Yamashita I
Center for Gene Science, Hiroshima University, Japan.
Mol Gen Genet. 1993 Dec;241(5-6):616-26. doi: 10.1007/BF00279904.
The SUD1 gene was identified during a hunt for mutants that are able to express an sta1 gene (encoding an extracellular glucoamylase) lacking an upstream activation sequence (UAS) for transcription. A null allele of sud1 alleviated the transcriptional defect of the UAS-less sta1 and also suppressed mutations in trans-acting genes (GAM1/SNF2 and GAM3/ADR6) required for transcription of STA1. The mutation also increased expression from various core promoters (CYC1, CUP1, HIS3, PUT1, and PUT2), suggesting that the SUD1 protein is a global transcriptional regulator that plays a negative role at or near the TATA element. However, the SUD1 function was ineffective on promoters containing a UAS from either STA1 or GAL10 under derepressed conditions. The sud1 mutation suppressed the salt-sensitive cell growth phenotype caused by elevated levels of the TATA-binding protein (SPT15), further suggesting a transcriptional role for SUD1. sud1 cells showed additional pleiotropic phenotypes: temperature-sensitive (ts) growth, reduced efficiencies of sporulation, and sensitivity to heat shock and nitrogen starvation. The SUD1 gene is predicted to encode a 64 kDa, hydrophilic protein.
在寻找能够表达缺乏转录上游激活序列(UAS)的sta1基因(编码一种细胞外葡糖淀粉酶)的突变体过程中,鉴定出了SUD1基因。sud1的无效等位基因缓解了无UAS的sta1的转录缺陷,并且还抑制了STA1转录所需的反式作用基因(GAM1/SNF2和GAM3/ADR6)中的突变。该突变还增加了各种核心启动子(CYC1、CUP1、HIS3、PUT1和PUT2)的表达,这表明SUD1蛋白是一种全局转录调节因子,在TATA元件处或其附近起负作用。然而,在去阻遏条件下,SUD1功能对含有来自STA1或GAL10的UAS的启动子无效。sud1突变抑制了由TATA结合蛋白(SPT15)水平升高引起的盐敏感细胞生长表型,进一步表明SUD1具有转录作用。sud1细胞表现出其他多效性表型:温度敏感(ts)生长、孢子形成效率降低以及对热休克和氮饥饿敏感。预测SUD1基因编码一种64 kDa的亲水性蛋白。