Sucrose is not only the carbon source for starch synthesis, but also a signal molecule. Alone or in coordination with ABA, it can regulate the expression of genes involved in starch synthesis. To investigate the molecular mechanisms underlying this effect, maize endosperms were collected from Zea mays L. B73 inbred line 10 d after pollination and treated with sucrose, ABA, or sucrose plus ABA at 28 °C in the dark for 24 h. RNA-sequence analysis of the maize endosperm transcriptome revealed 47 candidate transcription factors among the differentially expressed genes. We therefore speculate that starch synthetic gene expression is regulated by transcription factors induced by the combination of sucrose and ABA. ZmEREB156, a candidate transcription factor, is induced by sucrose plus ABA and is involved in starch biosynthesis. The ZmEREB156-GFP-fused protein was localized in the nuclei of onion epidermal cells and ZmEREB156 protein possessed strong transcriptional activation activity. Promoter activity of the starch-related genes Zmsh2 and ZmSSIIIa increased after overexpression of ZmEREB156 in maize endosperm. ZmEREB156 could bind to the ZmSSIIIa promoter but not the Zmsh2 promoter in a yeast one-hybrid system. Thus, ZmEREB156 positively modulates starch biosynthetic gene ZmSSIIIa via the synergistic effect of sucrose and ABA.

Palmitic acid, the most common saturated free fatty acid, can lead to lipotoxicity and apoptosis when overloaded in non-fat cells. Palmitic acid accumulation can induce pancreatic β-cell dysfunction and cardiac myocyte apoptosis. Under various cellular stresses, the activation of p53 signaling can lead to cell cycle arrest, DNA repair, senescence, or apoptosis, depending on the severity/type of stress. Nonetheless, the precise role of p53 in lipotoxicity induced by palmitic acid is not clear. Here, our results show that palmitic acid induces p53 activation in a dose- and time-dependent manner. Furthermore, loss of p53 makes cells sensitive to palmitic acid-induced apoptosis. These results were demonstrated in human colon carcinoma cells (HCT116) and primary mouse embryo fibroblasts (MEF) through analysis of DNA fragmentation, flow cytometry, colony formation, and Western blots. In the HCT116 p53^−/− cell line, palmitic acid induced greater reactive oxygen species formation compared to the p53^+/+ cell line. The reactive oxygen species (ROS) scavengers N-acetyl cysteine (NAC) and reduced glutathione (GSH) partially attenuated apoptosis in the HCT116 p53^−/− cell line but had no obvious effect on the p53^+/+ cell line. Furthermore, p53 induced the expression of its downstream target genes, p21 and Sesn2, in response to ROS induced by palmitic acid. Loss of p21 also leads to more palmitic acid-induced cell apoptosis in the HCT116 cell line compared with HCT116 p53^+/+ and HCT116 p53^−/−. In a mouse model of obesity, glucose tolerance test assays showed higher glucose levels in p53^−/− mice that received a high fat diet compared to wild type mice that received the same diet. There were no obvious differences between p53^−/− and p53^+/+ mice that received a regular diet. We conclude that p53 may provide some protection against palmitic acid- induced apoptosis in cells by targeting its downstream genes in response to this stress.

Maize is one of the three major crops worldwide based on its yield and quality. Starch is crucial to both the yield and quality of maize as it accounts more than 60% of the seed weight, and its structure influences the quality of the crop. Starch synthase I (SSI) contributes to the majority of the starch synthase activity in the maize endosperm. An in-depth understanding of the starch synthesis regulatory mechanism would provide opportunities for improving the yield and quality of maize. In this study, ZmPLATZ2, a plant AT-rich sequence and zinc-binding protein (PLATZ) transcription factor related to starch synthesis, was selected based on co-expression analysis. The semiquantitative RT-PCR and qRT-PCR assays revealed that ZmPLATZ2 had a high expression in the endosperm, and reached the peak at 12 days after pollination (DAP). Different treatments demonstrated that ZmPLATZ2 was downregulated by the presence of sucrose. Subsequent transactivation and subcellular localization analyses showed that ZmPLATZ2 was localized in the nuclei without transactivation. Yeast one-hybrid and transient expression in maize endosperm indicated that ZmPLATZ2 could bind to the promoters of ZmSSI, ZmISA1, and ZmISA2 and increase their gene expression. After ZmPLATZ2 overexpression in rice, four starch synthesis genes were significantly upregulated in the transgenic plant, including the OsSSI gene. In vitro DAP-seq data showed that ZmPLATZ2 could bind to the CAAAAAAA element. In conclusion, our data support that ZmPLATZ2 binds to the CAAAAAAA element in the ZmSSI promoter and mediates the Glu signal pathway.

Background: Short internodes contribute to plant dwarfism, which is exceedingly beneficial for crop production. However, the underlying mechanisms of internode elongation are complicated and have been not fully understood.Results: Here, we report a maize dwarf mutant,dwarf2014(d2014), which displays shortened lower internodes. Map-based cloning revealed that thed2014gene is a novelbr2allele with a splicing variation, resulting in a higher expression ofBR2-T02instead of normalBR2-T01. Then, we found that the internode elongation ind2014/br2exhibited a pattern of inhibition-normality-inhibition (transient for the ear-internode), correspondingly, at the 6-leaf, 12-leaf and 14-leaf stages. Indeed,BR2encodes a P-glycoprotein1 (PGP1) protein that functions in auxin efflux, and our in situ hybridization assay showed thatBR2was mainly expressed in vascular bundles of the node and internode. Furthermore, significantly higher auxin concentration was detected in the stem apex ofd2014at the 6-leaf stage and strictly in the node region for the ear-internode at the 14-leaf stage. In such context, we propose that BR2/PGP1 transports auxin from node to internode through the vascular bundles, and excessive auxin accumulation in the node (immediately next to the intercalary meristem) region suppresses internode elongation ofd2014.Conclusions: These findings suggest that low auxin levels mediated by BR2/PGP1 in the intercalary meristem region are crucial for internode elongation.