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首页> 外文期刊>Molecular and Cellular Biology >ADA3: a gene, identified by resistance to GAL4-VP16, with properties similar to and different from those of ADA2.
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ADA3: a gene, identified by resistance to GAL4-VP16, with properties similar to and different from those of ADA2.

机译：ADA3：通过对GAL4-VP16的抗性鉴定的基因，具有与ADA2相似和不同的特性。

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摘要

We describe the isolation of a yeast gene, ADA3, mutations in which prevent the toxicity of GAL4-VP16 in vivo. Toxicity was previously proposed to be due to the trapping of general transcription factors required at RNA polymerase II promoters (S. L. Berger, B. Pi?a, N. Silverman, G. A. Marcus, J. Agapite, J. L. Regier, S. J. Triezenberg, and L. Guarente, Cell 70:251-265, 1992). trans activation by VP16 as well as the acidic activation domain of GCN4 is reduced in the mutant. Other activation domains, such as those of GAL4 and HAP4, are only slightly affected in the mutant. This spectrum is similar to that observed for mutants with lesions in ADA2, a gene proposed to encode a transcriptional adaptor. The ADA3 gene is not absolutely essential for cell growth, but gene disruption mutants grow slowly and are temperature sensitive. Strains doubly disrupted for ada2 and ada3 grow no more slowly than single mutants, providing further evidence that these genes function in the same pathway. Selection of initiation sites by the general transcriptional machinery in vitro is altered in the ada3 mutant, providing a clue that ADA3 could be a novel general transcription factor involved in the response to acidic activators.
机译：我们描述了酵母基因ADA3突变的分离，其中该突变阻止了GAL4-VP16在体内的毒性。以前曾提出毒性是由于捕获RNA聚合酶II启动子所需的一般转录因子（SL Berger，B.Pi？a，N.Silverman，GA Marcus，J.Agapite，JL Regier，SJ Triezenberg和L. Guarente，Cell 70：251-265，1992）。在突变体中，VP16的反式激活以及GCN4的酸性激活结构域减少。其他激活域，例如GAL4和HAP4的激活域，在突变体中仅受到轻微影响。该光谱类似于在ADA2中发现的具有突变的突变体，该基因被提议编码转录接头。 ADA3基因对于细胞生长不是绝对必需的，但是基因破坏突变体生长缓慢且对温度敏感。对ada2和ada3双重破坏的菌株的生长不会比单个突变体慢得多，这进一步证明了这些基因在同一途径中起作用。 ada3突变体改变了体外一般转录机制对起始位点的选择，提示ADA3可能是参与对酸性激活剂反应的新型一般转录因子。

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