Journal of Integrative Plant Biology最新文献

Waterlogging stress is a major abiotic stress that severely limits plant growth and development. However, little is known about the effects of waterlogging stress on the growth and development of gymnosperms. In this study, we demonstrated that the TgRAV1–TgWRKY74–TgACS13 module regulates ethylene-enhanced root vitality during waterlogging stress in the gymnosperm Torreya grandis. Root vitality, the physiological status of root tissues, reflects their metabolic activity and cell viability of roots. Waterlogging stress induces ethylene accumulation in T. grandis roots, thereby enhancing root vitality. The ethylene biosynthesis gene TgACS13 positively regulates root vitality under waterlogging stress by increasing ethylene levels. The transcription factors TgWRKY74 and TgRAV1 directly regulate TgACS13 expression by binding to its promoter. Furthermore, waterlogging stress activates TgWRKY74 to promote TgACS13 transcription and alleviates the inhibitory effect of TgRAV1 on its expression, resulting in ethylene-enhanced root vitality during waterlogging stress. In addition, TgRAV1 interacts with TgWRKY74 both in vivo and in vitro, reducing the transcriptional activity of TgWRKY74 by inhibiting its DNA-binding ability without affecting the transcriptional activity of TgRAV1. Therefore, the TgRAV1–TgWRKY74 module finely tunes TgACS13 expression to regulate ethylene accumulation through multiple mechanisms, thereby maintaining the vitality of T. grandis roots exposed to waterlogging stress.

The conversion of starch into sugar during postharvest banana (Musa acuminata, AAA group) ripening significantly influences fruit quality. Ethylene response factors (ERFs) regulate fruit ripening through ethylene signaling, while redox modifications affect their activity by post-translational changes. This study identifies MaERF95L, an EDLL-domain ERF in banana, as a central regulator of starch-to-sugar metabolism during postharvest ripening. Using electrophoretic mobility shift and dual-luciferase reporter assays, we demonstrate that MaERF95L directly binds to and activates the expression of six genes related to starch degradation and sucrose synthesis (MaGWD1, MaAMY3, MaBAM1, MaHK5, MaPGI1, and MaUPG3). MaERF95L overexpression accelerates starch degradation and sugar accumulation in both banana and tomato fruits during ripening. Notably, methionine (Met, M)-based oxidation modifications (e.g., Met-16 and Met-77) suppress MaERF95L's transcriptional regulatory function. Simulating oxidation by Met→glutamine (Gln, Q) substitutions (MaERF95L^M16Q/M77Q) alters its subcellular localization and also impairs its DNA-binding and transcriptional activation capabilities. In contrast, blocking oxidation by Met→Valine (Val, V) substitutions (MaERF95L^M16V/M77V) maintains its transcriptional activation activity. Furthermore, transient overexpression of MaERF95L^M16Q/M77Q in bananas reduced MaERF95L's activation of genes related to starch degradation and sucrose synthesis, and starch-to-sugar conversion. However, the overexpression of MaERF95L^M16V/M77V showed no effect on MaERF95L's activation function. These findings reveal a Met oxidation-sensitive regulatory mechanism connecting reactive oxygen species signaling to carbohydrate metabolism, providing molecular insights into quality formation regulation during ripening and potential strategies for reducing postharvest losses in climacteric fruits.

Endoplasmic reticulum-associated degradation (ERAD) is an important mechanism for degrading misfolded proteins, and is mediated by different complexes containing several conserved ER-localized ubiquitin ligases, such as Hrd1, Doa10, and gp78. Recent studies have shown that the ERAD machinery is conserved in eukaryotes. However, it remains unknown whether plants have gp78 homologs. We report a functional study of Arabidopsis homologs of gp78 and their involvement in ERAD. T-DNA insertion mutations in Arabidopsis gp78 genes, AtGP78A and AtGP78B, increased degradation of mutated brassinosteroid (BR) receptors, bri1-5 and bri1-9, leading to lower activation of the signaling protein BES1, and thereby enhancing the dwarf phenotypes of bri1-5/9. This is different from the effects of knockout in known ERAD components, which suppress the dwarf phenotypes of bri1-5/9. AtGP78s interacted with and affected the stability of AtOS9, but not other components in the AtHRD1 complex. AtOS9 accumulated in atgp78a-1 atgp78b bri1-5/9, and knockout of AtOS9 rescued the enhanced-dwarf phenotypes of atgp78a-1 atgp78b bri1-5/9. We determined that AtGP78s were involved in plant ERAD by modulating the stability of AtOS9. Taken together, our results not only reveal AtGP78s as new ERAD components but also reveal a relationship between AtGP78s and the AtHRD1 complex in plants.