Suzuki Y, Nishizawa M
Department of Microbiology, Keio University School of Medicine, Tokyo, Japan.
Mol Cell Biol. 1994 Jun;14(6):3791-9. doi: 10.1128/mcb.14.6.3791-3799.1994.
GAL11 is an auxiliary transcription factor that functions either positively or negatively, depending on the structure of the target promoters and the combination of DNA-bound activators. In this report, we demonstrate that a gal11 delta mutation caused a decrease in the length of the telomere C1-3A tract, a derepression of URA3 when it is placed next to telomere, and an increase in accessibility of the telomeric region to dam methylase, indicating that GAL11 is involved in the regulation of the structure and the position effect of telomeres. The defective position effect in a gal11 delta strain was suppressed by overproduction of SIR3, whereas overexpression of GAL11 failed to restore the telomere position effect in a sir3 delta strain. Hyperproduced GAL11 could partially suppress the defect in silencing at HMR in a sir1 delta mutant but not that in a sir3 delta mutant, suggesting that GAL11 can replace SIR1 function partly in the silencing of HMR. Overproduced SIR3 also could restore silencing at HMR in sir1 delta cells. In contrast, SIR1 in a multicopy plasmid relieved the telomere position effect, especially in a gal11 delta mutant. Since chromatin structure is thought to play a major role in the silencing at both the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by the HM loci and telomeres, GAL11 is likely to participate in the regional regulation of transcription by modulating the chromatin structure.
GAL11是一种辅助转录因子，其功能取决于靶启动子的结构以及与DNA结合的激活因子的组合，可发挥正向或负向作用。在本报告中，我们证明gal11δ突变导致端粒C1 - 3A序列长度缩短，当URA3位于端粒附近时其表达去抑制，并且端粒区域对dam甲基化酶的可及性增加，这表明GAL11参与端粒结构和位置效应的调控。gal11δ菌株中缺陷的位置效应可通过过量表达SIR3来抑制，而过量表达GAL11未能恢复sir3δ菌株中的端粒位置效应。过量产生的GAL11可部分抑制sir1δ突变体中HMR位点沉默的缺陷，但不能抑制sir3δ突变体中的缺陷，这表明GAL11在HMR位点沉默中可部分替代SIR1的功能。过量表达的SIR3也可恢复sir1δ细胞中HMR位点的沉默。相反，多拷贝质粒中的SIR1可缓解端粒位置效应，尤其是在gal11δ突变体中。由于染色质结构被认为在HM位点和端粒的沉默中起主要作用，GAL11可能通过调节染色质结构参与HM位点和端粒区域的转录调控。
