RESUMO
Understanding the genetic and molecular basis of grain yield is important for maize improvement. Here, we identified 49 consensus quantitative trait loci (cQTL) controlling maize yield-related traits using QTL meta-analysis. Then, we collected yield-related traits associated SNPs detected by association mapping and identified 17 consensus significant loci. Comparing the physical positions of cQTL with those of significant SNPs revealed that 47 significant SNPs were located within 20 cQTL regions. Furthermore, intensive reviews of 31 genes regulating maize yield-related traits found that the functions of many genes were conservative in maize and other plant species. The functional conservation indicated that some of the 575 maize genes (orthologous to 247 genes controlling yield or seed traits in other plant species) might be functionally related to maize yield-related traits, especially the 49 maize orthologous genes in cQTL regions, and 41 orthologous genes close to the physical positions of significant SNPs. In the end, we prospected on the integration of the public sources for exploring the genetic and molecular mechanisms of maize yield-related traits, and on the utilization of genetic and molecular mechanisms for maize improvement. Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-021-01214-3.
RESUMO
OBJECTIVE: To analyze the CD40-mediated in vitro proliferation and invasiveness of lung cancer cell H1299, and explore the role of phosphatidylinositol-3-kinase-protein kinase B (PI3K-AKT) signaling pathway in the above-mentioned process. METHODS: Cell counting kit-8 (CCK-8) assay was used to detect the proliferation of tumor cells. And scratch test and Transwell chambers were applied to detect the migration and invasiveness of H1299. Western blot was utilized to examine the expressions of AKT and p-AKT and enzyme-linked immunosorbent assay (ELISA) for the CD40-mediated secretion of MMP-9. RESULTS: According to the CCK-8 test, the absorbance of 5C11 groups at different timepoints was significantly higher than the control group (1.72 ± 0.18), especially when the concentration was 10 mg/L at 96 hour (2.75 ± 0.35, P < 0.05). In scratch test, the scratching width of 5C11 groups was significantly shorter than control group (1.62 ± 0.32 mm), especially when the concentration was 10 mg/L (0.05 ± 0.01 mm, P < 0.05). Western blot showed that the level of p-AKT protein increased at 10 minutes after activating by the signal of CD40 on H1299 cells. It was higher (0.65 ± 0.28) than the un-activating group (0.33 ± 0.16) at 30 min (P < 0.05). Upon the addition of LY294002, 5C11-mediated up-regulation of p-AKT was inhibited. In Transwell invasion assay, the number of cells on membranes in 5C11 group (168 ± 31) were significantly higher than the control group (105 ± 19, P < 0.05) and there was no significant difference between the 5C11-added LY294002 group (118 ± 21) and the control group (P < 0.05). The expression of MMP-9 of 5C11 group (192 ± 31 ng/L) was higher than that of the control group (110 ± 23 ng/L, P < 0.05) and no significant difference existed between the 5C11-added LY294002 group (120 ± 21 ng/L) and the control group (P < 0.05). CONCLUSION: The in vitro proliferation and invasiveness of lung cancer H1299 may be regulated by the CD40-mediated activation of PI3K-AKT signaling pathway.