The G proteinα-subunit,GPA1,is an integral component of several signaling pathways in plants,including response to abiotic stress.However,the molecular mechanism behind these processes remains largely unknown in the ...The G proteinα-subunit,GPA1,is an integral component of several signaling pathways in plants,including response to abiotic stress.However,the molecular mechanism behind these processes remains largely unknown in the cucumber plant(Cucumis sativus L.).In order to further understand the role of CsGPA1 in cucumber under drought stress,changes in plant growth,physiological parameters,and gene expression of CsAQPs were all measured under water stress induced by polyethylene glycol(PEG)using wild type(WT)and CsGPA1-interference(RNAi)cucumber seedlings.Our results demonstrated that the RNAi plants had lower drought tolerance,displaying seriously withered leaves,lower relative growth rate,lower root-shoot ratio,and lower root activity under drought stress compared to WT plants.Physiological studies indicated that the suppression of CsGPA1 weakened drought stress tolerance due to higherwater loss rate in the leaves,higher levels of hydrogen peroxide(H2O2),increased malondialdehyde(MDA)content,lower free proline content,lower soluble sugar content,lower soluble protein content,and decreased antioxidant enzyme activities.qRT-PCR analysis demonstrated that the interference of CsGPA1 up-regulated the expression of most AQP genes(except for CsPIP2;3 in leaves)and down-regulated the expression of CsPIP1;2,CsPIP1;4,CsPIP2;1,and CsPIP2;4 in roots under drought stress when compared to WT plants.Our results demonstrated that CsGPA1 could function as a positive regulator in drought stress response by decreasing the accumulation of reactive oxygen species(ROS),improving permeable potentials,and reducing water loss in cucumber plants.展开更多
Background:Nasopharyngeal carcinoma(NPC)is one of the most prevalent cancers in Southeast Asia.Sirtuin 2(SIRT2)is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerou...Background:Nasopharyngeal carcinoma(NPC)is one of the most prevalent cancers in Southeast Asia.Sirtuin 2(SIRT2)is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerous biological processes.However,Its function in NPC remains uncertain.The primary aim of this study is to clarify the role of SIRT2 in NPC.Methods:In this research,we examined the effect of SIRT2 silencing on NPC cell proliferation and colony formation using vitro NPC cell lines.Co-immunoprecipitation and mass spectrometry was applied to identify SIRT2-interacting proteins in NPC cells.Results:In comparison to nasopharyngeal epithelial NP69 cells,SIRT2 was up-regulated in multiple NPC cell lines,particularly in CNE2 cells.SIRT2 knockdown abrogated CNE2 cell proliferation and colony formation,whereas SIRT2 overexpression promoted HNE1 cell proliferation and colony formation.The SIRT2-interacting proteins were gathered in gene expression and regulation processes including RNA processing and translation.Among the SIRT2-interacting proteins,there were multiple DEAD-box(DDX)family members.Of note,silencing of DDX24 phenocopied the effect of SIRT2 knockdown on NPC growth.Overexpression of DDX24 restored SIRT2-depleted CNE2 cells to proliferative and colony formation.Conclusions:Our study indicates that SIRT2 can interact with DDX24 to enhance NPC growth.The clinical relevance of SIRT2 and DDX24 in NPC warrants further investigation.展开更多
p53 is a well-known tumor suppressor. However, the regulatory mechanism（s） for p53 expression in B lymphoma cells, and the possible role of p53 in the development of the radioresistance in tumor cells are largely un...p53 is a well-known tumor suppressor. However, the regulatory mechanism（s） for p53 expression in B lymphoma cells, and the possible role of p53 in the development of the radioresistance in tumor cells are largely unknown. A human B lymphoma cell line, Karpas1106 （k1106）, was used as a model of radioresistance. Apoptosis of k1106 cells was determined using flow cytometry. Expression of p53 was assessed using real time RT-PCR and western blotting. The results showed that irradiation at 8 Gy induced apoptosis in up to 40% of k1106 cells. At the same time, the irradiation markedly increased IL-6 production of the k1106 cells. When k1106 cells were cocultured with regulatory T cells （Tregs） and irradiated, the rate of apoptotic k1106 cells was significantly reduced, indicating an acquired resistance to irradiation. IL-6 derived from the irradiation-treated k1106 cells induced IL-17 expression in Tregs. The IL- 17＋Foxp3＋ T cells suppressed p53 expression in k1106 cells. Collectively, irradiated k1106 cells induce the expression of IL-17 in Tregs, which interferes with the expression of p53 protein in k1106 cells and thereby represses irradiation-triggered apoptosis in k1106 cells.展开更多
基金This work was supported by the earmarked fund for The National Key Research and Development Program of China(Grant No.2018YFD1000800)National Nature Science Foundation of China(Grant No.32072650)+1 种基金Science and Technology Innovation Program of the Chinese Academy of Agricultural Sciences(Grant No.CAAS-ASTIP-IVFCAAS)the support by the Key Laboratory of Horticultural Crop Biology and Germplasm Innovation,Ministry of Agriculture,China.
