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.
Composting represents a crucial component of sustainable waste management, providing significant resource recovery and environmental advantages. However, nitrogen loss during composting remains a significant challenge, necessitating the development of a predictive model for nitrogen loss during the composting process. This investigation implemented five machine learning models, utilizing 307 data points encompassing composting strategies, physicochemical properties, and composting time stages, to predict nitrogen loss during organic solid waste composting. The findings demonstrated that the adaptive boosting (AdaBoost) algorithm achieved optimal performance with a coefficient of determination of 0.847 after eliminating redundant features (scale and C/N). Moreover, Shapley additive explanation analysis identified several key factors significantly influencing nitrogen losses during composting, including composting time stages, bulking agents, raw materials, and ammonium nitrogen levels. Notably, the initial phase of composting emerged as the most critical period for nitrogen loss. The utilization of sawdust, rice husk, and corn stalk as bulking agents enhanced nitrogen retention in compost. Furthermore, implementing static aeration for ventilation and applying chemical additives effectively reduced nitrogen losses during the composting process. These results provide a scientific foundation for identifying optimal composting conditions to minimize nitrogen loss, thereby offering practical guidance for effective composting operations.
The tobacco whitefly, Bemisia tabaci, is a notorious pest affecting various crops globally, and it exhibits high levels of resistance to various insecticides. Afidopyropen is a recently commercialized pyropene insecticide for B. tabaci control with high selectivity and a novel mode of action. We previously identified a high level of afidopyropen resistance in a field-collected population after selection in the lab, and named it the HD-Afi strain. In the present study, minimal cross-resistance in the HD-Afi strain was found between afidopyropen and other common chemical agents. However, the P450 enzyme activity in HD-Afi was 2.18 times the level in susceptible strain HD-S. Expression analysis revealed that two of 12 candidate P450 genes, namely CYP6DW3 and CYP4C64, were significantly up-regulated in HD-Afi. Silencing CYP6DW3 and CYP4C64 by RNA interference (RNAi) substantially increased the susceptibility of whitefly adults, confirming their involvement in afidopyropen resistance. Homology modeling and molecular docking analyses demonstrated stable binding of afidopyropen to CYP6DW3 and CYP4C64, with binding free energies of –6.87 and –6.11 kcal mol–1, respectively. The findings of this study suggest that the induction of CYP6DW3 and CYP4C64 facilitates afidopyropen detoxification, contributing to the development of resistance in B. tabaci.
Dehydrin (DHN) enhances plant resistance to environmental stress by regulating the synthesis of osmotic adjustment substances and scavenging reactive oxygen species. However, the role of PbDHN3 under salt stress remains unclear. In this study, salt stress induced high expression of PbDHN3, and the overexpression of PbDHN3 (OE-PbDHN3) enhanced plant growth under salt stress compared to wild-type (WT) plants. OE-PbDHN3 plants exhibited higher chlorophyll content and root growth capacity than WT plants under salt stress. Transcriptome analysis revealed that PbDHN3 expression is associated with ethylene signaling pathways. OE-PbDHN3 transgenic plants substantially influenced ethylene content and the expression of related genes. Following treatment with exogenous ethephon, the transgenic lines notably inhibited the processes of ethylene synthesis and signaling transduction. OE-PbDHN3 transgenic lines treated with exogenous ethylene and the ethylene inhibitor 1-MCP demonstrated significant inhibition of ethylene synthesis and signaling transduction, while promoting root development and chlorophyll content. Under salt stress, OE-PbDHN3 downregulated the expression of ethylene biosynthesis genes PbACO1-like and PbACO2, and signal transduction genes PbEIN3-like during the initial stress phase. This early regulation mitigated the adverse effects of salt stress on the plants. These findings demonstrate that PbDHN3 ameliorates the ethylene-mediated plant growth phenotype under salt stress through regulation of ethylene synthesis and signal transduction.
A novel live attenuated vaccine candidate protects chickens against subtype B avian metapneumovirus
Avian metapneumovirus (aMPV) is a highly contagious pathogen that causes acute upper respiratory tract diseases in chickens and turkeys, resulting in serious economic losses. Subtype B aMPV has recently become the dominant epidemic strain in China. We developed an attenuated aMPV subtype B strain by serial passaging in Vero cells and evaluated its safety and efficacy as a vaccine candidate. The safety test showed that after the 30th passage, the LN16-A strain was fully attenuated, as clinical signs of infection and histological lesions were absent after inoculation. The LN16-A strain did not revert to a virulent strain after five serial passages in chickens. The genomic sequence of LN16-A differed from that of the parent wild-type LN16 (wtLN16) strain and had nine amino acid mutations. In chickens, a single immunization with LN16-A induced robust humoral and cellular immune responses, including the abundant production of neutralizing antibodies, CD4+ T lymphocytes, and the Th1 (IFN-γ) and Th2 (IL-4 and IL-6)
cytokines. We also confirmed that LN16-A provided 100% protection against subtype B aMPV and significantly reduced viral shedding and turbinate inflammation. Our findings suggest that the LN16-A strain is a promising live attenuated vaccine candidate that can prevent infection with subtype B aMPV.