Hall Julie A, McElwee Matthew K, Freedman Jonathan H
Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America.
Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America.
PLoS One. 2017 Jun 20;12(6):e0177432. doi: 10.1371/journal.pone.0177432. eCollection 2017.
It has been proposed that aging results from the lifelong accumulation of intracellular damage via reactions with reactive oxygen species (ROS). Metallothioneins are conserved cysteine-rich proteins that function as efficient ROS scavengers and may affect longevity. To better understand mechanisms controlling metallothionein expression, the regulatory factors and pathways that controlled cadmium-inducible transcription of the C. elegans metallothionein gene, mtl-1, were identified. The transcription factor ATF-7 was identified in both ethylmethanesulfonate mutagenesis and candidate gene screens. PMK-1 and members of the insulin signaling pathway, PDK-1 and AKT-1/2, were also identified as mtl-1 regulators. Genetic and previous results support a model for the regulation of cadmium-inducible mtl-1 transcription based on the derepression of the constitutively active transcription factor ELT-2. In addition, knockdown of the mammalian homologs of PDK1 and ATF7 in HEK293 cells resulted in changes in metallothionein expression, suggesting that this pathway was evolutionarily conserved. The insulin signaling pathway is known to influence the aging process; however, various factors responsible for affecting the aging phenotype are unknown. Identification of portions of the insulin signaling pathway as regulators of metallothionein expression supports the hypothesis that longevity is affected by the expression of this efficient ROS scavenger.
有人提出,衰老是由于细胞内通过与活性氧(ROS)反应而造成的终身损伤积累所致。金属硫蛋白是保守的富含半胱氨酸的蛋白质,其功能是高效的ROS清除剂,可能影响寿命。为了更好地理解控制金属硫蛋白表达的机制,确定了控制秀丽隐杆线虫金属硫蛋白基因mtl-1镉诱导转录的调控因子和途径。在甲磺酸乙酯诱变和候选基因筛选中均鉴定出转录因子ATF-7。PMK-1以及胰岛素信号通路成员PDK-1和AKT-1/2也被鉴定为mtl-1的调节因子。遗传学和先前的研究结果支持一个基于组成型活性转录因子ELT-2去抑制作用的镉诱导mtl-1转录调控模型。此外,在HEK293细胞中敲低PDK1和ATF7的哺乳动物同源物导致金属硫蛋白表达发生变化,这表明该途径在进化上是保守的。已知胰岛素信号通路会影响衰老过程;然而,影响衰老表型的各种因素尚不清楚。将胰岛素信号通路的部分鉴定为金属硫蛋白表达的调节因子,支持了寿命受这种高效ROS清除剂表达影响的假说。