Nakai H, Kruklitis R
Department of Biochemistry and Molecular Biology, Georgetown University Medical Center, Washington, D.C. 20007, USA.
J Biol Chem. 1995 Aug 18;270(33):19591-8. doi: 10.1074/jbc.270.33.19591.
Upon catalyzing strand transfer, the Mu transposase (MuA) remains tightly bound to the resulting transposition intermediate, the strand transfer complex (STC), and poses an impediment to host replication proteins. Additional host factors, which can be resolved into two fractions (Mu Replication Factor alpha and beta; MRF alpha and MRF beta), are required to disassemble the MuA complex and initiate DNA synthesis. MRF alpha modifies the protein content of the STC, removing MuA from the DNA in the process. The MRF beta promotes initiation of the Mu DNA synthesis on the STC altered by the MRF alpha. These host factors cannot promote initiation of Mu DNA synthesis if the STC is damaged by partial proteolysis. Moreover, the mutant protein MuA211 cannot be removed from the STC by MRF alpha, blocking initiation of DNA synthesis. These results indicate that MuA in the STC plays a critical function in beginning a sequence of events leading to the establishment of a Mu replication fork.
在催化链转移时，Mu转座酶（MuA）仍紧密结合于产生的转座中间体——链转移复合物（STC），并对宿主复制蛋白构成障碍。需要其他宿主因子（可分为两部分，即Mu复制因子α和β；MRFα和MRFβ）来拆解MuA复合物并启动DNA合成。MRFα改变STC的蛋白质组成，在此过程中从DNA上移除MuA。MRFβ促进在经MRFα改变的STC上启动Mu DNA合成。如果STC因部分蛋白水解而受损，这些宿主因子就无法促进Mu DNA合成的起始。此外，突变蛋白MuA211不能被MRFα从STC上移除，从而阻断了DNA合成的起始。这些结果表明，STC中的MuA在启动一系列导致Mu复制叉建立的事件中发挥着关键作用。
