The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway plays a crucial role in innate immunity by inducing antiviral proteins in response to interferon signals.  Marek’s disease virus (MDV), a member of the alphaherpesvirus family, exerts potent tumorigenic and immunosuppressive effects.  Recent studies have primarily focused on the tumorigenic mechanisms of MDV, and the mechanism of immune evasion has not been fully understood.  In this study, we showed that MDV reduced the production of interferon-stimulated genes (ISGs) by inhibiting the phosphorylation and nuclear translocation of STAT1.  Using a dual-luciferase reporter system, we screened for viral proteins that significantly suppress interferon-stimulated response element (ISRE) promoter activity.  Meq overexpression markedly reduced ISRE promoter activity and ISG expression, whereas infection with Meq-deficient MDV induced higher ISG production in vitro and in vivo than infection with wild-type MDV.  Meq also inhibited the phosphorylation and nuclear translocation of STAT1.  Further experiments showed that Meq interacted with JAK1 and tyrosine kinase 2 (TYK2) and thereby inhibited JAK1–STAT1 interactions.  Meq degraded TYK2 via a caspase-mediated pathway.  The Meq-deficient MDV mutant replicated less efficiently than the wild-type MDV, both in vitro and in vivo.  Collectively, these findings demonstrate that Meq played an immunosuppressive role in MDV by attenuating the JAK–STAT signaling pathway, which facilitated escape from innate immune surveillance mechanisms.

Asynchronous seed development complicates soybean response to post-flowering high-temperature (HT) stress. To elucidate the mechanisms underlying HT-induced yield reduction after flowering, soybean plants were subjected to a six-day HT treatment in a greenhouse beginning at the opening of the first flower. HT reduced seed number and impaired pod and seed development at the initial flowering nodes, as evidenced by the decline in size and fresh weight. HT downregulated genes related to DNA replication, cell division, lipid metabolism, and secondary metabolism. Notably, auxin signaling and cell cycle factors emerged as central regulatory networks governing seed development. HT downregulated the expression of critical cell cycle components, including cyclins, kinesins, MAD2, and RAD, the latter two containing auxin-responsive elements. Moreover, HT reduced auxin levels in fertilized ovaries, while exogenous auxin (0.1 nM 1-Naphthaleneacetic acid) treatment alleviated HT-induced seed developmental restriction, mainly by increasing cell number and size. Auxin treatment further improved pod set, pod and seed number, and grain weight under HT stress. These results suggest that the cell cycle suppression is determinant for growth retardation in synergy with reduced auxin levels in soybean seeds, and auxin supplementation could enhance soybean adaptation to post-flowering HT stress.