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作 者:Kangdi Hu Wanjie Li Jiaxin Gao Qizheng Liu Haitao Wang Yue Wang Jianli Sang
机构地区:[1]Key Laboratory of Cell Proliferation and Regulation Biology,Ministry of Education,College of Life Science,Beijing Normal University [2]School of Biotechnology and Food Engineering,Hefei University of Technology [3]Institute of Molecular and Cell Biology,Agency for Science,Technology and Research (A*STAR)
出 处:《Chinese Science Bulletin》2014年第31期4060-4068,共9页
基 金:supported by the National Natural Science Foundation of China(31270113,31300133);the Beijing Natural Science Foundation(5132019);the Fundamental Research Foundation for the Central Universities(105566GK);Open Fund of Key Laboratory of Cell Proliferation and Regulation Biology,Ministry of Education
摘 要:To study the function of CaPpt1,we deleted PPT1 gene from the Candida albicans genome by sequentially replacing the entire coding region with the selectable markers ARG4 and HIS1.The results showed that the deletion of Ppt1 did not affect the hyphal formation of C.albicans under serum induction and caused enhanced sensitivity to DNA damage,Calcofluor white and saltinduced stress.We also found that Ppt1 was not required for the phenotypic response of cells treated with the genotoxins,methylmethane sulfonate and hydroxyurea.Flow cytometric analyses indicated that ppt1D cells and wild-type cells showed similar G2/M arrest profiles when exposed to DNA damage stress.Ppt1 was not required for the activation of the DNA damage response pathway,as indicated by normal phosphorylation of Rad53 and Rfa2 in ppt1D cells under DNA damage stress.We suggest that Ppt1 plays important roles in response to various stress conditions in C.albicans.To study the function of CaPptl, we deleted PPT1 gene from the Candida albicans genome by sequentially replacing the entire coding region with the selectable markers ARG4 and HIS1. The results showed that the deletion of Pptl did not affect the hyphal formation of C. albicans under serum induction and caused enhanced sensitivity to DNA damage, Calcofluor white and salt- induced stress. We also found that Pptl was not required for the phenotypic response of cells treated with the genotoxins, methylmethane sulfonate and hydroxyurea. Flow cytometric analyses indicated that pptlA cells and wild-type cells showed similar G2/M arrest profiles when exposed to DNA damage stress. Pptl was not required for the activation of the DNA damage response pathway, as indicated by normal phosphorylation of Rad53 and Rfa2 in pptlA cells under DNA damage stress. We suggest that Pptl plays important roles in response to various stress conditions in C. albicans.
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