論文

査読有り 国際誌
2020年9月

Interaction between the ins/IGF-1 and p38 MAPK signaling pathways in molecular compensation of sod genes and modulation related to intracellular ROS levels in C. elegans.

Biochemistry and biophysics reports
  • Sumino Yanase
  • ,
  • Kayo Yasuda
  • ,
  • Naoaki Ishii

23
開始ページ
100796
終了ページ
100796
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrep.2020.100796

Superoxide dismutases, which catalytically remove intracellular superoxide radicals by the disproportionation of molecular oxygen and hydrogen peroxide, are encoded by the sod-1 to -5 genes in the nematode C. elegans. Expression of the sod genes is mutually compensatory for the modulation of intracellular oxidative stress during aging. Interestingly, several-fold higher expression of the sod-1 to -4 was induced in a sod-5 deletion mutant, despite the low expression levels of sod-5 in wild-type animals. Consequently, this molecular compensation facilitated recovery of lifespan in the sod-5 mutant. In previous reports, two transcription factors DAF-16 and SKN-1 are associated with the compensatory expression of sod genes, which are downstream targets of the ins/IGF-1 and p38 MAPK signaling pathways activated under oxidative and heavy metal stresses, respectively. Here, we show that p38 MAPK signaling regulates induction of not only the direct expression of sod-1, -2 and -4 but also the indirect modulation of DAF-16 targets, such as sod-3 and -5 genes. Moreover, a SKN-1 target, the insulin peptide gene ins-5, partially mediates the expression of DAF-16 targets via p38 MAPK signaling. These findings suggest that the interaction of ins/IGF-1 and p38 MAPK signaling pathways plays an important role in the fine-tuning of molecular compensation among sod genes to protect against mitochondrial oxidative damage during aging.

リンク情報
DOI
https://doi.org/10.1016/j.bbrep.2020.100796
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32875124
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7451853

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