Pectin methylesterase inhibitors GhPMEI53 and AtPMEI19 improve seed germination by modulating cell wall plasticity in cotton and Arabidopsis

The germination process of seeds is influenced by the interplay between two opposing factors,pectin methylesterase(PME)and pectin methylesterase inhibitor(PMEI),which collectively regulate patterns of pectin methylesterification.Despite the recognized importance of pectin methylesterification in seed germination,the specific mechanisms that govern this process remain unclear.In this study,we demonstrated that the overexpression of GhPMEI53is associated with a decrease in PME activity and an increase in pectin methylesterification.This leads to seed cell wall softening,which positively regulates cotton seed germination.AtPMEI19,the homologue in Arabidopsis thaliana,plays a similar role in seed germination to GhPMEI53,indicating a conserved function and mechanism of PMEI in seed germination regulation.Further studies revealed that GhPMEI53 and AtPMEI19 directly contribute to promoting radicle protrusion and seed germination by inducing cell wall softening and reducing mechanical strength.Additionally,the pathways of abscicic acid(ABA)and gibberellin(GA)in the transgenic materials showed significant changes,suggesting that GhPMEI53/AtPMEI19-mediated pectin methylesterification serves as a regulatory signal for the related phytohormones involved in seed germination.In summary,GhPMEI53 and its homologs alter the mechanical properties of cell walls,which influence the mechanical resistance of the endosperm or testa.Moreover,they impact cellular phytohormone pathways(e.g.,ABA and GA)to regulate seed germination.These findings enhance our understanding of pectin methylesterification in cellular morphological dynamics and signaling transduction,and contribute to a more comprehensive understanding of the PME/PMEI gene superfamily in plants.

YTE-17 inhibits colonic carcinogenesis by resetting antitumor immune response via Wnt5a/JNK mediated metabolic signaling

The density and composition of lymphocytes infiltrating colon tumors serve as predictive factors for the clinical outcome of colon cancer.Our previous studies highlighted the potent anti-cancer properties of the principal compounds found in Garcinia yunnanensis(YTE-17),attributing these effects to the regu-lation of multiple signaling pathways.However,knowledge regarding the mechanism and effect of YTE-17 in the prevention of colorectal cancer is limited.In this study,we conducted isobaric tags for relative and absolute quantification(iTRAQ)analysis on intestinal epithelial cells(IECs)exposed YTE-17,both in vitro and in vivo,revealing a significant inhibition of the Wnt family member 5a(Wnt5a)/c-Jun N-terminal kinase(JNK)signaling pathway.Subsequently,we elucidated the influence and mechanism of YTE-17 on the tumor microenvironment(TME),specifically focusing on macrophage-mediated T helper 17(Th17)cell induction in a colitis-associated cancer(CAC)model with Wnt5a deletion.Additionally,we performed the single-cell RNA sequencing(scRNA-seq)on the colonic tissue from the Wnt5a-deleted CAC model to characterize the composition,lineage,and functional status of immune mesenchymal cells during different stages of colorectal cancer(CRC)progression.Remarkably,our findings demon-strate a significant reduction in M2 macrophage polarization and Th17 cell phenotype upon treatment with YTE-17,leading to the restoration of regulatory T(Treg)/Th17 cell balance in azoxymethane(AOM)/dextran sodium sulfate(DSS)model.Furthermore,we also confirmed that YTE-17 effectively inhibited the glycolysis of Th17 cells in both direct and indirect co-culture systems with M2 macrophages.Notably,our study shed light on potential mechanisms linking the non-canonical Wnt5a/JNK signaling pathway and well-established canonical b-catenin oncogenic pathway in vivo.Specifically,we proposed that Wnt5a/JNK signaling activity in IECs promotes the development of cancer stem cells with b-catenin activity within the TME,involving macrophages and T cells.In summary,our study undergoes the po-tential of YTE-17 as a preventive strategy against CRC development by addressing the imbalance with the immune microenvironment,thereby mitigating the risk of malignancies.