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The two multi-subunit complexes, Polycomb Repressive Complex 1 and 2 (PRC1/2), act synergistically during development to maintain the gene silencing state among different species. In contrast with mammals and Drosophila melanogaster, the enzyme activities and components of the PRC1 complex in plants are not fully conserved. In addition, the mutual recruitment of PRC1 and PRC2 in plants differs from that observed in mammals and Drosophila. Polycomb Group (PcG) proteins and their catalytic activity play an indispensable role in transcriptional regulation, developmental processes, and the maintenance of cellular identity. In plants, PRC1 and PRC2 deposit H2Aub and H3K27me3, respectively, and also play an important role in influencing three-dimensional (3D) chromatin structure. With the development of high-throughput sequencing techniques and computational biology, remarkable progress has been made in the field of plant 3D chromatin structure, and PcG has been found to be involved in the epigenetic regulation of gene expression by mediating the formation of 3D chromatin structures. At the same time, some genetic evidence indicates that PcG enables plants to better adapt to and resist a wide range of stresses by dynamically regulating gene expression. In the following review, we focus on the recruitment relationship between PRC1 and PRC2, the crucial role of PcG enzyme activity, the effect of PcG on 3D chromatin structure, and the vital role of PcG in environmental stress in plants. Full article

Progestin-only long-acting reversible-contraceptive (pLARC)-exposed endometria displays decidualized human endometrial stromal cells (HESCs) and hyperdilated thin-walled fragile microvessels. The combination of fragile microvessels and enhanced tissue factor levels in decidualized HESCs generates excess thrombin, which contributes to abnormal uterine bleeding (AUB) by inducing inflammation, aberrant angiogenesis, and proteolysis. The- zinc finger and BTB domain containing 16 (ZBTB16) has been reported as an essential regulator of decidualization. Microarray studies have demonstrated that ZBTB16 levels are induced by medroxyprogesterone acetate (MPA) and etonogestrel (ETO) in cultured HESCs. We hypothesized that pLARC-induced ZBTB16 expression contributes to HESC decidualization, whereas prolonged enhancement of ZBTB16 levels triggers an inflammatory milieu by inducing pro-inflammatory gene expression and tissue-factor-mediated thrombin generation in decidualized HESCs. Thus, ZBTB16 immunostaining was performed in paired endometria from pre- and post-depo-MPA (DMPA)-administrated women and oophorectomized guinea pigs exposed to the vehicle, estradiol (E₂), MPA, or E₂ + MPA. The effect of progestins including MPA, ETO, and levonorgestrel (LNG) and estradiol + MPA + cyclic-AMP (E₂ + MPA + cAMP) on ZBTB16 levels were measured in HESC cultures by qPCR and immunoblotting. The regulation of ZBTB16 levels by MPA was evaluated in glucocorticoid-receptor-silenced HESC cultures. ZBTB16 was overexpressed in cultured HESCs for 72 h followed by a ± 1 IU/mL thrombin treatment for 6 h. DMPA administration in women and MPA treatment in guinea pigs enhanced ZBTB16 immunostaining in endometrial stromal and glandular epithelial cells. The in vitro findings indicated that: (1) ZBTB16 levels were significantly elevated by all progestin treatments; (2) MPA exerted the greatest effect on ZBTB16 levels; (3) MPA-induced ZBTB16 expression was inhibited in glucocorticoid-receptor-silenced HESCs. Moreover, ZBTB16 overexpression in HESCs significantly enhanced prolactin (PRL), insulin-like growth factor binding protein 1 (IGFBP1), and tissue factor (F3) levels. Thrombin-induced interleukin 8 (IL-8) and prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA levels in control-vector-transfected HESCs were further increased by ZBTB16 overexpression. In conclusion, these results supported that ZBTB16 is enhanced during decidualization, and long-term induction of ZBTB16 expression by pLARCs contributes to thrombin generation through enhancing tissue factor expression and inflammation by enhancing IL-8 and PTGS2 levels in decidualized HESCs. Full article