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Autoregulation in the Biosynthesis of Ribosomes

机译：核糖体生物合成中的自动调节

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The synthesis of ribosomes in Saccharomyces cerevisiae consumes a prodigious amount of the cell's resources and, consequently, is tightly regulated. The rate of ribosome synthesis responds not only to nutritional cues but also to signals dependent on other macromolecular pathways of the cell, e.g., a defect in the secretory pathway leads to severe repression of transcription of both rRNA and ribosomal protein genes. A search for mutants that interrupted this repression revealed, surprisingly, that inactivation of RPL1B, one of a pair of genes encoding the 60S ribosomal protein L1, almost completely blocked the repression of rRNA and ribosomal protein gene transcription that usually follows a defect in the secretory pathway. Further experiments showed that almost any mutation leading to a defect in 60S subunit synthesis had the same effect, whereas mutations affecting 40S subunit synthesis did not. Although one might suspect that this effect would be due to a decrease in the initiation of translation or to the presence of half-mers, i.e., polyribosomes awaiting a 60S subunit, our data show that this is not the case. Rather, a variety of experiments suggest that some aspect of the production of defective 60S particles or, more likely, their breakdown suppresses the signal generated by a defect in the secretory pathway that represses ribosome synthesis.
机译：酿酒酵母（Saccharomyces cerevisiae）中的核糖体合成消耗了大量细胞资源，因此受到严格监管。核糖体合成的速率不仅对营养提示有反应，而且对依赖于细胞其他大分子途径的信号也有反应，例如，分泌途径的缺陷导致rRNA和核糖体蛋白基因的转录受到严重抑制。令人惊讶的是，搜索中断这种抑制的突变体后发现， RPL1B 的失活（编码60S核糖体蛋白L1的一对基因之一）几乎完全阻止了rRNA和核糖体蛋白基因转录的抑制。通常跟随分泌途径的缺陷。进一步的实验表明，几乎所有导致60S亚基合成缺陷的突变都具有相同的作用，而影响40S亚基合成的突变则没有。尽管可能会怀疑这种作用是由于翻译起始次数减少或半聚体（即等待60S亚基的多核糖体）的存在所致，但我们的数据表明并非如此。而是，各种实验表明，缺陷60S颗粒产生的某些方面，或更可能是它们的分解，抑制了分泌途径缺陷抑制核糖体合成而产生的信号。

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