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The complete mitogenome of Gymnosoma dolycoridis Dupuis, 1960 was determined in this study. It is 15,185 bp in length, consisting of 13 protein-coding genes (PCG), 22 transfer RNA genes, two ribosomal RNA genes and one non-coding control region. The A + T content of the mitogenome is 78.5%. A maximum-likelihood phylogenetic tree built on 13 PCGs of 15 tachinid species indicated that Gymnosoma dolycoridis is clustered with other members of the subfamily Phasiinae as conventional taxonomy predicted.

Zinnia elegans Jacq. is an important, globally cultivated ornamental plant. In August 2021, a leaf spot disease was observed in zinnia in Shibing County, Guizhou, China, with an incidence of approximately 60%. Pathogens were isolated and purified from the infected leaves by tissue isolation, and pathogen strain BRJ2 was confirmed as the pathogen causing the leaf spot. Based on morphology and ITS, TEF-1α, and TUB2 sequence analyses, the pathogen was identified as Nigrospora musae (McLennan and Hoëtte). The mycelial growth rate method was used to determine the in vitro toxicity of five fungicides to the pathogen. The results showed that 10% difenoconazole provided the strongest inhibitory effect on N. musae, with a concentration for 50% of maximal effect (EC50) of 0.0658 mg/L; 75% trifloxystrobin·tebuconazole had the second greatest effect, with an EC50 of 0.1802 mg/L. This study provides the first report that N. musae caused leaf spot disease in Z. elegans and provides important guidance for the effective prevention and control of this disease in Guizhou.

The present study was designed to explore the role of soluble guanylate cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/PKG pathway in sulfur dioxide (SO2)-induced vasodilation. We showed that SO2 induced a concentration-dependent relaxation of phenylephrine (PE)-precontracted rat aortic rings in association with an increase in cGMP concentration, whereas L-aspartic acid β-hydroxamate (HDX), an inhibitor of SO2 synthase, contracted rings in a dose-dependent manner. Pretreatment of aortic rings with the sGC inhibitor ODQ (30 µM) attenuated the vasodilatory effects of SO2, suggesting the involvement of cGMP pathway in SO2-induced vasodilation. Mechanistically, SO2 upregulated the protein levels of sGC and PKG dimers, while HDX inhibited it, indicating SO2 could promote cGMP synthesis through sGC activation. Furthermore, the dimerization of sGC and PKG and vasodilation induced by SO2 in precontracted rings were significantly prevented by thiol reductants dithiothreitol (DTT). In addition, SO2 reduced the activity of phosphodiesterase type 5 (PDE5), a cGMP-specific hydrolytic enzyme, implying that SO2 elevated cGMP concentration by inhibiting its hydrolysis. Hence, SO2 exerted its vasodilatory effects at least partly by promoting disulfide-dependent dimerization of sGC and PKG, resulting in an activated sGC/cGMP/PKG pathway in blood vessels. These findings revealed a new mode of action and mechanisms by which SO2 regulated the vascular tone. [ABSTRACT FROM AUTHOR]