Bedwell Gregory J, Prevelige Peter E
Department of Microbiology, University of Alabama at Birmingham, 845 19th St. South, Birmingham, AL 35294, United States; Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, 3 Blackfan Circle, Boston, MA 02115, United States.
Department of Microbiology, University of Alabama at Birmingham, 845 19th St. South, Birmingham, AL 35294, United States.
Virology. 2017 May;505:127-138. doi: 10.1016/j.virol.2017.02.019. Epub 2017 Feb 24.
The portal vertex in dsDNA bacteriophage serves as the site for genome encapsidation and release. In several of these viruses, efficient termination of DNA packaging has been shown to be dependent on the density of packaged DNA. The portal protein has been implicated as being part of the sensor that regulates packaging termination through DNA-dependent conformational changes during packaging. The mechanism by which DNA induces these conformational changes remains unknown. In this study, we explore how point mutants in the portal core can result in changes in genome packaging density in P22. Mutations in the portal core that subtly alter the structure or dynamics of the protein result in an increase in the amount of DNA packaged. The magnitude of the change is amino acid and location specific. Our findings suggest a mechanism wherein compression of the portal core is an essential aspect of signal transmission during packaging.
双链 DNA 噬菌体中的门户顶点是基因组包装和释放的位点。在其中几种病毒中，已证明 DNA 包装的有效终止取决于包装 DNA 的密度。门户蛋白被认为是传感器的一部分，该传感器在包装过程中通过依赖于 DNA 的构象变化来调节包装终止。DNA 诱导这些构象变化的机制仍然未知。在本研究中，我们探索了门户核心中的点突变如何导致 P22 中基因组包装密度的变化。门户核心中的突变会微妙地改变蛋白质的结构或动力学，从而导致包装的 DNA 量增加。变化的幅度具有氨基酸和位置特异性。我们的研究结果表明了一种机制，其中门户核心的压缩是包装过程中信号传递的一个重要方面。
