Abstract：
We previously found that overexpression of phosphate starvation-responsive genes by disrupting PHO80 led to a shortened replicative lifespan in yeast. To identify lifespan-related genes, we screened upregulated genes in the pho80Δ mutant and focused on the VTC genes, which encode the vacuolar polyphosphate (polyP) polymerase complex. VTC1/VTC2/VTC4 deletion restored the lifespan and intracellular polyP levels in pho80Δ. In the wild type, overexpression of VTC5 or a combination of the other VTCs caused high polyP accumulation and shortened lifespan. Similar phenotypes were caused by the deletion of polyP phosphatase genes-vacuolar PPN1 and cytosolic PPX1. The polyP-accumulating strains exhibited stress sensitivities. Thus, we demonstrated that polyP metabolic enzymes participate in replicative lifespan, and extreme polyP accumulation shortens the lifespan.
摘要：
我们先前发现，通过破坏PHO80过度表达磷酸盐饥饿反应基因会导致酵母中复制寿命缩短。为了识别与寿命相关的基因，我们在pho80Δ突变体中筛选了上调的基因，并专注于VTC基因，其编码液泡多磷酸盐(polyP)聚合酶复合物。VTC1/VTC2/VTC4缺失恢复了pho80Δ的寿命和细胞内polyP水平。在野生型中,VTC5的过表达或其他VTC的组合导致高polyP积累和寿命缩短。类似的表型是由polyP磷酸酶基因-液泡PPN1和胞质PPX1的缺失引起的。聚磷菌株表现出应激敏感性。因此，我们证明了polyP代谢酶参与复制寿命，极端的聚磷积累缩短了寿命。
