The zinc finger protein (ZFP) family is one of plants’ most diverse family of transcription factors. These proteins with finger-like structural domains have been shown to play a critical role in plant responses to abiotic stresses such as drought. This study aimed to systematically characterize Triticum aestivum ZFPs (TaZFPs) and understand their roles under drought stress. A total of 9 TaC2H2, 38 TaC3HC4, 79 TaCCCH, and 143 TaPHD were identified, which were divided into 4, 7, 12, and 14 distinct subgroups based on their phylogenetic relationships, respectively. Segmental duplication dominated the evolution of four subfamilies and made important contributions to the large-scale amplification of gene families. Syntenic relationships, gene duplications, and Ka/Ks result consistently indicate a potential strong purifying selection on TaZFPs. Additionally, TaZFPs have various abiotic stress-associated cis-acting regulatory elements and have tissue-specific expression patterns showing different responses to drought and heat stress. Therefore, these genes may play multiple functions in plant growth and stress resistance responses. This is the first comprehensive genome-wide analysis of ZFP gene families in T. aestivum to elucidate the basis of their function and resistance mechanisms, providing a reference for precise manipulation of genetic engineering for drought resistance in T. aestivum.

SET-domain-containing 2 (SETD2) is known as the major trimethyltransferase that regulates the methylation of histone H3 lysine 36 (H3K36), which has been found frequently mutated in IBD samples. Although SETD2 deficiency has been proven to modulate oxidative stress, the specific mechanisms of SETD2 in IBD are still little known. To investigate the possible role of SETD2 in IBD, we generated and genotyped epithelium-specific deletion of Setd2 ( Setd2 ^Vil-KO ) progeny mice to establish mice IBD pathology model and then studied molecular expression differences at mRNA and protein levels in the intestinal epithelial tissue of Setd2 ^Vil-KO mice. Compared with Setd2 ^F/F mice, the tissue of Setd2 ^Vil-KO mice showed increases in oxidative stress and cell apoptosis level via RT-qPCR, while TUNEL assay and immunofluorescence showed significantly enhanced apoptotic signaling and FasL expression. Together, our findings highlight that SETD2 regulates oxidative stress and FasL-induced apoptosis in Setd2 ^Vil-KO mice intestinal epithelial cells through epigenetics mechanisms, which plays an essential role in IBD pathogenesis. Therefore, our study provides new insights into the prevention and therapy of IBD from the perspective of epigenetic regulation.