Wickner S, Hoskins J, McKenney K
Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):7903-7. doi: 10.1073/pnas.88.18.7903.
DnaK is a major heat shock protein of Escherichia coli and the homolog of hsp70 in eukaryotes. We demonstrate the mechanism by which DnaK and another heat shock protein, DnaJ, render the plasmid P1 initiator RepA 100-fold more active for binding to the P1 origin of replication. Activation is the conversion of RepA dimers into monomers in an ATP-dependent reaction and the monomer form binds with high affinity to oriP1 DNA. Reversible chemical denaturants also convert RepA dimers to monomers and simultaneously activate oriP1 DNA binding. Increasing protein concentration converts monomers to dimers and deactivates RepA. Based on our data and previous work, we present a model for heat shock protein action under normal and stress conditions.
DnaK是大肠杆菌的一种主要热休克蛋白,也是真核生物中hsp70的同源物。我们证明了DnaK和另一种热休克蛋白DnaJ使质粒P1起始子RepA与P1复制起点结合的活性提高100倍的机制。激活是指在ATP依赖的反应中,RepA二聚体转化为单体,单体形式以高亲和力与oriP1 DNA结合。可逆化学变性剂也能将RepA二聚体转化为单体,并同时激活oriP1 DNA结合。增加蛋白质浓度会使单体转化为二聚体,并使RepA失活。基于我们的数据和之前的研究工作,我们提出了一个在正常和应激条件下热休克蛋白作用的模型。