RESULTS: We show that Rasd1 is expressed in vasopressin neurons of the PVN and SON, within which mRNA levels are induced by hyperosmotic cues. Dexamethasone treatment of AtT20 cells decreased forskolin stimulation of c-Fos, Nr4a1 and phosphorylated CREB expression, effects that were mimicked by overexpression of Rasd1, and inhibited by knockdown of Rasd1. These effects were dependent upon isoprenylation, as both farnesyltransferase inhibitor FTI-277 and CAAX box deletion prevented Rasd1 inhibition of cAMP-induced gene expression. Injection of lentiviral vector into rat SON expressing Rasd1 diminished, whereas CAAX mutant increased, cAMP inducible genes in response to osmotic stress.
CONCLUSIONS: We have identified two mechanisms of Rasd1 induction in the hypothalamus, one by elevated glucocorticoids in response to stress, and one in response to increased plasma osmolality resulting from osmotic stress. We propose that the abundance of RASD1 in vasopressin expressing neurons, based on its inhibitory actions on CREB phosphorylation, is an important mechanism for controlling the transcriptional responses to stressors in both the PVN and SON. These effects likely occur through modulation of cAMP-PKA-CREB signaling pathway in the brain.
METHOD: An electronic search to collate all the information on studies on homeobox gene expression in odontogenic lesions was carried out in four databases (PubMed, EBSCO host, Web of Science and Cochrane Library) with selected keywords. All papers which reported expression of homeobox genes in odontogenic lesions were considered.
RESULTS: A total of eleven (11) papers describing expression of homeobox genes in odontogenic lesions were identified. Methods of studies included next generation sequencing, microarray analysis, RT-PCR, Western blotting, in situ hybridization, and immunohistochemistry. The homeobox reported in odontogenic lesions includes LHX8 and DLX3 in odontoma; PITX2, MSX1, MSX2, DLX, DLX2, DLX3, DLX4, DLX5, DLX6, ISL1, OCT4 and HOX C in ameloblastoma; OCT4 in adenomatoid odontogenic tumour; PITX2 and MSX2 in primordial odontogenic tumour; PAX9 and BARX1 in odontogenic keratocyst; PITX2, ZEB1 and MEIS2 in ameloblastic carcinoma while there is absence of DLX2, DLX3 and MSX2 in clear cell odontogenic carcinoma.
CONCLUSIONS: This paper summarized and reviews the possible link between homeobox gene expression in odontogenic lesions. Based on the current available data, there are insufficient evidence to support any definite role of homeobox gene in odontogenic lesions.
OBJECTIVE: We previously identified AtWRKY50 as a transcriptional activator of SAR gene PR1. Although PR1 accumulates to high levels in plants after attack by pathogens, its function is still elusive. Here we investigated the effects of overexpression of several WRKY proteins, including AtWRKY50, on the metabolome of Arabidopsis thaliana.
METHODS: The influence of overexpression of WRKY proteins on the metabolites of Arabidopsis was investigated by using an NMR spectroscopy-based metabolomic approach. The 1H NMR data was analysed using the multivariate data analysis methods, such as principal component analysis, hierarchical cluster analysis and partial least square-discriminant analysis.
RESULTS: The results showed that the metabolome of transgenic Arabidopsis seedlings overexpressing AtWRKY50 was different from wild type Arabidopsis and transgenic Arabidopsis overexpressing other WRKY genes. Amongst other metabolites, sinapic acid and 1-O-sinapoyl-β-D-glucose especially appeared to be the most prominent discriminating metabolites, accumulating to levels 2 to 3 times higher in the AtWRKY50 overexpressor lines.
CONCLUSION: Our results indicate a possible involvement of AtWRKY50 in secondary metabolite production in Arabidopsis, in particular of hydroxycinnamates such as sinapic acid and 1-O-sinapoyl-β-D-glucose.
SIGNIFICANCE: Mutant HRAS drives metastasis of head and neck cancer by switching off the Hippo pathway to activate the YAP1-AXL axis and to stimulate lymphovascular angiogenesis.