4.2 Article

Ultraviolet light activates PMK-1/p38 MAPK signaling via MOM-4 and JKK-1 in Caenorhabditis elegans

Journal

TOXICOLOGY RESEARCH
Volume 9, Issue 4, Pages 461-466

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/toxres/tfaa041

Keywords

C. elegans; ultraviolet; JKK-1; PMK-1; MOM-4

Categories

Funding

  1. National Natural Science Foundation of China [81200044, 81402904]
  2. Science and Technology Commission of Shanghai Municipality [13ZR1426900, 15411963900]
  3. Innovation program of Shanghai Municipal Education Commission [12ZZ117]
  4. Biomedical Engineering Cross-fund of Shanghai Jiaotong University [YG2012MS57]

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P38 mitogen-activated protein kinase (p38 MAPK) plays an important role in innate immunity and is activated by ultraviolet (UV) radiation. However, the molecular mechanism underlying UV stress remains unclear. In this study, we reported that UV activated PMK-1/p38 MAPK signaling via JKK-1 and MOM-4 in Caenorhabditis elegans. In C. elegans, different UV radiation doses resulted in PMK-1 phosphorylation. However, pmk-1 mutants failed to demonstrate an altered survival time in response to UV when compared with wild-type worms. Further analysis showed that JKK-1, but not SEK-1 mutants, displayed impaired PMK-1 activation following UV irradiation, suggesting that JKK-1 is the upstream MAP2K for the activation of PMK-1 in C. elegans under UV stimulation. UV-induced activation of PMK-1 was markedly reduced in MOM-4, but not in NSY-1 and DLK-1 mutant worms, suggesting that MOM-4 is the upstream MAP3K regulator of PMK-1 activation in response to UV stress in C. elegans. Additionally, daf-16 mutants displayed a shorter lifespan under UV stress, but UV-induced activation of PMK-1 was not markedly reduced in daf-16 and age-1 mutant worms. Our results revealed the signaling pathway involved in PMK-1 activation in C. elegans in response to UV radiation.

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