Department of Pathology, Stanford University Medical School, Stanford, CA, USA; Department of Molecular Biosciences, University of Texas Austin, Austin, TX, USA.
Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, San Diego, CA, USA.
Dev Cell. 2019 Mar 25;48(6):811-826.e6. doi: 10.1016/j.devcel.2019.01.019. Epub 2019 Feb 21.
Caenorhabditis elegans provides an amenable system to explore whether newly composed ribosomes are required to progress through development. Despite the complex pattern of tissues that are formed during embryonic development, we found that null homozygotes lacking any of the five different ribosomal proteins (RPs) can produce fully functional first-stage larvae, with similar developmental competence seen upon complete deletion of the multi-copy ribosomal RNA locus. These animals, relying on maternal but not zygotic contribution of ribosomal components, are capable of completing embryogenesis. In the absence of new ribosomal components, the resulting animals are arrested before progression from the first larval stage and fail in two assays for postembryonic plasticity of neuronal structure. Mosaic analyses of larvae that are a mixture of ribosome-competent and non-competent cells suggest a global regulatory mechanism in which ribosomal insufficiency in a subset of cells triggers organism-wide growth arrest.
秀丽隐杆线虫为研究新合成的核糖体是否是发育所必需的提供了一个合适的系统。尽管胚胎发育过程中形成的组织模式复杂，但我们发现，缺乏五种不同核糖体蛋白（RP）的纯合缺失突变体可以产生完全功能的第一期幼虫，并且在完全缺失多拷贝核糖体 RNA 基因座的情况下，也能看到相似的发育能力。这些动物依赖于母源而不是合子的核糖体成分，能够完成胚胎发生。在没有新的核糖体成分的情况下，产生的动物在从第一期幼虫阶段向前推进之前就被阻止，并且在两个用于检测神经元结构后生可塑性的实验中失败。对由核糖体功能正常和功能不正常的细胞组成的嵌合体幼虫进行的嵌合分析表明，存在一种全局调控机制，其中细胞亚群中的核糖体不足会引发整个生物体的生长停滞。
