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ATR-Chk1-Cdc25信号通路参与盘基网柄菌G2/M转变期的调控
  • ISSN号:1000-5641
  • 期刊名称:《华东师范大学学报:自然科学版》
  • 时间:0
  • 分类:Q952.6[生物学—动物学]
  • 作者机构:[1]华东师范大学生命科学学院,上海200062
  • 相关基金:中国国家自然科学基金(30970316)
中文摘要:

显微镜观察盘基网柄菌野生型KAx-3细胞和突变型RNAi—allC细胞,计数结果表明后者的单细胞繁殖速度约为前者的8倍.为探究该突变型盘基网柄菌细胞周期缩短的原因,用荧光定量PCR和westernblot研究了ATRChklCdc25信号通路在其中的可能作用.实验结果表明:RNAiallC细胞中cdc25基因相对表达量约为KAx-3细胞的8倍,丽其Cbkl与ATR基因的相对表达量却明显低于KAx-3细胞.突变细胞中Cdc25蛋白含量高于KAx-3细胞,但其Chkl蛋白含量却显著低于KAx-3细胞.这些数据表明,两种类型细胞之间的ATR、Chkl、Cdc25在mRNA水平和蛋白表达上均存在差异,特别是ATR基因表达量的不同明显影响chKl和Cdc25的表达量,提示ATR—Chkl—Cdc25信号通路应该在一定程度上参与了盘基网柄菌细胞周期G2/M期的调控.

英文摘要:

The cell proliferation of wild type KAx-3 and mutant type RNAi-allC observed by light microscope and cell counting, The latter was divided 8 time faste than the former. To eval uate the reason why RNAi-allC cell cycle shortened, the function of ATR-Chkl-Cdc25 signaling pathway were explored by quantitative PCR and western blot techniques. The results showed the differences of ATR, Chkl, Cdc25 in mRNA contents and protein level existed in KAx-3 and RNAi-allC cells, that is, the expression of ATR and Chlel ratio of RNAi-allC to KAx-3 was 0.69:1 and 0.1:1 respectively; the expression of Cdc25 in RNAi allC cells was 8 times that of KAx-3 cells. The data suggested that once the expression of ATR had little change, Chkl andCdc25 expression changed greatly. Western blotting results were consistent with Q-PCR re- ports. The Chkl protein contents were significantly less in mutant type RNAi-allC than that in KAx-3cells; the Cdc25 protein contents were higher in RNAi-aI1C cells. The above mentioned results suggest that ATR-Chk1-Cdc25 signaling pathway involved in the regulation of the G2/M phase in Dictyostelium discoideum.

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期刊信息
  • 《华东师范大学学报:自然科学版》
  • 中国科技核心期刊
  • 主管单位:中华人民共和国教育部
  • 主办单位:华东师范大学
  • 主编:郑伟安
  • 地址:上海中山北路3663号
  • 邮编:200062
  • 邮箱:xblk@xb.ecnu.edu.cn
  • 电话:021-62233703
  • 国际标准刊号:ISSN:1000-5641
  • 国内统一刊号:ISSN:31-1298/N
  • 邮发代号:4-359
  • 获奖情况:
  • 中国综合性科技类核心期刊
  • 国内外数据库收录:
  • 俄罗斯文摘杂志,美国化学文摘(网络版),美国数学评论(网络版),德国数学文摘,美国剑桥科学文摘,中国中国科技核心期刊,中国北大核心期刊(2004版),中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2014版),中国北大核心期刊(2000版)
  • 被引量:6600