Furter-Graves E M, Hall B D, Furter R
Institute for Cell Biology, Swiss Federal Institute of Technology, ETH-Hönggerberg, Zürich.
Nucleic Acids Res. 1994 Nov 25;22(23):4932-6. doi: 10.1093/nar/22.23.4932.
The yeast shi mutation affects the spacing between the TATA promoter element and transcription initiation sites; for the H2B and ADH1 genes, a series of start sites located approximately 50-80 bp downstream of TATA is used in addition to the wild-type initiation sites located at around 100 bp from TATA (1). Here, the yeast SHI wild-type gene has been isolated by complementation and shown to be identical to RPB9, the gene encoding a small subunit of RNA polymerase II. A point mutation in the shi gene, changing a cysteine residue in a putative zinc ribbon motif into a phenylalanine residue, was demonstrated to permit the observed usage of upstream initiation sites. Deletion of the non-essential SHI gene also results in usage of upstream initiation sites and causes conditional growth defects.
酵母shi突变影响TATA启动子元件与转录起始位点之间的间距；对于H2B和ADH1基因，除了位于距TATA约100 bp处的野生型起始位点外，还使用了一系列位于TATA下游约50 - 80 bp处的起始位点(1)。在这里，酵母SHI野生型基因已通过互补分离出来，并显示与RPB9相同，RPB9是编码RNA聚合酶II小亚基的基因。shi基因中的一个点突变，将假定的锌带基序中的一个半胱氨酸残基变为苯丙氨酸残基，被证明允许观察到的上游起始位点的使用。非必需的SHI基因的缺失也会导致上游起始位点的使用，并导致条件性生长缺陷。
