DNA-Protein Interactions Unit, School of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, UK.
Nucleic Acids Res. 2013 Jan;41(2):1081-90. doi: 10.1093/nar/gks1210. Epub 2012 Dec 5.
The mechanism by which a double-stranded DNA break is produced following collision of two translocating Type I Restriction-Modification enzymes is not fully understood. Here, we demonstrate that the related Type ISP Restriction-Modification enzymes LlaGI and LlaBIII can cooperate to cleave DNA following convergent translocation and collision. When one of these enzymes is a mutant protein that lacks endonuclease activity, DNA cleavage of the 3'-5' strand relative to the wild-type enzyme still occurs, with the same kinetics and at the same collision loci as for a reaction between two wild-type enzymes. The DNA nicking activity of the wild-type enzyme is still activated by a protein variant entirely lacking the Mrr nuclease domain and by a helicase mutant that cannot translocate. However, the helicase mutant cannot cleave the DNA despite the presence of an intact nuclease domain. Cleavage by the wild-type enzyme is not activated by unrelated protein roadblocks. We suggest that the nuclease activity of the Type ISP enzymes is activated following collision with another Type ISP enzyme and requires adenosine triphosphate binding/hydrolysis but, surprisingly, does not require interaction between the nuclease domains. Following the initial rapid endonuclease activity, additional DNA cleavage events then occur more slowly, leading to further processing of the initial double-stranded DNA break.
双链 DNA 断裂是如何在两种迁移的 I 型限制修饰酶碰撞后产生的,其机制尚未完全阐明。在这里,我们证明相关的 I 型 ISP 限制修饰酶 LlaGI 和 LlaBIII 可以在收敛迁移和碰撞后合作切割 DNA。当其中一种酶是一种缺乏内切酶活性的突变蛋白时,相对于野生型酶,3'-5'链的 DNA 切割仍然会发生,其动力学和野生型酶之间的反应相同。野生型酶的 DNA 切口活性仍然被完全缺乏 Mrr 核酸酶结构域的蛋白质变体和不能迁移的解旋酶突变体激活。然而,尽管存在完整的核酸酶结构域,解旋酶突变体仍然不能切割 DNA。野生型酶的切割不能被不相关的蛋白路障激活。我们认为,I 型 ISP 酶的核酸酶活性在与另一种 I 型 ISP 酶碰撞后被激活,需要三磷酸腺苷结合/水解,但令人惊讶的是,不需要核酸酶结构域之间的相互作用。在初始快速内切酶活性之后,随后会发生较慢的额外 DNA 切割事件,导致初始双链 DNA 断裂的进一步处理。