Genome Sequencing and Analysis Reveal Potential High-Valued Metabolites Synthesized by Lasiodiplodia iranensis DWH-2.

Lasiodiplodia sp. is a typical opportunistic plant pathogen, which can also be classified as an endophytic fungus. In this study, the genome of a jasmonic-acid-producing Lasiodiplodia iranensis DWH-2 was sequenced and analyzed to understand its application value. The results showed that the L. iranensis DWH-2 genome was 43.01 Mb in size with a GC content of 54.82%. A total of 11,224 coding genes were predicted, among which 4776 genes were annotated based on Gene Ontology. Furthermore, the core genes involved in the pathogenicity of the genus Lasiodiplodia were determined for the first time based on pathogen-host interactions. Eight Carbohydrate-Active enzymes (CAZymes) genes related to 1,3-ß-glucan synthesis were annotated based on the CAZy database and three relatively complete known biosynthetic gene clusters were identified based on the Antibiotics and Secondary Metabolites Analysis Shell database, which were associated with the synthesis of 1,3,6,8-tetrahydroxynaphthalene, dimethylcoprogen, and (R)-melanin. Moreover, eight genes associated with jasmonic acid synthesis were detected in pathways related to lipid metabolism. These findings fill the gap in the genomic data of high jasmonate-producing strains.

High production of jasmonic acid by Lasiodiplodia iranensis using solid-state fermentation: Optimization and understanding.

BACKGROUND: Jasmonic acid (JA) is a plant hormone involved in regulating developmental and growth controls as well as photosynthesis. In addition, this hormone protects the plant against insects and has good applications in agriculture, the flavored industry and other fields. Filamentous fungus generally produces JA using liquid static culture. In the present study, a solid-state fermentation (SSF) method is developed for high production of JA using Lasiodiplodia iranensis. MAIN METHODS AND MAJOR RESULTS: By selecting the solid substrate and optimizing the initial water content, inoculum volume, loading volume and other culture conditions, the maximum JA yield reached 5306.38 mg kg-1 when fermented for 12 days in a petri dish containing a medium with crushed wheat as the solid substrate and 75% initial water content. The logistic and Luedeking-Piret models were used to characterize the relationship between microbial growth and product synthesis in the SSF process, and the maximum JA production is predicted to be 5263.23 mg kg-1 , which is close to the experimental value. Liquid chromatography with tandem mass spectrometry (LC-MS/MS) is used to examine the metabolic changes that develop during fermentation. The results indicate that JA biosynthesis occurs in the α-linolenic acid metabolic pathway, of which 13(S)-HpOTrE is a key intermediate metabolite and both 13(S)-HOTrE and traumatic acid are byproducts of the branches of its synthesis. CONCLUSIONS AND IMPLICATIONS: The results of this study provide a method for obtaining high JA yields by SSF, and offer new insights for understanding the production of JA by fungal fermentation.

Protective effects of selenium yeast against cadmium-induced necroptosis through miR-26a-5p/PTEN/PI3K/AKT signaling pathway in chicken kidney.

Cadmium (Cd) is a ubiquitous environmental pollutant of increasing worldwide concern to both humans and animals. Selenium yeast (Se-Y) is an organic selenium source that has been shown an advantage in antagonizing Cd-induced liver necroptosis in chicken. Herein, we described the discovery path of Se-Y antagonism in Cd-induced renal necroptosis in chicken through targeting miR-26a-5p/PTEN/PI3K/AKT signaling pathway. We set up four groups of chickens at random: control group (0.5 mg/kg Na2SeO3), Se-Y group (0.5 mg/kg Se-Y), Se-Y+Cd group (0.5 mg/kg Se-Y and 150 mg/kg CdCl2) and Cd group (150 mg/kg CdCl2 and 0.5 mg/kg Na2SeO3). Interestingly, we found Se-Y, but not Na2SeO3, significantly blocked Cd accumulation in the kidney and alleviated Cd-induced necroptosis through inhibiting the expression of RIP1, RIP3 and MLKL. Se-Y, activated miR-26a-5p expression, thereby down-regulated the expression of PTEN, resulting in the up-regulation of PI3K/AKT signaling pathway and the inhibition of oxidative stress in both Se-Y and Cd treated chickens. Besides that, Se-Y could also specifically reduce the expression levels of heat shock protein 60 (HSP60), HSP70 and HSP90 in Se-Y and Cd co-treated chickens. Taken together, our results showed that Se-Y has an added value to antagonize Cd-induced necroptosis in chicken kidney by regulating the miR-26a-5p/PTEN/PI3K/AKT signaling pathway and HSPs, indicating that Se-Y could serve as an effective antagonist on Cd-induced renal necroptosis in chickens.