Department of Biological Sciences, Lehigh University, Bethlehem, PA 18015, USA.
FEBS Lett. 2010 Sep 24;584(18):4037-40. doi: 10.1016/j.febslet.2010.08.020. Epub 2010 Aug 20.
Ctf7/Eco1-dependent acetylation of Smc3 is essential for sister chromatid cohesion. Here, we use epitope tag-induced lethality in cells diminished for Ctf7/Eco1 activity to map cohesin architecture in vivo. Tagging either Smc1 or Mcd1/Scc1, but not Scc3/Irr1, appears to abolish access to Smc3 in ctf7/eco1 mutant cells, suggesting that Smc1 and Smc3 head domains are in direct contact with each other and also with Mcd1/Scc1. Thus, cohesin complexes may be much more compact than commonly portrayed. We further demonstrate that mutation in ELG1 or RFC5 anti-establishment genes suppress tag-induced lethality, consistent with the notion that the replication fork regulates Ctf7/Eco1.
Ctf7/Eco1 依赖性 Smc3 乙酰化对于姐妹染色单体黏合是必需的。在这里，我们使用 Ctf7/Eco1 活性降低的细胞中表位标记诱导的致死性来体内作图黏合复合物结构。标记 Smc1 或 Mcd1/Scc1，但不是 Scc3/Irr1，似乎会在 ctf7/eco1 突变细胞中消除 Smc3 的可及性，表明 Smc1 和 Smc3 头部结构域直接相互接触，也与 Mcd1/Scc1 相互接触。因此，黏合复合物可能比通常描绘的更紧凑。我们进一步证明，ELG1 或 RFC5 抗起始基因的突变可以抑制标记诱导的致死性，这与复制叉调节 Ctf7/Eco1 的观点一致。
