Abstract
The red-eared slider (Trachemys scripta elegans), identified as one of the 100 most invasive species in the world, is a freshwater turtle originally from the eastern United States and northeastern Mexico. Field investigations have shown that T. s. elegans can survive and lay eggs in saline habitats. In order to understand the molecular mechanisms of salinity adaptation, high-throughput RNA-Seq was utilized to identify the changes in gene expression profiles in the liver of T. s. elegans in response to elevated salinity. We exposed individuals to 0, 5, or 15 psu (practical salinity units) for 30 days. A total of 157.21 million reads were obtained and assembled into 205138 unigenes with an average length of 620 bp and N50 of 964 bp. Of these, 1019 DEGs (differentially expressed genes) were found in the comparison of 0 vs. 5 psu, 1194 DEGs in 0 vs. 15 psu and 1180 DEGs in 5 vs. 15 psu, which are mainly related to macromolecule metabolic process, ion transport, oxidoreductase activity and generation of precursor metabolites and energy by GO (Gene Ontology) enrichment analyses. T. s. elegans can adapt itself into salinity by balancing the entry of sodium and chloride ions via the up-regulation expression genes of ion transport (potassium voltage-gated channel subfamily H member 5, KCNH5; erine/threonine-protein kinase 32, STK32; salt-inducible kinase 1, SIK1; adiponectin, ACDC), and by accumulating plasma urea and free amino acid via the up-regulation expression genes of amino acid metabolism (ornithine decarboxylase antizyme 3, OAZ3; glutamine synthetase, GLUL; asparaginase-like protein 1b, ASRGL; L-amino-acid oxidase-like, LAAO; sodium-dependent neutral amino acid transporter B, SLC6A15s; amino acid permease, SLC7A9) in response to osmotic regulation. An investment of energy to maintain their homeostatic balance is required to salinity adaptation, therefore, the genes related to energy production and conversion (F-ATPase protein 6, ATP6; cytochrome c oxidase subunit I, COX1; cytochrome c oxidase subunit III, COX3; cytochrome b, CYTb; cytochrome P450 17A1, CYP17A1) were up-regulated with the increase of gene expression associated with lipid metabolism (apolipoprotein E precursor, APoE; coenzyme Q-binding protein, CoQ10; high-density lipoprotein particle, SAA) and carbohydrate metabolism (HK, MIP). These findings improve our understanding of the underlying molecular mechanisms involved in salinity adaptation and provide general guidance to illuminate the invasion potential of T. s. elegans into saline environments.
Highlights
The red-eared slider (Trachemys scripta elegans) has been introduced into diverse aquatic habitats worldwide via the pet-release pathway and, as a result, is classified as a highly invasive species by the International Union for Conservation of Nature (Luiselli et al, 1997; Martins, Assalim & Molina, 2014)
Because we haven’t got the genome of T. s. elegans yet, a transcriptome was used as a reference to identify the differentially expressed genes induced by salinity exposure
We report the first transcriptome analysis of T. s. elegans under salinity stress
Summary
The red-eared slider (Trachemys scripta elegans) has been introduced into diverse aquatic habitats worldwide (including many countries in Africa, Asia and Europe as well as Australia) via the pet-release pathway and, as a result, is classified as a highly invasive species by the International Union for Conservation of Nature (Luiselli et al, 1997; Martins, Assalim & Molina, 2014). It is native to freshwater habitats in 19 states of the eastern United States and two states of northeastern Mexico (Mittermeier et al, 2015) These turtles have been found to lay eggs in the low salinity (0.1–26 ) estuary of the Nandujiang in Hainan Province, China (Liu et al, 2011; Yang & Shi, 2014). Elegans in the Lake Pontchartrain Basin of Louisiana suggest that these turtles may serve as a sentinel species for elevated salinity in environments where salinity is rising due to saltwater intrusion (Thompson, Franck & Valverde, 2011). The invasion potential and the mechanism of response to salinity adaptation of T. s. elegans is of serious concern
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