Fujiwara D, Yoshimoto H, Sone H, Harashima S, Tamai Y
Central Laboratories for Key Technology, Kirin Brewery Co. Ltd., Kanagawa, Japan.
Yeast. 1998 Jun 15;14(8):711-21. doi: 10.1002/(SICI)1097-0061(19980615)14:8<711::AID-YEA263>3.0.CO;2-8.
The ATF1 gene encodes an alcohol acetyl transferase which catalyzes the synthesis of acetate esters from acetyl CoA and several kinds of alcohols. ATF1 expression is repressed by unsaturated fatty acids or oxygen. Analysis using ATF1-lacZ fusion plasmid revealed that ATF1 gene expression is widely repressed by a variety of unsaturated fatty acids, and the degree of ATF1 transcriptional repression varies according to the structure of the unsaturated fatty acids. Interestingly, it was noted that the degree of ATF1 transcriptional repression was related to the melting point of unsaturated fatty acids added to the medium. The OLE1 gene, which encodes delta-9 fatty acid desaturase, has been reported to be repressed by unsaturated fatty acids. Transcription of OLE1 was also repressed by a wide variety of unsaturated fatty acids under anaerobic conditions. The degree of transcriptional repression of OLE1 was also related to the melting point of the added unsaturated fatty acids. Therefore, it is considered that ATF1 and OLE1 transcription are regulated in response to cell membrane fluidity. As has been reported for OLE1, the repression of ATF1 by unsaturated fatty acids was relieved in a disruptant carrying a faa1 and faa4 double mutation, two fatty acid activation genes. However, the ATF1 transcript in this double gene disruptant was repressed by oxygen. These results suggested that ATF1 transcription was co-regulated by the same mechanism as the OLE1 gene and that unsaturated fatty acids and oxygen repressed the ATF1 transcript by a different regulation pathway.
ATF1基因编码一种乙醇乙酰转移酶，该酶催化由乙酰辅酶A和几种醇合成乙酸酯。ATF1的表达受到不饱和脂肪酸或氧气的抑制。使用ATF1 - lacZ融合质粒进行的分析表明，ATF1基因的表达受到多种不饱和脂肪酸的广泛抑制，并且ATF1转录抑制的程度根据不饱和脂肪酸的结构而有所不同。有趣的是，注意到ATF1转录抑制的程度与添加到培养基中的不饱和脂肪酸的熔点有关。据报道，编码δ-9脂肪酸去饱和酶的OLE1基因也受到不饱和脂肪酸的抑制。在厌氧条件下，OLE1的转录也受到多种不饱和脂肪酸的抑制。OLE1转录抑制的程度也与添加的不饱和脂肪酸的熔点有关。因此，认为ATF1和OLE1的转录是根据细胞膜流动性进行调节的。正如关于OLE1的报道，在携带faa1和faa4双突变（两个脂肪酸激活基因）的破坏株中，不饱和脂肪酸对ATF1的抑制作用得到缓解。然而，在这个双基因破坏株中，ATF1转录本受到氧气的抑制。这些结果表明，ATF1转录与OLE1基因通过相同的机制共同调节，并且不饱和脂肪酸和氧气通过不同的调节途径抑制ATF1转录本。
