Normant Vincent, Beaudoin Jude, Labbé Simon
From the Département de Biochimie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec J1E 4K8, Canada.
From the Département de Biochimie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Quebec J1E 4K8, Canada
J Biol Chem. 2015 Sep 11;290(37):22622-37. doi: 10.1074/jbc.M115.674556. Epub 2015 Jul 30.
Sense and antisense transcripts produced from convergent gene pairs could interfere with the expression of either partner gene. In Schizosaccharomyces pombe, we found that the iss1(+) gene produces two transcript isoforms, including a long antisense mRNA that is complementary to the meiotic cum1(+) sense transcript, inhibiting cum1(+) expression in vegetative cells. Inhibition of cum1(+) transcription was not at the level of its initiation because fusion of the cum1(+) promoter to the lacZ gene showed that activation of the reporter gene occurs in response to low copper conditions. Further analysis showed that the transcription factor Cuf1 and conserved copper-signaling elements (CuSEs) are required for induction of cum1(+)-lacZ transcription under copper deficiency. Insertion of a multipartite polyadenylation signal immediately downstream of iss1(+) led to the exclusive production of a shorter iss1(+) mRNA isoform, thereby allowing accumulation of cum1(+) sense mRNA in copper-limited vegetative cells. This finding suggested that the long iss1(+) antisense mRNA could pair with cum1(+) sense mRNA, thereby producing double-stranded RNA molecules that could induce RNAi. We consistently found that mutant strains for RNAi (dcr1Δ, ago1Δ, rdp1Δ, and clr4Δ) are defective in selectively eliminating cum1(+) sense transcript in the G1 phase of the cell cycle. Taken together, these results describe the first example of a copper-regulated meiotic gene repressed by an antisense transcription mechanism in vegetative cells.
由同向基因对产生的正义和反义转录本可能会干扰任何一个伙伴基因的表达。在粟酒裂殖酵母中,我们发现iss1(+)基因产生两种转录本异构体,包括一种长反义mRNA,它与减数分裂期的cum1(+)正义转录本互补,在营养细胞中抑制cum1(+)的表达。cum1(+)转录的抑制并非发生在其起始水平,因为cum1(+)启动子与lacZ基因的融合表明,报告基因的激活是对低铜条件的响应。进一步分析表明,转录因子Cuf1和保守的铜信号元件(CuSEs)是铜缺乏时诱导cum1(+)-lacZ转录所必需的。在iss1(+)下游紧邻插入一个多聚腺苷酸化信号,导致只产生较短的iss1(+) mRNA异构体,从而使cum1(+)正义mRNA在铜限制的营养细胞中积累。这一发现表明,长iss1(+)反义mRNA可以与cum1(+)正义mRNA配对,从而产生可诱导RNA干扰的双链RNA分子。我们一致发现,RNA干扰的突变菌株(dcr1Δ、ago1Δ、rdp1Δ和clr4Δ)在细胞周期的G1期选择性消除cum1(+)正义转录本方面存在缺陷。综上所述,这些结果描述了营养细胞中一个通过反义转录机制被铜调节的减数分裂基因的首个例子。