Li B, Nierras C R, Warner J R
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Mol Cell Biol. 1999 Aug;19(8):5393-404. doi: 10.1128/MCB.19.8.5393.
The ribosomal proteins (RPs) of Saccharomyces cerevisiae are encoded by 137 genes that are among the most transcriptionally active in the genome. These genes are coordinately regulated: a shift up in temperature leads to a rapid, but temporary, decline in RP mRNA levels. A defect in any part of the secretory pathway leads to greatly reduced ribosome synthesis, including the rapid loss of RP mRNA. Here we demonstrate that the loss of RP mRNA is due to the rapid transcriptional silencing of the RP genes, coupled to the naturally short lifetime of their transcripts. The data suggest further that a global inhibition of polymerase II transcription leads to overestimates of the stability of individual mRNAs. The transcription of most RP genes is activated by two Rap1p binding sites, 250 to 400 bp upstream from the initiation of transcription. Rap1p is both an activator and a silencer of transcription. The swapping of promoters between RPL30 and ACT1 or GAL1 demonstrated that the Rap1p binding sites of RPL30 are sufficient to silence the transcription of ACT1 in response to a defect in the secretory pathway. Sir3p and Sir4p, implicated in the Rap1p-mediated repression of silent mating type genes and of telomere-proximal genes, do not influence such silencing of RP genes. Sir2p, implicated in the silencing both of the silent mating type genes and of genes within the ribosomal DNA locus, does not influence the repression of either RP or rRNA genes. Surprisingly, the 180-bp sequence of RPL30 that lies between the Rap1p sites and the transcription initiation site is also sufficient to silence the Gal4p-driven transcription in response to a defect in the secretory pathway, by a mechanism that requires the silencing region of Rap1p. We conclude that for Rap1p to activate the transcription of an RP gene it must bind to upstream sequences; yet for Rap1p to repress the transcription of an RP gene it need not bind to the gene directly. Thus, the cell has evolved a two-pronged approach to effect the rapid extinction of RP synthesis in response to the stress imposed by a heat shock or by a failure of the secretory pathway. Calculations based on recent transcriptome data and on the half-life of the RP mRNAs suggest that in a rapidly growing cell the transcription of RP mRNAs accounts for nearly 50% of the total transcriptional events initiated by RNA polymerase II. Thus, the sudden silencing of the RP genes must have a dramatic effect on the overall transcriptional economy of the cell.
酿酒酵母的核糖体蛋白(RPs)由137个基因编码,这些基因是基因组中转录活性最高的基因之一。这些基因受到协同调控:温度升高会导致RP mRNA水平迅速但暂时下降。分泌途径任何部分的缺陷都会导致核糖体合成大幅减少,包括RP mRNA的快速丢失。在此,我们证明RP mRNA的丢失是由于RP基因的快速转录沉默,以及其转录本天然较短的寿命。数据还表明,对聚合酶II转录的全局抑制会导致对单个mRNA稳定性的高估。大多数RP基因的转录由两个Rap1p结合位点激活,位于转录起始点上游250至400 bp处。Rap1p既是转录激活剂又是转录沉默剂。RPL30与ACT1或GAL1之间启动子的交换表明,RPL30的Rap1p结合位点足以响应分泌途径缺陷而沉默ACT1的转录。参与Rap1p介导的沉默交配型基因和端粒近端基因抑制的Sir3p和Sir4p,并不影响RP基因的这种沉默。参与沉默交配型基因和核糖体DNA位点内基因沉默的Sir2p,不影响RP或rRNA基因的抑制。令人惊讶的是,位于Rap1p位点和转录起始位点之间的180 bp的RPL30序列也足以响应分泌途径缺陷而沉默Gal4p驱动的转录,其机制需要Rap1p的沉默区域。我们得出结论,Rap1p要激活RP基因的转录,它必须结合到上游序列;然而,Rap1p要抑制RP基因的转录,它不必直接结合到该基因。因此,细胞进化出了一种双管齐下的方法,以响应热休克或分泌途径故障所施加的应激,实现RP合成的快速终止。基于最近的转录组数据和RP mRNA半衰期的计算表明,在快速生长的细胞中,RP mRNA的转录占RNA聚合酶II启动的总转录事件的近50%。因此,RP基因的突然沉默必定会对细胞的整体转录经济性产生巨大影响。