Genome-wide identification and expression analysis of MYB gene family in Cajanus cajan and CcMYB107 improves plant drought tolerance.

MYB transcription factor (TF) is one of the largest superfamilies that play a vital role in multiple plant biological processes. However, the MYB family has not been comprehensively identified and functionally verified in Cajanus cajan, which is the sixth most important legume crop. Here, 170 CcR2R3-MYBs were identified and divided into 43 functional subgroups. Segmental and tandem duplications and alternative splicing events were found and promoted the expansion of the CcR2R3-MYB gene family. Functional prediction results showed that CcR2R3-MYBs were mainly involved in secondary metabolism, cell fate and identity, developmental processes, and responses to abiotic stress. Cis-acting element analysis of promoters revealed that stress response elements were widespread in the above four functional branches, further suggesting CcR2R3-MYBs were extensively involved in abiotic stress response. The transcriptome data and qRT-PCR results indicated that most of the CcR2R3-MYB genes responded to various stresses, of which the expression of CcMYB107 was significantly induced by drought stress. Overexpression of CcMYB107 enhanced antioxidant enzyme activity and increased proline and lignin accumulation, thus improving the drought resistance of C. cajan. Furthermore, Overexpression of CcMYB107 up-regulated the expression of stress-related genes and lignin biosynthesis genes after drought stress. Our findings established a strong foundation for the investigation of biological function of CcR2R3-MYB TFs in C. cajan.

Genome-wide transcriptome analysis and characterization of the cytochrome P450 flavonoid biosynthesis genes in pigeon pea (Cajanus cajan).

MAIN CONCLUSION: 226 CcCYP450 genes were identified at the genomic level and were classified into 45 clades based on phylogenetic analysis. CcCYP75B165 gene was found that might play important roles in the biosynthesis of flavonoids in pigeon pea, and was significantly induced by methyl jasmonate (MeJA). The cytochrome P450 mono-oxygenase (CYP450) superfamily plays a key role in the flavonoid biosynthesis pathway and resists different kinds of stresses. Several CYP450 genes have been identified to be involved in the biosynthesis of crop protection agents. However, the CcCYP450 genes from pigeon pea have not been identified. Here, 226 CcCYP450 genes were identified at the genomic level by analysing the gene structure, distribution on chromosomes, gene duplication, and conserved motifs and were classified into 45 clades based on phylogenetic analysis. RNA-seq analysis revealed clear details of CcCYP450 genes that varied with time of MeJA (methyl jasmonate) induction. Among them, six CcCYP450 subfamily genes were found that might play important roles in the biosynthesis of flavonoids in pigeon pea. The overexpression of CcCYP75B165 in pigeon pea significantly induced the accumulation of genistin and downregulated the contents of cajaninstilbene acid, apigenin, isovitexin, and genistein and the expression of flavonoid synthase genes. This study provides theoretical guidance and plant genetic resources for cultivating new pigeon pea varieties with high flavonoid contents and exploring the molecular mechanisms of the biosynthesis of flavonoids under MeJA treatment.

Propofol pretreatment alleviates mast cell degranulation by inhibiting SOC to protect the myocardium from ischemia-reperfusion injury.

Propofol (PPF) has a protective effect on myocardial ischemia-reperfusion (I/R) injury (MIRI). The purpose of this study was to investigate whether the myocardial protective effect of propofol is related to the inhibition of mast cell degranulation and explore the possible mechanisms involved. Our in vivo results showed that compared with the sham group, cardiac function, infarct size, histopathological damage, apoptosis, and markers of myocardial necrosis were significantly increased in the ischemia-reperfusion group, and propofol pretreatment alleviated these effects. In the coculture system, propofol-treated mast cells reduced their tryptase activity, resulting in cardiomyocyte protective effects, such as decreased apoptosis of cardiomyocytes and decreased expression of myocardial necrosis markers. Finally, experimental results in vitro revealed that thapsigargin (TG) can increase mast cell degranulation, tryptase release, calcium ion concentration, and the expression of STIM1 and Orai1 induced by H/R, but propofol pretreatment can partially reverse the above effects. These results suggested that the cardioprotective effect of propofol is achieved in part by inhibiting calcium influx through store-operated Ca2+ channels (SOCs) and thus alleviating mast cell degranulation.

COX-2 expression is correlated with VEGF-C, lymphangiogenesis and lymph node metastasis in human cervical cancer.

Lymphangiogenesis has been shown to promote lymph node metastasis in cancers, making it an important target in cancer therapy. Vascular endothelial growth factor (VEGF)-C is upregulated in various tumors/cancers and is one of the most potent growth factors for inducing lymphangiogenesis and promoting lymph node metastasis (LNM). Likewise, cyclooxygenase (COX)-2 plays major roles in carcinogenesis, tumor growth and metastasis via multiple mechanisms including inactivation of host antitumor immunity and promotion of tumor cell migration, tumor cell invasiveness and tumor-associated angiogenesis and lymphangiogenesis. We previously demonstrated an association between COX-2 and VEGF-C in an in vitro model of lung cancer. However, little is known about the regulation of VEGF-C by COX-2 in cervical cancer. In this study, we measured the COX-2 and VEGF-C expressions by immunohistochemistry in 23 LNM-positive and 20 LNM-negative cervical cancer specimens. We then examined the correlations among the expressions and the lymphatic microvessel density (LMVD) and ultrastructural changes to the lymphatic vessel walls by enzyme histochemical staining and electron microscopy. In addition, we used the HeLa cervical cancer cell line to explore the in vitro regulation of VEGF-C by COX-2 and its metabolite, PGE(2), using siRNA-mediated gene silencing and EP receptor blockade. The LNM-positive specimens exhibited significantly higher VEGF-C expression, COX-2 expression and LMVD than the LNM-negative specimens. Furthermore, there were strong correlations between the levels of COX-2 expression and the levels of VEGF-C expression and secretion and a significant positive association between the LMVD and LNM. siRNA-mediated knockdown of COX-2 expression inhibited VEGF-C mRNA expression while EP1 and EP4 receptor antagonists reduced the VEGF-C protein level and tyrosine phosphorylation of Src kinase. Moreover, inhibition of Src kinase with the tyrosine kinase inhibitor PP1 attenuated VEGF-C expression. Collectively, our data provide evidence for a clinical association between COX-2 and VEGF-C expressions in cervical cancer. EP1 and EP4 receptors may be involved in the COX-2-mediated regulation of VEGF-C protein and mRNA expressions. Src may be a downstream mediator of EP1 and EP4 receptors. COX-2 inhibition may diminish LNM by suppressing VEGF-C-mediated lymphangiogenesis.