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.

中文翻译：

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紫外线通过秀丽隐杆线虫中的MOM-4和JKK-1激活PMK-1 / p38 MAPK信号传导。

P38丝裂原活化蛋白激酶（p38 MAPK）在先天免疫中起重要作用，并被紫外线（UV）激活。但是，紫外线应力的分子机制仍不清楚。在这项研究中，我们报道了秀丽隐杆线虫中的紫外线通过JKK-1和MOM-4激活了PMK-1 / p38 MAPK信号传导。在秀丽隐杆线虫中，不同的紫外线辐射剂量导致PMK-1磷酸化。但是，与野生型蠕虫相比，pmk-1突变体未能表现出对紫外线响应的存活时间改变。进一步的分析表明，JKK-1（而不是SEK-1突变体）在紫外线照射后显示出受损的PMK-1活化，表明JKK-1是秀丽隐杆线虫中PMK-1活化的上游MAP2K 。在紫外线刺激下。UV诱导的PMK-1激活在MOM-4中显着降低，但在NSY-1和DLK-1突变蠕虫中却没有显着降低，这表明MOM-4是PMK-1激活响应于UV胁迫的上游MAP3K调节剂。秀丽隐杆线虫。此外，daf-16突变体在紫外线胁迫下显示出较短的寿命，但在daf-16和age-1突变体蠕虫中，紫外线诱导的PMK-1活化并未显着降低。我们的结果揭示了响应线虫紫外线辐射线虫中PMK-1激活的信号通路。