Colombo Chiara Vittoria, Casari Erika, Gnugnoli Marco, Corallo Flavio, Tisi Renata, Longhese Maria Pia
Dipartimento di Biotecnologie e Bioscienze, Università degli Studi di Milano - Bicocca, 20126 Milano, Italy.
Nucleic Acids Res. 2024 Dec 11;52(22):13849-13864. doi: 10.1093/nar/gkae1049.
The yeast Sae2 protein, known as CtIP in mammals, once phosphorylated at Ser267, stimulates the endonuclease activity of the Mre11-Rad50-Xrs2 (MRX) complex to cleave DNA ends that possess hairpin structures or protein blocks, such as the Spo11 transesterase or trapped topoisomerases. Stimulation of the Mre11 endonuclease by Sae2 depends on a Rad50-Sae2 interaction, but the mechanism by which this is achieved remains to be elucidated. Through genetic studies, we show that the absence of the last 23 amino acids from the Sae2 C-terminus specifically impairs MRX-dependent DNA cleavage events, while preserving the other Sae2 functions. Employing AlphaFold3 protein structure predictions, we found that the Rad50-Sae2 interface involves not only phosphorylated Ser267 but also the phosphorylated Thr279 residue and the C-terminus of Sae2. This region engages in multiple interactions with residues that are mutated in rad50-s mutants, which are known to be specifically defective in the processing of Spo11-bound DNA ends. These interactions are critical for stabilizing the association between Sae2 and Rad50, thereby ensuring the correct positioning of Mre11 in its active endonucleolytic state.
酵母中的Sae2蛋白,在哺乳动物中称为CtIP,一旦在Ser267位点磷酸化,就会刺激Mre11-Rad50-Xrs2(MRX)复合物的核酸内切酶活性,以切割具有发夹结构或蛋白质阻断的DNA末端,例如Spo11转酯酶或被困的拓扑异构酶。Sae2对Mre11核酸内切酶的刺激依赖于Rad50-Sae2相互作用,但其实现机制仍有待阐明。通过遗传学研究,我们发现Sae2 C末端缺失最后23个氨基酸会特异性损害依赖MRX的DNA切割事件,同时保留Sae2的其他功能。利用AlphaFold3蛋白质结构预测,我们发现Rad50-Sae2界面不仅涉及磷酸化的Ser267,还涉及磷酸化的Thr279残基和Sae2的C末端。该区域与rad50-s突变体中发生突变的残基进行多种相互作用,已知rad50-s突变体在处理与Spo11结合的DNA末端时存在特异性缺陷。这些相互作用对于稳定Sae2和Rad50之间的结合至关重要,从而确保Mre11在其活性核酸内切酶状态下的正确定位。