Vidal M, Gaber R F
Department of Biochemistry, Molecular Biology, Northwestern University, Evanston, Illinois 60208-3500.
Mol Cell Biol. 1991 Dec;11(12):6317-27. doi: 10.1128/mcb.11.12.6317-6327.1991.
In Saccharomyces cerevisiae, TRK1 and TRK2 encode the high- and low-affinity K+ transporters, respectively. In cells containing a deletion of TRK1, transcription levels of TRK2 are extremely low and are limiting for growth in media containing low levels of K+ (Trk- phenotype). Recessive mutations in RPD1 and RPD3 suppress the TRK2, conferring an approximately fourfold increase in transcription. rpd3 mutations confer pleiotropic phenotypes, including (i) mating defects, (ii) hypersensitivity to cycloheximide, (iii) inability to sporulate as homozygous diploids, and (iv) constitutive derepression of acid phosphatase. RPD3 was cloned and is predicted to encode a 48-kDa protein with no extensive similarity to proteins contained in current data bases. Deletion of RPD3 is not lethal but confers phenotypes identical to those caused by spontaneous mutations. RPD3 is required for both full repression and full activation of transcription of target genes including PHO5, STE6, and TY2. RPD3 is the second gene required for this function, since RPD1 is also required. The effects of mutations in RPD1 and RPD3 are not additive, suggesting that these genes are involved in the same transcriptional regulatory function or pathway.
在酿酒酵母中，TRK1和TRK2分别编码高亲和力和低亲和力的钾离子转运蛋白。在缺失TRK1的细胞中，TRK2的转录水平极低，限制了细胞在低钾培养基中的生长（Trk-表型）。RPD1和RPD3中的隐性突变抑制了TRK2，使转录增加约四倍。rpd3突变赋予多种表型，包括：（i）交配缺陷；（ii）对环己酰亚胺过敏；（iii）作为纯合二倍体无法形成孢子；（iv）酸性磷酸酶的组成型去阻遏。RPD3被克隆出来，预计编码一种48 kDa的蛋白质，与现有数据库中的蛋白质没有广泛的相似性。缺失RPD3并不致命，但赋予与自发突变相同的表型。RPD3对于包括PHO5、STE6和TY2在内的靶基因转录的完全抑制和完全激活都是必需的。RPD3是该功能所需的第二个基因，因为RPD1也是必需的。RPD1和RPD3突变的影响不是累加的，表明这些基因参与相同的转录调节功能或途径。