文摘The G proteinα-subunit,GPA1,is an integral component of several signaling pathways in plants,including response to abiotic stress.However,the molecular mechanism behind these processes remains largely unknown in the cucumber plant(Cucumis sativus L.).In order to further understand the role of CsGPA1 in cucumber under drought stress,changes in plant growth,physiological parameters,and gene expression of CsAQPs were all measured under water stress induced by polyethylene glycol(PEG)using wild type(WT)and CsGPA1-interference(RNAi)cucumber seedlings.Our results demonstrated that the RNAi plants had lower drought tolerance,displaying seriously withered leaves,lower relative growth rate,lower root-shoot ratio,and lower root activity under drought stress compared to WT plants.Physiological studies indicated that the suppression of CsGPA1 weakened drought stress tolerance due to higherwater loss rate in the leaves,higher levels of hydrogen peroxide(H2O2),increased malondialdehyde(MDA)content,lower free proline content,lower soluble sugar content,lower soluble protein content,and decreased antioxidant enzyme activities.qRT-PCR analysis demonstrated that the interference of CsGPA1 up-regulated the expression of most AQP genes(except for CsPIP2;3 in leaves)and down-regulated the expression of CsPIP1;2,CsPIP1;4,CsPIP2;1,and CsPIP2;4 in roots under drought stress when compared to WT plants.Our results demonstrated that CsGPA1 could function as a positive regulator in drought stress response by decreasing the accumulation of reactive oxygen species(ROS),improving permeable potentials,and reducing water loss in cucumber plants.
基金supported by 2017 Guangxi Appropriate Technology Development and Application Project(S2017013)the Project of Guangxi Health Department(Grant Nos.Z20190059 and Z20181011).
文摘Background:Nasopharyngeal carcinoma(NPC)is one of the most prevalent cancers in Southeast Asia.Sirtuin 2(SIRT2)is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerous biological processes.However,Its function in NPC remains uncertain.The primary aim of this study is to clarify the role of SIRT2 in NPC.Methods:In this research,we examined the effect of SIRT2 silencing on NPC cell proliferation and colony formation using vitro NPC cell lines.Co-immunoprecipitation and mass spectrometry was applied to identify SIRT2-interacting proteins in NPC cells.Results:In comparison to nasopharyngeal epithelial NP69 cells,SIRT2 was up-regulated in multiple NPC cell lines,particularly in CNE2 cells.SIRT2 knockdown abrogated CNE2 cell proliferation and colony formation,whereas SIRT2 overexpression promoted HNE1 cell proliferation and colony formation.The SIRT2-interacting proteins were gathered in gene expression and regulation processes including RNA processing and translation.Among the SIRT2-interacting proteins,there were multiple DEAD-box(DDX)family members.Of note,silencing of DDX24 phenocopied the effect of SIRT2 knockdown on NPC growth.Overexpression of DDX24 restored SIRT2-depleted CNE2 cells to proliferative and colony formation.Conclusions:Our study indicates that SIRT2 can interact with DDX24 to enhance NPC growth.The clinical relevance of SIRT2 and DDX24 in NPC warrants further investigation.
文摘p53 is a well-known tumor suppressor. However, the regulatory mechanism（s） for p53 expression in B lymphoma cells, and the possible role of p53 in the development of the radioresistance in tumor cells are largely unknown. A human B lymphoma cell line, Karpas1106 （k1106）, was used as a model of radioresistance. Apoptosis of k1106 cells was determined using flow cytometry. Expression of p53 was assessed using real time RT-PCR and western blotting. The results showed that irradiation at 8 Gy induced apoptosis in up to 40% of k1106 cells. At the same time, the irradiation markedly increased IL-6 production of the k1106 cells. When k1106 cells were cocultured with regulatory T cells （Tregs） and irradiated, the rate of apoptotic k1106 cells was significantly reduced, indicating an acquired resistance to irradiation. IL-6 derived from the irradiation-treated k1106 cells induced IL-17 expression in Tregs. The IL- 17＋Foxp3＋ T cells suppressed p53 expression in k1106 cells. Collectively, irradiated k1106 cells induce the expression of IL-17 in Tregs, which interferes with the expression of p53 protein in k1106 cells and thereby represses irradiation-triggered apoptosis in k1106 cells.
