Department of Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Department of Zoology, University of British Columbia, Vancouver, BC, Canada.
Dev Cell. 2018 Jan 8;44(1):42-55.e4. doi: 10.1016/j.devcel.2017.12.007.
Wild-type Drosophila cells can remove cells heterozygous for ribosomal protein mutations (known as "Minute" mutant cells) from genetic mosaics, a process termed cell competition. The ribosomal protein S12 was unusual because cells heterozygous for rpS12 mutations were not competed by wild-type, and a viable missense mutation in rpS12 protected Minute cells from cell competition with wild-type cells. Furthermore, cells with Minute mutations were induced to compete with one another by altering the gene dose of rpS12, eliminating cells with more rpS12 than their neighbors. Thus RpS12 has a special function in cell competition that defines the competitiveness of cells. We propose that cell competition between wild-type and Minute cells is initiated by a signal of ribosomal protein haploinsufficiency mediated by RpS12. Since competition between cells expressing different levels of Myc did not require RpS12, other kinds of cell competition may be initiated differently.
野生型果蝇细胞可以从遗传嵌合体中去除携带核糖体蛋白突变的杂合子细胞(称为“微小”突变细胞),这个过程称为细胞竞争。核糖体蛋白 S12 很特别,因为携带 rpS12 突变的杂合子细胞不会被野生型细胞竞争,而 rpS12 中的一个可行的错义突变可以保护微小细胞免受与野生型细胞的细胞竞争。此外,通过改变 rpS12 的基因剂量,使带有微小突变的细胞相互诱导竞争,从而消除了比其邻居拥有更多 rpS12 的细胞。因此,RpS12 在定义细胞竞争力的细胞竞争中具有特殊功能。我们提出,野生型和微小细胞之间的细胞竞争是由 RpS12 介导的核糖体蛋白单倍不足信号引发的。由于表达不同水平 Myc 的细胞之间的竞争不需要 RpS12,因此其他类型的细胞竞争可能以不同的方式启动。