期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2020
卷号：117
期号：39
页码：24019-24021
DOI：10.1073/pnas.2016446117
出版社：The National Academy of Sciences of the United States of America
摘要：For well over a century, geneticists have relentlessly bombarded the genome of the fruit fly Drosophila melanogaster with increasingly sophisticated mutagenic agents (1). Collectively, these loss-of-function studies have been astoundingly informative, providing fundamental breakthroughs in nearly all fields of biology (2, 3). Initially, such studies relied on mutagens that attack the genome in quasirandom locations, such as X-rays, mutagenic chemicals, and transposable elements. The application of RNA interference (RNAi) to Drosophila genetics made it possible to intentionally target the transcript of any specific gene of interest and, with the Gal4-UAS system, to do so with precise spatial and temporal control (4, 5). The field was revolutionized again 7 y ago, when CRISPR-Cas9–based genome editing was demonstrated in Drosophila , making it possible to mutate and rewrite the genome of the fruit fly with ease, specificity, and scalability that were previously unimaginable (6). Yet for all of the profound properties of Cas9, the powerhouse RNA-guided DNase at the center of this technical revolution, there are downsides to relying solely on this particular nuclease for genome editing. Indeed, a growing number of alternative CRISPR approaches have been described in recent years, based on both naturally occurring and laboratory-evolved CRISPR-family proteins. To date, however, none of these alternatives have been effectively adapted for in vivo studies in Drosophila . In PNAS, Port et al. (7) provide such a demonstration, focusing on the Cas12a enzyme (formerly known as Cpf1). Cas12a displays a number of intriguing properties that make it a broadly useful complement to Cas9 (Fig. 1) and a valuable tool to continue the collective interrogation on the Drosophila genome.
