The freshwater red-eared slider (Trachemys scripta elegans) is found not only in freshwater but also in coastal saline habitats. Hyperosmotic salinity can induce cell damage. p53, regarded as the guardian of the genome, is very important and versatile in response to the change of environment. In this study, the role of p53 in T. s. elegans under environmental salinity change will be explored. The results indicated that amino acid sequence of p53 showed high similarity to p53 of other species. In addition, the expression of p53 showed differences in various tissues under normal condition. Under salinity stress, the mRNA levels of p53 in the liver increased significantly at 48 h with 15‰ group (15 practical salinity units-exposed group). In the heart, p53 mRNA levels increased at 6 h in 5‰ (5 practical salinity units) and 15‰ groups. Furthermore, the changes of p21 mRNA expression levels in liver and heart were similar to p53, while cyclin D1, cyclin-dependent kinase4 (CDK4) and cyclin-dependent kinase6 (CDK6) showed opposite changes to p53. Moreover, Bax and caspase 3 mRNA expression levels were similar to p53, respectively, while Bcl-2 showed opposite changes. The positive cells of apoptosis were found in the liver of 15‰ at 48 h and 30 d of chronic stress. Taken together, these results indicated that the T. s. elegans may protect itself by regulating cell cycle progression and apoptosis of damaged cells under salinity stress, which played an important role for T. s. elegans in salinity adaptation.

Additional Metadata
Keywords Apoptosis, Biological invasive, Cell cycle arrest, Gene cloning, Gene expression, Salinity adaptation
Persistent URL dx.doi.org/10.1016/j.cbpc.2019.03.011
Journal Comparative Biochemistry and Physiology - C Toxicology and Pharmacology
Citation
Li, W. (Weihao), Li, N. (Na), Liang, L. (Lingyue), Yu, Q. (Qifan), Ren, P. (Peng), Shi, H. (Haitao), … Ding, L. (Li). (2019). Regulation of p53 in the red-eared slider (Trachemys scripta elegans) in response to salinity stress. Comparative Biochemistry and Physiology - C Toxicology and Pharmacology, 221, 49–58. doi:10.1016/j.cbpc.2019.03.011