The role of tumor suppressor protein p53 in the mud crab (Scylla paramamosain) after Vibrio parahaemolyticus infection
文献类型： 外文期刊
作者： Cheng, Chang-Hong 1 ; Ma, Hai-Tao 2 ; Ma, Hong-Ling 1 ; Liu, Guang-Xin 1 ; Deng, Yi-Qin 1 ; Feng, Juan 1 ; Wang, Li-Ca 1 ;
作者机构： 1.Chinese Acad Fishery Sci, South China Sea Fisheries Res Inst, Key Lab South China Sea Fishery Resources Exploit, Minist Agr & Rural Affairs, Guangzhou 510300, Guangdong, Peoples R China
2.Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, Guangzhou 510301, Peoples R China
关键词： P53; Scylla paramamosain; Vibrio parahaemolyticus; DNA damage
期刊名称：COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY （ 影响因子：3.228； 五年影响因子：3.289 ）
ISSN： 1532-0456
年卷期： 2021 年 246 卷
页码：
收录情况： SCI
摘要： The tumor suppressor protein p53 plays important roles in DNA repair, cell cycle and genetic stability. In the present study, a p53 gene in the mud crab (Scylla paramamosain) (designated as Sp-53) was identified and characterized. The open reading frame of Sp-53 was comprised a 1383 bp, which encoded a putative protein of 460 amino acids. Sp-53 is expressed in all examined tissues, with the highest expression in hepatopancreas and hemocytes. Vibrio parahaemolyticus infection induced oxidative stress, and led to DNA damage. The Sp-53 transcriptions in hepatopancreas were significantly up-regulated after V. parahaemolyticus infection. RNA interference (RNAi) experiment was used to understand the roles of Sp-53 in response to V. parahaemolyticus infection. Knocking down Sp-53 in vivo significantly reduced the expression of the Mn-SOD, Gpx3 and caspase 3 after V. parahaemolyticus infection. Moreover, the mortality of mud crabs and DNA damage in Sp-53-silenced mud crab challenged with V. parahaemolyticus were significantly higher than those in the control group. All these results suggested that Sp-53 played an important role in responses to V. parahaemolyticus infection through its participation in regulation of antioxidant defense, DNA repair and apoptosis.
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