The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway plays a critical role in host defense against viral infections. Here, we report the use of the Drosophila model system to investigate the modulation of the JAK/STAT pathway by the white spot syndrome virus (WSSV) protein WSV181. WSV181 overexpression in transgenic flies resulted in the downregulation of STAT92E and STAT92E-targeted genes. This result indicates that WSV181 can suppress JAK/STAT signaling by controlling STAT92E expression. An infection experiment was carried out on transgenic Drosophila infected with Drosophila C virus and on Litopenaeus vannamei injected with recombinant WSV181 and WSSV. The increased viral load and suppressed transcript levels of JAK/STAT pathway components indicate that WSV181 can promote viral proliferation by inhibiting the JAK/STAT pathway. This study provided evidence for the role of WSV181 in viral replication and revealed a new mechanism through which WSSV evades host immunity to maintain persistent infection.

Background Abscisic acid (ABA) plays an important role in plant growth and adaptation through the ABA signaling pathway. The ABA-responsive element binding (AREB/ABF) family transcriptional factors are central regulators that integrate ABA signaling with various signaling pathways. It has long been known that ABA inhibits rhizobial infection and nodule formation in legumes, but the underlying molecular mechanisms remain elusive. Results Here, we show that nodulation is very sensitive to ABA and exogenous ABA dramatically inhibits rhizobial infection and nodule formation in soybean. In addition, we proved that GmbZIP1, an AREB/ABF transcription factor, is a major regulator in both nodulation and plant response to ABA in soybean. GmbZIP1 was specifically expressed during nodule formation and development. Overexpression of GmbZIP1 resulted in reduced rhizobial infection and decreased nodule number. Furthermore, GmbZIP1 is responsive to ABA, and ectopic overexpression of GmbZIP1 increased sensitivity of Arabidopsis plants to ABA during seed germination and postgerminative growth, and conferred enhanced drought tolerance of plants. Remarkably, we found that GmbZIP1 directly binds to the promoter of GmENOD40–1, a marker gene for nodule formation, to repress its expression. Conclusion Our results identified GmbZIP1 as a node regulator that integrates ABA signaling with nodulation signaling to negatively regulate nodule formation.

The aim of this study is to explore the effect of flavonoids from Rosa roxburghii Tratt (FRRT) on doxorubicin (DOX)-induced autophagy of myocardial cells. Primary isolation and culture of myocardial cells and H9C2 myocardial cell lines from 1 to 3-day-old rats were performed, myocardial cells were incubated using 5 μmol/L DOX and a cardiotoxicity model was established, intervention was conducted via FRRT, and the ultrastructure of myocardial cells was observed under a transmission electron microscope. The expressions of LC3-II and P62 proteins were detected through immunofluorescence and Western blotting. The ultrastructure showed a large quantity of autophagic vacuoles of the cells in DOX group with poor cell state. After the FRRT intervention, only a small quantity of autophagic vacuoles appeared in the myocardial cells, and there were many coarse microvilli on the cell surface. The expression of P62 protein was reduced in DOX group, while that in FRRT group was increased (p < 0.01). In conclusion, FRRT exerts a protective effect in the DOX-induced cardiotoxicity by downregulating DOX-induced autophagy of myocardial cells.

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