Weidner Julie, Wang Congwei, Prescianotto-Baschong Cristina, Estrada Alejandro F, Spang Anne
Growth & Development, Biozentrum, University of Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland.
J Cell Sci. 2014 May 1;127(Pt 9):1992-2004. doi: 10.1242/jcs.142083. Epub 2014 Feb 25.
Numerous mRNAs are degraded in processing bodies (P bodies) in Saccharomyces cerevisiae. In logarithmically growing cells, only 0-1 P bodies per cell are detectable. However, the number and appearance of P bodies change once the cell encounters stress. Here, we show that the polysome-associated mRNA-binding protein Scp160 interacts with P body components, such as the decapping protein Dcp2 and the scaffold protein Pat1, presumably, on polysomes. Loss of either Scp160 or its interaction partner Bfr1 caused the formation of Dcp2-positive structures. These Dcp2-positive foci contained mRNA, because their formation was inhibited by the presence of cycloheximide. In addition, Scp160 was required for proper P body formation because only a subset of bona fide P body components could assemble into the Dcp2-positive foci in Δscp160 cells. In either Δbfr1 or Δscp160 cells, P body formation was uncoupled from translational attenuation as the polysome profile remained unchanged. Collectively, our data suggest that Bfr1 and Scp160 prevent P body formation under normal growth conditions.
酿酒酵母中许多mRNA在加工小体（P小体）中被降解。在对数生长期的细胞中，每个细胞只能检测到0 - 1个P小体。然而，一旦细胞遇到压力，P小体的数量和外观就会发生变化。在这里，我们表明多聚核糖体相关的mRNA结合蛋白Scp160与P小体成分相互作用，例如去帽蛋白Dcp2和支架蛋白Pat1，大概是在多聚核糖体上相互作用。Scp160或其相互作用伴侣Bfr1的缺失导致Dcp2阳性结构的形成。这些Dcp2阳性病灶含有mRNA，因为它们的形成受到环己酰亚胺的抑制。此外，正确形成P小体需要Scp160，因为在Δscp160细胞中，只有一部分真正的P小体成分能够组装成Dcp2阳性病灶。在Δbfr1或Δscp160细胞中，P小体的形成与翻译衰减解偶联，因为多聚核糖体谱保持不变。总体而言，我们的数据表明Bfr1和Scp160在正常生长条件下可防止P小体的形成。
