The increasing salinity of agricultural lands highlights the urgent need to improve salt tolerance in crops, a critical factor for ensuring food security. Epigenetic mechanisms are pivotal in plant adaptation to salt stress. This review elucidates the complex roles of DNA methylation, histone modifications, histone variants, and non-coding RNAs in the fine-tuning of gene expression in response to salt stress. It emphasizes how heritable changes, which do not alter the DNA sequence but significantly impact plant phenotype, contribute to this adaptation. DNA methylation is notably prevalent under high-salinity conditions and is associated with changes in gene expression that enhance plant resilience to salt. Modifications in histones, including both methylation and acetylation, are directly linked to the regulation of salt-tolerance genes. The presence of histone variants, such as H2A.Z, is altered under salt stress, promoting plant adaptation to high-salinity environments. Additionally, non-coding RNAs, such as miRNAs and lncRNAs, contribute to the intricate gene regulatory network under salt stress. This review also underscores the importance of understanding these epigenetic changes in developing plant stress memory and enhancing stress tolerance.

Neutralizing antibodies (NAbs) have attracted attention as tools for achieving PRRSV control and prevention, but viral antigenic variation undermines the abilities of NAbs elicited by attenuated PRRSV vaccines to confer full protection against heterogeneous PRRSV field isolates. As demonstrated in this study, the monoclonal antibody (mAb) mAb-PN9cx3 exhibited broad-spectrum recognition and neutralizing activities againstPRRSV-1andPRRSV-2strains in vitro. Furthermore, in vivo experiments revealed that the administration of two 10-mg doses of mAb-PN9cx3 before and after the inoculation of piglets with heterologous PRRSV isolates (HP-PRRSV-JXA1 or PRRSV NADC30-like strain HNhx) resulted in significant reduction of the PRRSV-induced pulmonary pathological changes and virus loads in porcine alveolar macrophages (PAMs) compared with the results obtained with mAb-treated isotype controls. Moreover, minimal hilar lymph node PRRSV antigen levels were observed in mAb-PN9cx3-treated piglets. A transcriptome profile analysis of PAMs extracted from lung tissues of piglets belonging to different groups (except for antibody-isotype controls) indicated that mAb-PN9cx3 treatment reversed the PRRSV infection-induced alterations in expression profiles. A gene ontology (GO) enrichment analysis of these genes traced their functions to pathways that included the immune response, inflammatory response, and response to steroid hormone, and their functions in oogenesis and positive regulation of angiogenesis have been implicated in PRRSV pathogenesis. Overall, NADC30-like HNhx infection affected more gene pathways than HP-PRRSV infection. In conclusion, our research describes a novel immunologic approach involving the use of mAbs that confer cross-protection against serious illness resulting from infection with heterogeneousPRRSV-2isolates, which is a feat that has not yet been achieved through vaccination. Ultimately, mAb-PN9cx3 will be a powerful addition to our current arsenal for achieving PRRSV prevention and eradication.

High salinity stress promotes plant ethylene biosynthesis and triggers the ethylene signaling response. However, the precise mechanism underlying how plants transduce ethylene signaling in response to salt stress remains largely unknown. In this study, we discovered that SALT OVERLY SENSITIVE 2 (SOS2) inhibits the kinase activity of CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) by phosphorylating the 87th serine (S87). This phosphorylation event activates the ethylene signaling response, leading to enhanced plant salt resistance. Furthermore, through genetic analysis, we determined that the loss of CTR1 or the gain of SOS2-mediated CTR1 phosphorylation both contribute to improved plant salt tolerance. Additionally, in the sos2 mutant, we observed compromised proteolytic processing of ETHYLENE INSENSITIVE 2 (EIN2) and reduced nuclear localization of EIN2 C-terminal fragments (EIN2-C), which correlates with decreased accumulation of ETHYLENE INSENSITIVE 3 (EIN3). Collectively, our findings unveil the role of the SOS2-CTR1 regulatory module in promoting the activation of the ethylene signaling pathway and enhancing plant salt tolerance.