Researchers at the University of Minnesota have discovered a molecular¹ security system in human cells that deactivates² and degrades foreign DNA³. This discovery could open the door to major improvements in genetic⁵ engineering and gene⁴ therapy technologies. Led by Reuben Harris, associate professor of biochemistry生物化学, molecular biology and biophysics in the College of Biological Sciences, the report's findings will be published online by Nature Structural⁶ and Molecular Biology on Jan. 10.

In the study, Harris and colleagues show how APOBEC3A, an enzyme酶 found in human immune cells, disables double-stranded foreign DNA by changing cytosines胞嘧啶 (one of the four main bases in DNA) to uracils尿嘧啶 (an atypical DNA base). Persisting DNA uracils result in mutations that disable the DNA. In addition, the authors show that other enzymes⁸ step in to degrade the uracil-containing foreign DNA and sweep its remains⁹ out of the cell.

"Scientists have known for a long time that some human cells take up DNA better than others, but we haven't had good molecular explanations," Harris says. "This is definitely one of the reasons. Foreign DNA restriction¹⁰ is a fundamental process that could have broad implications for a variety of genetic diseases."

By understanding how the mechanism¹¹ works, scientists can develop ways to manipulate it to enable more effective methods to swap¹²交换，交易 bad genes¹³ for good ones. Harris is also intrigued好奇的 to learn why the mechanism doesn't affect a cell's own DNA.

The discovery of an analogous类似的，可比拟的 foreign DNA restriction mechanism in bacteria launched the field of genetic engineering during the 1970s. Once bacterial¹⁶ DNA restriction enzymes were understood, their power was harnessed to cut and paste segments of DNA for a wide variety of therapeutic治疗的 and industrial purposes.