한빛사 논문
You Kyeong Jeong 1,5, SeokHoon Lee1,5, Gue-Ho Hwang1, Sung-Ah Hong 1, Se-eun Park1, Jin-Soo Kim 2,3, Jae-Sung Woo4,* and Sangsu Bae1,*
1Department of Chemistry and Research Institute for Convergence of Basic Sciences, Hanyang University, Seoul, South Korea. 2Center for Genome Engineering, Institute for Basic Science, Daejeon, South Korea. 3Department of Chemistry, Seoul National University, Seoul, South Korea. 4Department of Life Sciences, Korea University, Seoul, South Korea. 5These authors contributed equally: You Kyeong Jeong, SeokHoon Lee.
Correspondence to Jae-Sung Woo or Sangsu Bae.
Abstract
Adenine base editors (ABEs) catalyze specific A-to-G conversions at genomic sites of interest. However, ABEs also induce cytosine deamination at the target site. To reduce the cytosine editing activity, we engineered a commonly used adenosine deaminase, TadA7.10, and found that ABE7.10 with a D108Q mutation in TadA7.10 exhibited tenfold reduced cytosine deamination activity. The D108Q mutation also reduces cytosine deamination activity in two recently developed high-activity versions of ABE, ABE8e and ABE8s, and is compatible with V106W, a mutation that reduces off-target RNA editing. ABE7.10 containing a P48R mutation displayed increased cytosine deamination activity and a substantially reduced adenine editing rate, yielding a TC-specific base editing tool for TC-to-TT or TC-to-TG conversions that broadens the utility of base editors.
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