Hirschman J E, Durbin K J, Winston F
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Mol Cell Biol. 1988 Nov;8(11):4608-15. doi: 10.1128/mcb.8.11.4608-4615.1988.
The his4-912 delta mutation is an insertion of the long terminal repeat (delta) of the yeast retrotransposon Ty into the HIS4 promoter region, such that the delta is 97 base pairs upstream of the HIS4 transcription initiation site. Strains carrying the his4-912 delta allele are His- at 23 degrees C; this phenotype can be reversed either by growth at 37 degrees C or by mutations in trans-acting SPT genes. Under conditions in which his4-912 delta confers a His- phenotype. HIS4 transcription initiates at the delta initiation site, rather than at the HIS4 initiation site, producing a longer, nonfunctional transcript. Under conditions in which the strain is His+, transcription initiates at the wild-type HIS4 initiation site. To understand how transcription is balanced between the delta and HIS4 promoters, we have selected for cis-acting suppressors of his4-912 delta. Two classes defined by six independent mutations restore synthesis of a functional HIS4 transcript. The first class is an A-to-G base change 1 base upstream of the proposed delta TATA sequence. These mutants do not synthesize the delta-initiated transcript; instead, they synthesize only the wild-type HIS4 transcript. The second class of mutations alters base pairs surrounding the functional HIS4 TATA sequence. The two strongest His+ mutants of this class synthesize the wild-type HIS4 transcript at levels consistent with their His+ phenotype. Surprisingly, these two mutants also have a reduced level of the delta-initiated transcript relative to the his4-912 delta parent. Analysis of these mutants indicates that the level of transcription from one promoter can affect the level of transcription from the other promoter and suggests that delta and HIS4 transcription signals compete for initiation of transcription from each site.
his4-912δ突变是酵母逆转录转座子Ty的长末端重复序列(δ)插入到HIS4启动子区域,使得δ位于HIS4转录起始位点上游97个碱基对处。携带his4-912δ等位基因的菌株在23℃时为组氨酸缺陷型(His-);这种表型可以通过在37℃下生长或通过反式作用的SPT基因突变来逆转。在his4-912δ赋予组氨酸缺陷型表型的条件下,HIS4转录在δ起始位点起始,而不是在HIS4起始位点起始,产生更长的、无功能的转录本。在菌株为组氨酸野生型(His+)的条件下,转录在野生型HIS4起始位点起始。为了了解转录如何在δ和HIS4启动子之间保持平衡,我们筛选了his4-912δ的顺式作用抑制子。由六个独立突变定义的两类突变恢复了功能性HIS4转录本的合成。第一类是在假定的δTATA序列上游1个碱基处的A到G碱基变化。这些突变体不合成δ起始的转录本;相反,它们只合成野生型HIS4转录本。第二类突变改变了功能性HIS4 TATA序列周围的碱基对。这类中两个最强的His+突变体以与其His+表型一致的水平合成野生型HIS4转录本。令人惊讶的是,相对于his4-912δ亲本,这两个突变体的δ起始转录本水平也有所降低。对这些突变体的分析表明,一个启动子的转录水平可以影响另一个启动子的转录水平,并表明δ和HIS4转录信号竞争从每个位点起始转录。