The kernel setting of maize varies greatly because of the timing and intensity of water deficits. This variation can limit leaf productivity (source), the translocation of assimilated sugars (flow), and yield formation (sink). To explain the decline in kernel setting of maize under water deficits from the perspective of source-flow-sink, a 3-year experiment was conducted under a rain shelter. Five water regimes were studied. One regime included well-irrigated (CK) treatment. Four regimes involved water deficits: irrigation was withheld during the 6- to 8-leaf stage (V6−8), the 9- to 12-leaf stage (V9−12), the 13-leaf stage to tasseling stage (V13−T), and the silking stage to blister stage (R1−2). Water deficit effects on kernel setting began when the water deficit occurred at V9 and became more significant with time. Kernel weight was reduced by 12 and 11% when there were water deficits during V9−12 and V13−T, respectively. This was the result of reduced leaf area (limited source) and an altered vascular bundle in the ear peduncles (limited assimilate flow). The reduced vascular bundle number, rather than the ear peduncle cross-sectional area, significantly affected the final kernel weight when exposed to a water deficit prior to the silking stage. The water deficits prior to and close to the flowering stage significantly reduced ear kernel number; that is, 14 and 19% less during V13−T and R1−2, respectively, compared with the kernel number during the CK treatment. This reflects a smaller sink under water deficit conditions. Additionally, ovary size was reduced the most in the V13−T water deficit compared with other treatments. After rewatering, the water deficit before or during flowering stage continued to have residual effects on grain-filling in the late growth period. The grain-filling rate decreased under the V9−12 water deficit; the grain-filling duration shortened under the R1−2 water deficit; and both negative effects occurred under the V13−T water deficit. This study clearly indicated that (1) the water deficit during the vegetative organ rapid growth period both limited leaf source development and assimilate flow and slowed down kernel development, and (2) the water deficit just before and during flowering reduced kernel sink. Deficits at both times could retard grain-filling and reduce maize yield. The results of the present study might guide irrigation practices in irrigated maize or inform the management of sowing time in rainfed maize, to desynchronize the water deficit and the plant’s reactions to such deficits at different stages.
Colon cancer (CC) is one of the most frequent malignancies in the world, with a high rate of morbidity and death. In CC, necroptosis and long noncoding RNA (lncRNAs) are crucial, but the mechanism is not completely clear. The goal of this study was to create a new signature that might predict patient survival and tumor immunity in patients with CC. Expression profiles of necroptosis-related lncRNAs in 473 patients with CC were retrieved from the TCGA database. A consensus clustering analysis based on differentially expressed (DE) genes and a prognostic model based on least absolute shrinkage and selection operator (LASSO) regression analysis were conducted. Clinicopathological correlation analysis, expression difference analysis, PCA, TMB, GO analysis, KEGG enrichment analysis, survival analysis, immune correlation analysis, prediction of clinical therapeutic compounds, and qRT–PCR were also conducted. Fifty-six necroptosis-related lncRNAs were found to be linked to the prognosis, and consensus clustering analysis was performed. There were substantial variations in survival, immune checkpoint expression, clinicopathological correlations, and tumor immunity among the different subgroups. Six lncRNAs were discovered, and patients were split into high-risk and low-risk groups based on a risk score generated using these six lncRNAs. The survival time of low-risk patients was considerably longer than that of high-risk patients, indicating that these lncRNAs are directly associated with survival. The risk score was associated with the tumor stage, infiltration depth, lymph node metastasis, and distant metastasis. After univariate and multivariate Cox regression analysis, the risk score and tumor stage remained significant. Cancer- and metabolism-related pathways were enriched by KEGG analyses. Immune infiltration was shown to differ significantly between high- and low-risk patients in a tumor immunoassay. Eight compounds were screened out, and qRT–PCR confirmed the differential expression of the six lncRNAs. Overall, in CC, necroptosis-related lncRNAs have an important function, and the prognosis of patients with CC can be predicted by these six necroptosis-related lncRNAs. They may be useful in the future for customized cancer therapy.
Background: Mesangial collagen synthesis in renal glomeruli contributes to the pathogenesis of diabetic nephropathy (DN) which is one of the most serious complications of diabetes mellitus. However, the underlying mechanism of mesangial collagen synthesis is largely unknown. Methods: The differential expression of CHOP and TRIM13 which is a well-defined E3 ubiquitin ligase was compared in renal biopsy samples from DN/normal renal tissues, in isolated glomeruli of diabetic/control mice, as well as in high glucose (HG) or TGF-b1-stimulated renal mesangial cells. Then the relationship between TRIM13 and CHOP was explored using the ubiquitination assay. Findings: We found that the expression of TRIM13 was downregulated in renal biopsies, isolated glomeruli of diabetic mice, and HG/TGF-b1-stimulated renal mesangial cells, while the expression of CHOP was upregulated. An increased level of TRIM13 promoter methylation contributed to the deregulation of TRIM13 in renal glomeruli of DN. The ubiquitination assay confirmed that TRIM13 promoted ubiquitination and degradation of CHOP. Meanwhile, overexpressing TRIM13 attenuated DN-induced collagen synthesis and restored renal function in vitro and in vivo via downregulating CHOP. Interpretation: Our findings demonstrated that overexpressed TRIM13 suppresses mesangial collagen synthesis in DN by promoting ubiquitination of CHOP, suggesting TRIM13 as a potential therapeutic target in treating DN.
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