Hu Z, Gibson A W, Kim J H, Wojciechowicz L A, Zhang B, Michels C A
Departments of Biology and Biochemistry, Queens College and the Graduate School of CUNY, 65-30 Kissena Boulevard, Flushing, NY 11367, USA.
Curr Genet. 1999 Aug;36(1-2):1-12. doi: 10.1007/s002940050466.
MAL63 of the MAL6 locus and its homologues at the other MAL loci encode transcription activators required for the maltose-inducible expression of the MAL structural genes. We carried out a deletion analysis of LexA-MAL63 gene fusions to localize the functional domains of the Mal63 MAL-activator protein. Our results indicate that the sequence-specific DNA-binding domain of Mal63p is contained in residues 1-100; that residues 60-283 constitute a functional core region including the transactivation domain; that residues 251-299 are required to inhibit the activation function of Mal63p; and that the rest of the C-terminal region of the protein contains a maltose-responsive domain that acts to relieve the inhibitory effect on the activation function. Abundant overproduction of Mal63p does not overcome the negative regulation of MAL gene expression in the absence of maltose, suggesting that a titratable MAL-specific repressor similar to Gal80p is not involved in the negative regulation of the MAL-activator. A model for maltose-inducible autoregulation of the MAL-activator is presented.
MAL6位点的MAL63及其在其他MAL位点的同源物编码MAL结构基因麦芽糖诱导表达所需的转录激活因子。我们对LexA-MAL63基因融合体进行了缺失分析，以定位Mal63 MAL激活蛋白的功能结构域。我们的结果表明，Mal63p的序列特异性DNA结合结构域包含在第1至100位残基中；第60至283位残基构成一个功能核心区域，包括反式激活结构域；第251至299位残基是抑制Mal63p激活功能所必需的；并且该蛋白C末端区域的其余部分包含一个麦芽糖反应结构域，其作用是解除对激活功能的抑制作用。在没有麦芽糖的情况下，Mal63p的大量过量表达并不能克服MAL基因表达的负调控，这表明类似于Gal80p的可滴定MAL特异性阻遏物不参与MAL激活因子的负调控。本文提出了一个MAL激活因子麦芽糖诱导自调控的模型。
