Teeters Gary, Cucolo Christina E, Kasar Sagar N, Worley Melanie I, Siegrist Sarah E
Program in Fundamental Neuroscience, Department of Biology, University of Virginia, Charlottesville, VA, 22904, USA; Department of Biology, University of Virginia, Charlottesville, VA, 22904, USA.
Department of Biology, University of Virginia, Charlottesville, VA, 22904, USA.
Dev Biol. 2025 Apr;520:31-40. doi: 10.1016/j.ydbio.2024.12.017. Epub 2024 Dec 28.
The ability to induce cell death in a controlled stereotypic manner has led to the discovery of evolutionary conserved molecules and signaling pathways necessary for tissue growth, repair, and regeneration. Here we report the development of a new method to genetically induce cell death in a controlled stereotypic manner in Drosophila. This method has advantages over other current methods and relies on expression of the E. coli enzyme Nitroreductase (NTR) with exogenous application of the nitroimidazole prodrug, Ronidazole. NTR expression is controlled spatially using the GAL4/UAS system while temporal control of cell death is achieved through timed feeding of Ronidazole supplied in the diet. In cells expressing NTR, Ronidazole is converted to a toxic substance inducing DNA damage and cell death. Caspase cell death is achieved in a range of NTR-expressing cell types with Ronidazole feeding, including epithelial, neurons, and glia. Removing Ronidazole from the diet restores cell death to normal unperturbed levels. Unlike other genetic ablation methods, temporal control is achieved through feeding not temperature, circumventing developmental complications associated with temperature changes. Ronidazole-NTR also requires only two transgenes, a GAL4 driver and UAS-NTR, which is generated as a GFP-NTR fusion allowing for easy setup of large-scale screening of UAS-RNAi lines. Altogether, Ronidazole-NTR provides a new streamlined method for inducing cell death in Drosophila with temperature-independent ON/OFF control.
以可控的模式诱导细胞死亡的能力,已促成了对组织生长、修复和再生所必需的进化保守分子及信号通路的发现。在此,我们报告一种在果蝇中以可控的模式进行基因诱导细胞死亡的新方法的开发。该方法相较于其他现有方法具有优势,它依赖于大肠杆菌硝基还原酶(NTR)与硝基咪唑前药罗硝唑的外源应用的表达。利用GAL4/UAS系统在空间上控制NTR的表达,同时通过定时投喂添加在食物中的罗硝唑来实现细胞死亡的时间控制。在表达NTR的细胞中,罗硝唑被转化为一种有毒物质,诱导DNA损伤和细胞死亡。通过投喂罗硝唑,在一系列表达NTR的细胞类型中实现了半胱天冬酶细胞死亡,包括上皮细胞、神经元和神经胶质细胞。从食物中去除罗硝唑可使细胞死亡恢复到正常的未受干扰水平。与其他基因消融方法不同,时间控制是通过投喂而非温度来实现的,从而规避了与温度变化相关的发育并发症。罗硝唑 - NTR也只需要两个转基因,一个GAL4驱动子和UAS - NTR,它作为GFP - NTR融合体产生,便于对UAS - RNAi品系进行大规模筛选的设置。总之,罗硝唑 - NTR为在果蝇中诱导细胞死亡提供了一种新的简化方法,具有与温度无关的开/关控制。