Transcriptional changes in Candida albicans Genes by both farnesol and high cell density at an early stage of morphogenesis in N-acetyl-D-glucosamine medium.

Transcriptional changes in Candida albicans Genes by both farnesol and high cell density at an early stage of morphogenesis in N-acetyl-D-glucosamine medium.
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DOI:
10.3314/jjmm.48.159
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发表时间:
2007-01-01
期刊:
Nihon Ishinkin Gakkai zasshi = Japanese journal of medical mycology
影响因子:
--
通讯作者:
Kaminishi, Hidenori
Kaminishi, Hidenori
中科院分区:
其他
文献类型:
--
作者:
Cho, Tamaki;Aoyama, Toshihiro;Kaminishi, Hidenori

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通过法呢醇(一种群体感应分子)进行群体感应,调节白色念珠菌的毒力和形态发生。金合欢醇和白色念珠菌的高细胞密度在含有 N-乙酰基-D-葡萄糖胺的基本培养基中抑制菌丝形成。分析了 N-乙酰基-D-葡萄糖胺培养基中白色念珠菌群体感应早期阶段的全局转录谱。总共 53 个基因中有 22 个对金合欢醇和高细胞密度都有反应。根据计算机分析和之前发表的数据,其中 9 个基因(包括编码氨基酸生物合成的基因)受 Gcn4p 调节器控制。其他九个基因(包括编码中心碳代谢的基因)由负调节因子控制,包括 Nrg1p、Tup1p、Ssn6p 和/或 Mig1p。其他不受这些调节因子控制的基因包括与氧化应激、葡萄糖代谢和凝集相关的基因。本研究中与氨基酸生物合成和中心碳代谢相关的基因的表达与之前关于白色念珠菌被吞噬细胞内化并适应宿主挑战后的转录谱的报告相似。
Quorum sensing through farnesol, a quorum sensing molecule, regulates virulence and morphogenesis in Candida albicans. Farnesol and high cell density of C. albicans repress hyphal formation in a minimal medium containing N-acetyl-D-glucosamine. Global transcription profiling at an early stage of quorum sensing by C. albicans in the N-acetyl-D-glucosamine medium was analyzed. Twenty-two of a total of 53 genes responded to both farnesol and high cell density. From in silico analysis and previous published data, nine of these genes including those encoding amino acid biosynthesis were controlled by the Gcn4p regulator. Nine other genes which included genes encoding central carbon metabolism were controlled by negative regulators including Nrg1p, Tup1p, Ssn6p, and/or Mig1p. Other genes not controlled by these regulators included genes related to oxidative stress, glucose metabolism, and agglutination. Expression of genes related to amino acid biosynthesis and central carbon metabolism in this study is similar to a previous report of transcription profiling in C. albicans following its internalization by phagocyte cells and adaptation to host challenges.