[目的]探讨NDR1通过NOTCH1调控非小细胞肺癌(NSCLC)干细胞特性的潜在机制。[方法]采用流式细胞仪分析CD24-PE和CD44-FITC抗体标记的NSCLC细胞表面干细胞标志物的表达。通过ALDEFLUOR染色评估NSCLC细胞的醛脱氢酶活性,从而确定其干细胞...[目的]探讨NDR1通过NOTCH1调控非小细胞肺癌(NSCLC)干细胞特性的潜在机制。[方法]采用流式细胞仪分析CD24-PE和CD44-FITC抗体标记的NSCLC细胞表面干细胞标志物的表达。通过ALDEFLUOR染色评估NSCLC细胞的醛脱氢酶活性,从而确定其干细胞特性。采用免疫印迹法分析NOTCH1通路的激活情况。[结果]与对照组相比,过表达NDR1后,NSCLC细胞中CD24_(Low)/CD44_(High)细胞比例(37.81±3.63 vs 58.56±7.11;P<0.05)和ALDEFLUO细胞水平(15.17±3.13 vs 26.44±4.13;P<0.05)显著上升。过表达NDR1后,NSCLC细胞中NOTCH1表达水平上升。敲低NOTCH1后,NSCLC细胞中CD24_(Low)/CD44_(High)细胞比例(35.40±3.67 vs 5.04±1.16;P<0.05)和ALDEFLUO细胞水平(15.77±2.82 vs 5.28±0.89;P<0.05)显著下降。此外,敲低NOTCH1后,NSCLC细胞中NOTCH1、c-Myc和HES1的表达水平下降,而过表达NOTCH1后,这些基因表达水平上升。[结论]NDR1通过激活NOTCH1通路提升了NSCLC细胞的干细胞特性(37.81±3.63 vs 58.56±7.11)。展开更多
Plant pathogens rely on effector proteins to suppress host innate immune responses and facilitate colonization.Although the Phytophthora sojae RxLR effector Avh241 promotes Phytophthora infection,the molecular basis o...Plant pathogens rely on effector proteins to suppress host innate immune responses and facilitate colonization.Although the Phytophthora sojae RxLR effector Avh241 promotes Phytophthora infection,the molecular basis of Avh241 virulence remains poorly understood.Here we identified non-race specific disease resistance 1(NDR1)-like proteins,the critical components in plant effector-triggered immunity(ETI)responses,as host targets of Avh241.Avh241 interacts with NDR1 in the plasma membrane and suppresses NDR1-participated ETI responses.Silencing of GmNDR1s increases the susceptibility of soybean to P.sojae infection,and overexpression of GmNDR1s reduces infection,which supports its positive role in plant immunity against P.sojae.Furthermore,we demonstrate that GmNDR1 interacts with itself,and Avh241 probably disrupts the self-association of GmNDR1.These data highlight an effective counter-defense mechanism by which a Phytophthora effector suppresses plant immune responses,likely by disturbing the function of NDR1 during infection.展开更多
文摘[目的]探讨NDR1通过NOTCH1调控非小细胞肺癌(NSCLC)干细胞特性的潜在机制。[方法]采用流式细胞仪分析CD24-PE和CD44-FITC抗体标记的NSCLC细胞表面干细胞标志物的表达。通过ALDEFLUOR染色评估NSCLC细胞的醛脱氢酶活性,从而确定其干细胞特性。采用免疫印迹法分析NOTCH1通路的激活情况。[结果]与对照组相比,过表达NDR1后,NSCLC细胞中CD24_(Low)/CD44_(High)细胞比例(37.81±3.63 vs 58.56±7.11;P<0.05)和ALDEFLUO细胞水平(15.17±3.13 vs 26.44±4.13;P<0.05)显著上升。过表达NDR1后,NSCLC细胞中NOTCH1表达水平上升。敲低NOTCH1后,NSCLC细胞中CD24_(Low)/CD44_(High)细胞比例(35.40±3.67 vs 5.04±1.16;P<0.05)和ALDEFLUO细胞水平(15.77±2.82 vs 5.28±0.89;P<0.05)显著下降。此外,敲低NOTCH1后,NSCLC细胞中NOTCH1、c-Myc和HES1的表达水平下降,而过表达NOTCH1后,这些基因表达水平上升。[结论]NDR1通过激活NOTCH1通路提升了NSCLC细胞的干细胞特性(37.81±3.63 vs 58.56±7.11)。
基金supported by the Natural ScienceFoundation of Jiangsu Province(BK20190520)the NationalNatural Science Foundation of China(31721004,32001882)the National Postdoctoral Program for Innovative Talents(BX20180142)。
文摘Plant pathogens rely on effector proteins to suppress host innate immune responses and facilitate colonization.Although the Phytophthora sojae RxLR effector Avh241 promotes Phytophthora infection,the molecular basis of Avh241 virulence remains poorly understood.Here we identified non-race specific disease resistance 1(NDR1)-like proteins,the critical components in plant effector-triggered immunity(ETI)responses,as host targets of Avh241.Avh241 interacts with NDR1 in the plasma membrane and suppresses NDR1-participated ETI responses.Silencing of GmNDR1s increases the susceptibility of soybean to P.sojae infection,and overexpression of GmNDR1s reduces infection,which supports its positive role in plant immunity against P.sojae.Furthermore,we demonstrate that GmNDR1 interacts with itself,and Avh241 probably disrupts the self-association of GmNDR1.These data highlight an effective counter-defense mechanism by which a Phytophthora effector suppresses plant immune responses,likely by disturbing the function of NDR1 during infection.
