Kluyveromyces lactis Upc2p is an ortholog of Upc2p/Ecm22p transcription factors involved in regulation of sterol import and sterol homeostasis in Saccharomyces cerevisiae. In this work, we investigated the role of Upc2p in K. lactis. The absence of KlUpc2p significantly reduced the tolerance of mutant cells to antifungal azoles and Li⁺ cations. Reduced expression of genes from the late ergosterol pathway results in a decreased ergosterol content and altered plasma membrane‐associated functions in Klupc2 mutant cells—the plasma membrane is hyperpolarized, and its fluidity is reduced. KlUpc2p contributes to transcriptional upregulation of KlENA1, KlPMA1 and KlYAP1 under azole stress. Our study demonstrates that KlUpc2p is involved in the regulation of ergosterol homeostasis in K. lactis. The analysis of KlPMA1 and KlPDR12 transcripts in wild‐type and Klupc2Δ mutant strains showed that KlUpc2p acts as an activator or as a repressor depending upon its target.

中文翻译：

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UPC2基因缺失改变了乳酸克鲁维酵母中甾醇稳态和对代谢抑制剂的敏感性

Kluyveromyces lactis Upc2p 是 Upc2p/Ecm22p 转录因子的直向同源物，这些转录因子参与酿酒酵母中甾醇输入和甾醇稳态的调节。在这项工作中，我们调查了 Upc2p 在K. lactis 中的作用。没有吉隆坡Upc2p显著降低的突变体细胞，以抗真菌唑类和Li的公差⁺阳离子。来自晚期麦角甾醇途径的基因表达减少导致Klupc2突变细胞中麦角甾醇含量降低和质膜相关功能改变——质膜超极化，其流动性降低。吉隆坡Upc2p贡献的转录上调KlENA1, KlPMA1和KlYAP1在唑胁迫下。我们的研究表明，Kl Upc2p 参与了乳酸杆菌麦角甾醇稳态的调节。对野生型和Klupc2Δ突变株中KlPMA1和KlPDR12转录物的分析表明，Kl Upc2p 根据其靶标充当激活剂或阻遏物。