School of Physical Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Sci Rep. 2019 Apr 10;9(1):5891. doi: 10.1038/s41598-019-41975-8.
DNA condensation is a ubiquitous phenomenon in biology, yet the physical basis for it has remained elusive. Here, we have explored the mechanism of DNA condensation through the protamine-DNA interaction, and by examining on it the influence of DNA binding drugs. We observed that the DNA condensation is accompanied by B to Ψ-DNA transition as a result of DNA base pair distortions due to protamine binding, bringing about the formation of toroidal structure through coil-globule transition. The binding energetics suggested that electrostatic energy, bending energy and hydration energy must play crucial roles in DNA condensation. EtBr intercalation interferes with the protamine-DNA interaction, challenging the distortion of the DNA helix and separation of DNA base pairs by protamine. Thus, EtBr, by competing directly with protamine, resists the phenomenon of DNA condensation. On the contrary, netropsin impedes the DNA condensation by an allosteric mechanism, by resisting the probable DNA major groove bending by protamine. In summary, we demonstrate that drugs with distinct binding modes use different mechanism to interfere with DNA condensation.
DNA 凝聚是生物学中普遍存在的现象,但它的物理基础仍然难以捉摸。在这里,我们通过鱼精蛋白-DNA 相互作用研究了 DNA 凝聚的机制,并考察了 DNA 结合药物对其的影响。我们观察到,由于鱼精蛋白结合导致 DNA 碱基对扭曲,DNA 凝聚伴随着 B 到 Ψ-DNA 的转变,通过螺旋-球转变形成环形结构。结合能表明,静电能、弯曲能和水合能在 DNA 凝聚中必须发挥关键作用。溴化乙锭(EtBr)嵌入干扰鱼精蛋白-DNA 相互作用,挑战 DNA 螺旋的扭曲和鱼精蛋白分离 DNA 碱基对。因此,EtBr 通过与鱼精蛋白直接竞争,抵抗 DNA 凝聚现象。相反,净司他丁(netropsin)通过变构机制阻碍 DNA 凝聚,抵抗鱼精蛋白可能导致的 DNA 大沟弯曲。总之,我们证明了具有不同结合模式的药物通过不同的机制干扰 DNA 凝聚。