonsmokers. 117 eligible subjects were randomly assigned to receive 10 or 20 mg/d of lutein or placebo for 12 weeks. Levels of plasma carotenoid concentrations, total antioxidant capacity (TAOC), the lipoprotein profile, and antioxidant enzymes activities were determined at baseline and at 6, and 12 weeks after the initiation of treatment. Biomarkers of oxidative damage to protein and lipids, and C-reactive protein (CRP) concentrations were measured at baseline and after supplementation. RESULTS: Plasma lutein and TAOC significantly increased in both active treatment groups during 12 weeks. A significant reduction was found in malondialdehyde in the 20 mg lutein group. CRP concentration decreased in a dose-dependent manner for lutein supplementation, and there was a significant between-group difference in CRP between the 20 mg lutein and the placebo group. Serum CRP was directly related to the change in plasma lutein and TAOC for both active treatment groups. CONCLUSION: The results support the possibility that lutein supplementation reduce biomarkers of CVD risk via decreased lipid peroxidation and inflammatory response by increasing plasma lutein concentrations and antioxidant capacity.