Arabidopsis AGAMOUS-LIKE16 and SUPPRESSOR OF CONSTANS1 regulate the genome-wide expression and flowering time.

Flowering transition is tightly coordinated by complex gene regulatory networks, in which AGAMOUS-LIKE 16 (AGL16) plays important roles. Here, we identified the molecular function and binding properties of AGL16 and demonstrated its partial dependency on the SUPPRESSOR OF CONSTANS 1 (SOC1) function in regulating flowering. AGL16 bound to promoters of more than 2,000 genes via CArG-box motifs with high similarity to that of SOC1 in Arabidopsis (Arabidopsis thaliana). Approximately 70 flowering genes involved in multiple pathways were potential targets of AGL16. AGL16 formed a protein complex with SOC1 and shared a common set of targets. Intriguingly, only a limited number of genes were differentially expressed in the agl16-1 loss-of-function mutant. However, in the soc1-2 knockout background, AGL16 repressed and activated the expression of 375 and 182 genes, respectively, with more than a quarter bound by AGL16. Corroborating these findings, AGL16 repressed the flowering time more strongly in soc1-2 than in the Col-0 background. These data identify a partial inter-dependency between AGL16 and SOC1 in regulating genome-wide gene expression and flowering time, while AGL16 provides a feedback regulation on SOC1 expression. Our study sheds light on the complex background dependency of AGL16 in flowering regulation, thus providing additional insights into the molecular coordination of development and environmental adaptation.

A case-control study on the association of intestinal flora with ulcerative colitis.

The association between intestinal flora and ulcerative colitis (UC) was studied in order to provide a basis and method for clinical treatment. Fresh fecal samples were collected from 30 active UC patients and 10 healthy controls. The intestinal flora DNA from each sample was extracted and 16S rRNA gene sequencing was carried out using HiSeq platform to identify the intestinal flora in fecal samples. The richness and diversity of intestinal flora in UC patients were significantly lower than those in healthy control group (P < 0.05). Significant differences were observed between the intestinal flora-species of UC patients and healthy controls. Synergistetes (P < 0.01) and Firmicutes (P < 0.05), along with probiotics Veillonella (P < 0.01), Ruminococcus and Coprococcus (P < 0.05) in the UC patients were lower than that in the healthy controls significantly. Furthermore, compared with the control group, Tenericutes (P < 0.01) and intestinal pathogenic bacteria, including Bacteroides (P < 0.01), Escherichia and Sutterella (P < 0.05) were significantly increased. The incidence of UC is significantly associated with the changes in intestinal flora. Changes in intestinal flora may lead to a decrease in the diversity of intestinal flora or to the enrichment of a particular intestinal flora.

IL-6/STAT3/SOCS3 signaling pathway playing a regulatory role in ulcerative colitis carcinogenesis.

OBJECTIVE: Large-scale clinical studies have shown that ulcerative colities were related with colorectal cancer. In this study, animal model was established by AOM/DSS method to explore the activation of IL-6-STAT3-SOCS3 signaling pathway and the expression of pathway-related proteins in ulcerative colitis carcinogenesis, in order to lay a foundation for exploring the regulation mechanism of IL-6/STAT3/SOCS3 signaling pathway in ulcerative colitis carcinogenesis. METHOD: AOM/DSS modeling method was used to establish animal models of ulcerative colitis carcinogenesis; colonic mucosa specimens were collected at different time points for pathological examination. Immunohistochemical method and western blot were used to detect the expression of IL6, STAT3 and SOCS3 protein in the control group, UC model + empty vector group and UC model + STAT3 knockout group. RESULTS: In UC model + empty vector group, IL6 and STAT3 expression was increased as lesion degree increased (P < 0.05). The expression of SOCS3 was weakened and the degree of activation decreased (P < 0.05). IL6 expression increased in UC model + STAT3 knockout group (P < 0.05) while the expression of SOCS3 decreased; compared with the UC model + empty vector group, there was a significant difference (P < 0.05). CONCLUSION: The expression and activation of IL6 and STAT3 expression were enhanced in ulcerative colitis carcinogenesis, and their expression increased with the lesion degree increased, reflecting the disease progression to a certain extent. The expression and activation of SOCS3 expression decreased. STAT3 had a certain effect on the expression of SOCS3, playing a certain regulatory role in ulcerative colitis carcinogenesis.

[Influence of artificial pneumoperitoneal media on colon carcinoma cell proliferation in vitro].

OBJECTIVE: To evaluate the influence of different pneumoperitoneal media on colon carcinoma LS-174T cell proliferation in vitro. METHODS: The artificial pneumoperitoneum was established. The proliferation of LS-174T cells was detected by MTT assay and soft agar clone formation assay. Expression of HIF-1alpha and VEGF was examined by immunohistochemistry. Apoptosis of LS-174T cells was analyzed by AO/EB double fluorescein stain and flow cytometry. RESULTS: The growth speed and proliferating capacity of LS-174T cells in CO(2) pneumoperitoneum group[A:0.37 +/- 0.02,formation (32.8 +/- 3.6)%] were significantly higher than those in control group [A:0.33 +/- 0.01,formation (28.4 +/- 2.3)%] and He group [A:0.30 +/- 0.01,formation (23.5 +/- 2.7)%], meanwhile the He group was the lowest (P<0.01). Positive expression of HIF-1alpha and VEGF in CO(2) and He artificial pneumoperitoneum up-regulated significantly as compared to control group(P<0.01), meanwhile the above expression was higher in CO(2) group (P<0.01). The G(0 )/G(1) ratio in CO(2) group was the lowest as compared to control group and He group (P<0.01), and G(0 )/G(1) ratio in He group was higher than that of control group(P<0.01). Aapoptosis rate in He group was the highest as compared with the other two groups(P<0.01). CONCLUSION: CO(2) pneumoperitoneum has stronger effect on the proliferation of colon carcinoma cell LS-174T as compared to He pneumoperitoneum in vitro.