“…The CSR machinery responds to sodium-destabilized proteins by overexpressing molecular chaperones, such as heat shock proteins (T. G. Evans & Kultz, 2020), two of which were temporarily upregulated in Arabian pupfish at 24 hours, as well as in a hyperosmotic challenged Sacramento splittail population (Mundy et al, 2020). Rising intracellular sodium levels can also cause nucleic acid structural disruptions (T. G. Evans & Kultz, 2020), and consequently, increased expressions of DNA damage related genes are often reported as part of the CSR following hyperosmotic stress in teleosts (Brennan et al, 2015;Su, Ma, Zhu, Liu, & Gao, 2020;Whitehead et al, 2013). In Arabian pupfish several DNA damage related genes were transiently upregulated especially in the first 24 hours of exposure, like serum/glucocorticoid regulated kinase 1 (SGK1), and similarly increased in other fish following acute seawater challenges (T. G. Evans & Somero, 2008;Shaw et al, 2008).…”