Lee Myon-Hee, Cha Dong Seok, Mamillapalli Srivalli Swathi, Kwon Young Chul, Koo Hyeon-Sook
Department of Oncology, Brody School of Medicine, East Carolina University Greenville, NC 27834, USA ; Leo W. Jenkins Cancer Center, Brody School of Medicine, East Carolina University Greenville, NC 27834, USA ; Lineberger Comprehensive Cancer Center, University of North Carolina Chapel Hill, NC 27599, USA.
Department of Oncology, Brody School of Medicine, East Carolina University Greenville, NC 27834, USA ; Department of Oriental Pharmacy, College of Pharmacy, Woosuk University Jeonbuk 565-701, Republic of Korea.
Int J Biochem Mol Biol. 2014 May 15;5(1):11-20. eCollection 2014.
Ectopic expression of multi-transgenic copies can result in reduced expression of the transgene and can induce silence of endogenous gene; this process is called as co-suppression. Using a transgene-mediated co-suppression technique, we demonstrated the biological function of DNA topoisomerase-1 (top-1) in C. elegans development. Introduction of full-length top-1 transgene sufficiently induced the co-suppression of endogenous top-1 gene, causing embryonic lethality and abnormal germline development. We also found that the co-suppression of top-1 gene affected morphogenesis, lifespan and larval growth that were not observed in top-1 (RNAi) animals. Strikingly, co-suppression effects were significantly reduced by the elimination of top-1 introns, suggesting that efficient co-suppression may require intron(s) in C. elegans. Sequence analysis revealed that the introns 1 and 2 of top-1 gene possess consensus binding sites for several transcription factors, including MAB-3, LIN-14, TTX-3/CEH-10, CEH-1, and CEH-22. Among them, we examined a genetic link between ceh-22 and top-1. The ceh-22 is partially required for the specification of distal tip cells (DTC), which functions as a stem cell niche in the C. elegans gonad. Intriguingly, top-1 (RNAi) significantly enhanced DTC loss in ceh-22 mutant gonads, indicating that top-1 may play an important role in CEH-22-mediated DTC fate specification. Therefore, our findings suggest that transgene-mediated co-suppression facilitates the silencing of the specific genes and the study of gene function in vivo.
多个转基因拷贝的异位表达可导致转基因表达降低,并可诱导内源基因沉默;这一过程被称为共抑制。利用转基因介导的共抑制技术,我们证明了DNA拓扑异构酶-1(top-1)在秀丽隐杆线虫发育中的生物学功能。全长top-1转基因的导入充分诱导了内源top-1基因的共抑制,导致胚胎致死和生殖系发育异常。我们还发现,top-1基因的共抑制影响了形态发生、寿命和幼虫生长,而在top-1(RNA干扰)动物中未观察到这些现象。引人注目的是,去除top-1内含子后,共抑制效应显著降低,这表明在秀丽隐杆线虫中高效的共抑制可能需要内含子。序列分析显示,top-1基因的内含子1和2具有几个转录因子的共有结合位点,包括MAB-3、LIN-14、TTX-3/CEH-10、CEH-1和CEH-22。其中,我们研究了ceh-22与top-1之间的遗传联系。ceh-22在远端末梢细胞(DTC)的特化中部分发挥作用,DTC在秀丽隐杆线虫性腺中作为干细胞微环境起作用。有趣的是,top-1(RNA干扰)显著增强了ceh-22突变性腺中的DTC丢失,表明top-1可能在CEH-22介导的DTC命运特化中起重要作用。因此,我们的研究结果表明,转基因介导的共抑制促进了特定基因的沉默以及体内基因功能的研究。