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首页> 美国卫生研究院文献>PLoS Pathogens >A Comprehensive Functional Portrait of Two Heat Shock Factor-Type Transcriptional Regulators Involved in Candida albicans Morphogenesis and Virulence
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A Comprehensive Functional Portrait of Two Heat Shock Factor-Type Transcriptional Regulators Involved in Candida albicans Morphogenesis and Virulence

机译：涉及白色念珠菌的形态发生和毒力的两个热休克因子型转录调节剂的综合功能画像。

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摘要

Sfl1p and Sfl2p are two homologous heat shock factor-type transcriptional regulators that antagonistically control morphogenesis in Candida albicans, while being required for full pathogenesis and virulence. To understand how Sfl1p and Sfl2p exert their function, we combined genome-wide location and expression analyses to reveal their transcriptional targets in vivo together with the associated changes of the C. albicans transcriptome. We show that Sfl1p and Sfl2p bind to the promoter of at least 113 common targets through divergent binding motifs and modulate directly the expression of key transcriptional regulators of C. albicans morphogenesis and/or virulence. Surprisingly, we found that Sfl2p additionally binds to the promoter of 75 specific targets, including a high proportion of hyphal-specific genes (HSGs; HWP1, HYR1, ECE1, others), revealing a direct link between Sfl2p and hyphal development. Data mining pointed to a regulatory network in which Sfl1p and Sfl2p act as both transcriptional activators and repressors. Sfl1p directly represses the expression of positive regulators of hyphal growth (BRG1, UME6, TEC1, SFL2), while upregulating both yeast form-associated genes (RME1, RHD1, YWP1) and repressors of morphogenesis (SSN6, NRG1). On the other hand, Sfl2p directly upregulates HSGs and activators of hyphal growth (UME6, TEC1), while downregulating yeast form-associated genes and repressors of morphogenesis (NRG1, RFG1, SFL1). Using genetic interaction analyses, we provide further evidences that Sfl1p and Sfl2p antagonistically control C. albicans morphogenesis through direct modulation of the expression of important regulators of hyphal growth. Bioinformatic analyses suggest that binding of Sfl1p and Sfl2p to their targets occurs with the co-binding of Efg1p and/or Ndt80p. We show, indeed, that Sfl1p and Sfl2p targets are bound by Efg1p and that both Sfl1p and Sfl2p associate in vivo with Efg1p. Taken together, our data suggest that Sfl1p and Sfl2p act as central “switch on/off” proteins to coordinate the regulation of C. albicans morphogenesis.
机译：Sfl1p和Sfl2p是两个同源的热休克因子型转录调节因子，拮抗性控制白色念珠菌的形态发生，而完整的发病机理和毒力则是必需的。为了了解Sfl1p和Sfl2p如何发挥其功能，我们结合了全基因组的位置和表达分析，以揭示它们在体内的转录靶标以及白色念珠菌转录组的相关变化。我们显示Sfl1p和Sfl2p通过不同的结合基序绑定到至少113个共同目标的启动子，并直接调节白色念珠菌形态发生和/或毒力的关键转录调节因子的表达。出人意料的是，我们发现Sfl2p还与75个特异性靶标的启动子结合，包括高比例的菌丝特异性基因（HSG； HWP1，HYR1，ECE1等），揭示了Sfl2p与菌丝发育之间的直接联系。数据挖掘指向一个监管网络，其中Sfl1p和Sfl2p既是转录激活因子又是抑制因子。 Sfl1p直接抑制菌丝生长的正调控子（BRG1，UME6，TEC1，SFL2）的表达，同时上调与酵母形式相关的基因（RME1，RHD1，YWP1）和形态发生的阻遏物（SSN6，NRG1）。另一方面，Sfl2p直接上调HSG和菌丝生长激活剂（ UME6 ， TEC1 ），同时下调与酵母形式相关的基因和形态发生的阻遏物（ NRG1 ， RFG1 ， SFL1 ）。使用遗传相互作用分析，我们提供了Sfl1p和Sfl2p拮抗C的进一步证据。通过直接调节菌丝生长的重要调节子的表达来形成白色念珠菌的形态。生物信息学分析表明，Sfl1p和Sfl2p与其靶标结合是通过Efg1p和/或Ndt80p的共结合而发生的。我们确实表明，Sfl1p和Sfl2p靶标与Efg1p结合，并且Sfl1p和Sfl2p都与Efg1p关联了“体内”。两者合计，我们的数据表明Sfl1p和Sfl2p作为中央“开关”蛋白来协调C的调控。白色念珠的形态发生。

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