WRKY transcription factors constitute one of the largest transcription factor families in plants, and play crucial roles in plant growth and development, defense regulation and stress responses. However, knowledge about this family in maize is limited. In the present study, we identified a drought-induced WRKY gene, ZmWRKY106, based on the maize drought de novo transcriptome sequencing data. ZmWRKY106 was identified as part of the WRKYII group, and a phylogenetic tree analysis showed that ZmWRKY106 was closer to OsWRKY13. The subcellular localization of ZmWRKY106 was only observed in the nucleus. The promoter region of ZmWRKY106 included the C-repeat/dehydration responsive element (DRE), low-temperature responsive element (LTR), MBS, and TCA-elements, which possibly participate in drought, cold, and salicylic acid (SA) stress responses. The expression of ZmWRKY106 was induced significantly by drought, high temperature, and exogenous abscisic acid (ABA), but was weakly induced by salt. Overexpression of ZmWRKY106 improved the tolerance to drought and heat in transgenic Arabidopsis by regulating stress-related genes through the ABA-signaling pathway, and the reactive oxygen species (ROS) content in transgenic lines was reduced by enhancing the activities of superoxide dismutase (SOD), peroxide dismutase (POD), and catalase (CAT) under drought stress. This suggested that ZmWRKY106 was involved in multiple abiotic stress response pathways and acted as a positive factor under drought and heat stress.

Ectoin is an amino acid derivative that can create a balance between the osmotic pressure of cells and can protect enzymes, DNA proteins, and nucleic acids under extreme conditions. Ectoin has also been reported to slow skin aging. However, there are few reports on the protective effect of Ectoin on oxidative damage, especially on the regulation of PI3K/AKT-pathway-related genes at the mRNA level. UVA-induced oxidative stress injury and H₂O₂-induced oxidative stress injury are two common oxidative stress injury models. Skin fibroblasts produce a large number of ROS following excessive UV radiation or oxidative stimulation by H₂O₂, which further inhibits cell proliferation and causes cell apoptosis. In this study, UVA- and H₂O₂-induced oxidation models of human skin fibroblasts were established separately to investigate the protective effect of Ectoin. Further studies on the mechanisms involved, for example, the expression levels of genes associated with the PI3K/AKT signaling pathway and levels of antioxidant enzymes in cells, were determined. We found that Ectoin upregulated genes associated with the PI3K/AKT signaling pathway, including COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1, but decreased intracellular ROS levels and malondialdehyde (MDA), while increasing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In conclusion, our results indicate that Ectoin exerts protective properties by the upregulated genes COL1A1, COL1A2, FN1, IGF2, NR4A1, and PIK3R1 and upregulating antioxidative enzyme levels.

Heyndrickxia coagulans is widely used for industrial L-lactic acid production, but carbon catabolite repression (CCR) and its link to fermentative metabolism remain poorly understood. A ccpA deletion mutant (ΔccpA) and a complementation strain (C-ccpA) were constructed to investigated the physiological, enzymatic, and transcriptomic consequences of CcpA loss. Deletion of ccpA completely abolished glucose-mediated CCR, enabling simultaneous glucose–xylose co-utilization, and triggered a marked shift from L-lactic to mixed-acid fermentation, with an 82.5% reduction in lactate titer accompanied by 24.1-fold and 51.6-fold increases in acetate and formate, respectively. Enzyme activity assays showed that L-lactate dehydrogenase activity was reduced by half, whereas acetate kinase activity increased nearly six-fold. Transcriptomic analysis revealed downregulation of ldhL and upregulation of pflB and ackA. Scale-up fermentation in a 5 L bioreactor confirmed that the wild type directed 90.2% of carbon flux to lactate (yield, 0.95 g/g glucose), compared with only 24.5% in the mutant. All phenotypes were fully restored upon complementation. These results demonstrate that CcpA is as an indispensable dual regulator of both CCR and L-lactic fermentation, providing a foundation for rational metabolic engineering of H. coagulans.