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CNS翻译练习：Nature. 2010 Jul 25.光裂合酶修复紫外线引导的（6-4）光化产物的动力学和机制
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Nature. 2010 Jul 25. [Epub ahead of print]
Dynamics and mechanism of repair of ultraviolet-induced (6-4) photoproduct by photolyase.
Li J, Liu Z, Tan C, Guo X, Wang L, Sancar A, Zhong D.
Departments of Physics, Chemistry and Biochemistry, Programs of Biophysics, Chemical Physics and Biochemistry, 191 West Woodruff Avenue, The Ohio State University, Columbus, Ohio 43210, USA.
Abstract
One of the detrimental effects of ultraviolet radiation on DNA is the formation of the (6-4) photoproduct, 6-4PP, between two adjacent pyrimidine rings. This lesion interferes with replication and transcription, and may result in mutation and cell death. In many organisms, a flavoenzyme called photolyase uses blue light energy to repair the 6-4PP (ref. 3). The molecular mechanism of the repair reaction is poorly understood. Here, we use ultrafast spectroscopy to show that the key step in the repair photocycle is a cyclic proton transfer between the enzyme and the substrate. By femtosecond synchronization of the enzymatic dynamics with the repair function, we followed the function evolution and observed direct electron transfer from the excited flavin cofactor to the 6-4PP in 225 picoseconds, but surprisingly fast back electron transfer in 50 picoseconds without repair. We found that the catalytic proton transfer between a histidine residue in the active site and the 6-4PP, induced by the initial photoinduced electron transfer from the excited flavin cofactor to 6-4PP, occurs in 425 picoseconds and leads to 6-4PP repair in tens of nanoseconds. These key dynamics define the repair photocycle and explain the underlying molecular mechanism of the enzyme's modest efficiency.
光裂合酶修复紫外线引导的（6-4）光化产物的动力学和机制
Abstract
在两个相邻嘧啶环间形成（6-4）光化产物6-4PP是紫外线辐射有害作用之一。这种损伤干扰复制和转录,可能会导致突变和细胞死亡。在很多生物中，一种叫做光裂合酶的黄素酶利用蓝光的能量修复6-4PP(ref. 3)。修复反应的分子机制还不甚明了。本文我们利用超高速光谱仪显示了光循环修复的关键步骤是酶和底物的质子转移循环。利用飞秒同步化修复功能的酶动力学，我们跟踪了功能进化并在225皮秒观察到激发的黄素辅因子到6-4PP的直接电子转移，但令人吃惊的是50皮秒时快速回电子转移（？）却没有发生修复。我们发现组活性位点组氨酸残基和6-4PP之间质子转移催化作用，从已激发的黄素辅酶到6-4PP是由最初的光激发电子转移，发生在425皮秒，并且导致数十纳秒内6-4PP的修复。这些关键的动力学定义了光循环修复并解释了酶的适当效率的潜在分子机制。
https://blog.sciencenet.cn/blog-464637-356336.html
下一篇：CNS翻译练习：Cell. 2010 Jul 23.成骨细胞的胰岛素信号传导整合骨重建和能量代谢
Dynamics and mechanism of repair of ultraviolet-induced (6-4) photoproduct by photolyase.
Li J, Liu Z, Tan C, Guo X, Wang L, Sancar A, Zhong D.
Departments of Physics, Chemistry and Biochemistry, Programs of Biophysics, Chemical Physics and Biochemistry, 191 West Woodruff Avenue, The Ohio State University, Columbus, Ohio 43210, USA.
Abstract
One of the detrimental effects of ultraviolet radiation on DNA is the formation of the (6-4) photoproduct, 6-4PP, between two adjacent pyrimidine rings. This lesion interferes with replication and transcription, and may result in mutation and cell death. In many organisms, a flavoenzyme called photolyase uses blue light energy to repair the 6-4PP (ref. 3). The molecular mechanism of the repair reaction is poorly understood. Here, we use ultrafast spectroscopy to show that the key step in the repair photocycle is a cyclic proton transfer between the enzyme and the substrate. By femtosecond synchronization of the enzymatic dynamics with the repair function, we followed the function evolution and observed direct electron transfer from the excited flavin cofactor to the 6-4PP in 225 picoseconds, but surprisingly fast back electron transfer in 50 picoseconds without repair. We found that the catalytic proton transfer between a histidine residue in the active site and the 6-4PP, induced by the initial photoinduced electron transfer from the excited flavin cofactor to 6-4PP, occurs in 425 picoseconds and leads to 6-4PP repair in tens of nanoseconds. These key dynamics define the repair photocycle and explain the underlying molecular mechanism of the enzyme's modest efficiency.
光裂合酶修复紫外线引导的（6-4）光化产物的动力学和机制
Abstract
在两个相邻嘧啶环间形成（6-4）光化产物6-4PP是紫外线辐射有害作用之一。这种损伤干扰复制和转录,可能会导致突变和细胞死亡。在很多生物中，一种叫做光裂合酶的黄素酶利用蓝光的能量修复6-4PP(ref. 3)。修复反应的分子机制还不甚明了。本文我们利用超高速光谱仪显示了光循环修复的关键步骤是酶和底物的质子转移循环。利用飞秒同步化修复功能的酶动力学，我们跟踪了功能进化并在225皮秒观察到激发的黄素辅因子到6-4PP的直接电子转移，但令人吃惊的是50皮秒时快速回电子转移（？）却没有发生修复。我们发现组活性位点组氨酸残基和6-4PP之间质子转移催化作用，从已激发的黄素辅酶到6-4PP是由最初的光激发电子转移，发生在425皮秒，并且导致数十纳秒内6-4PP的修复。这些关键的动力学定义了光循环修复并解释了酶的适当效率的潜在分子机制。
https://blog.sciencenet.cn/blog-464637-356336.html
下一篇：CNS翻译练习：Cell. 2010 Jul 23.成骨细胞的胰岛素信号传导整合骨重建和能量代谢
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