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

机译:紫外线光通过MOM-4和Caenorhabditis elegans的MOM-4和JKK-1激活PMK-1 / P38 MAPK信号传导

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摘要

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.
机译:P38丝裂原激活的蛋白激酶(P38Mapk)在先天免疫中起重要作用,并通过紫外(UV)辐射激活。然而,紫外线应激的分子机制仍不清楚。在这项研究中,我们报道了紫外线激活的PMK-1 / P38 MAPK信号传导通过JKK-1和Caenorhabditis elegans中的MOM-4。在C.杆状杆菌中,不同的紫外线辐射剂量导致PMK-1磷酸化。然而,与野生型蠕虫相比,PMK-1突变体未能响应紫外线证明存在改变的存活时间。进一步的分析表明,在紫外线辐射后,JKK-1,但不是SEK-1突变体显示出PMK-1激活受损,表明JKK-1是在紫外线刺激下激活PMK-1的上游MAP2K。在MOM-4中显着降低了紫外线诱导的PMK-1的活化,但不在NSY-1和DLK-1突变虫中,表明MOM-4是响应于UV应力的PMK-1激活的上游MAP3K调节器C.秀丽隐形。另外,DAF-16突变体在紫外线应激下显示较短的寿命,但在DAF-16和A年龄-1突变虫中,UV诱导的PMK-1的激活并未显着降低。我们的结果揭示了C.杆状杆菌中的PMK-1活化的信号通路,响应于紫外线辐射。

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