Abstract
Temperature is one of the most prevalent environmental factors that affects the growth and development of organisms. The survival of aquatic animals is closely related to the changes in temperature, low temperature could cause physiological damage even death. In this study, we revealed the regulatory mechanisms of low-temperature stimulation from the transcriptomics in the hepatopancreas of the red swamp crayfish, Procambarus clarkii. Transcriptome sequencing revealed that lipid metabolism pathways were significantly enriched at low temperature. Crayfish improved their cold tolerance by increasing expression levels of thermogenic gene prdm16 and uncoupling protein genes ucp4 and ucp5. Furthermore, lipid and triglyceride content increased significantly in cold-sensitive crayfish, which in turn increased the expression levels of proinflammatory factors (cox2 and tgfβr) and the amount of hepatopancreas bacteria. In addition, low-temperature stimulation could cause more severe damage to cold-sensitive crayfish spermatophores, accompanied by downregulated of spermatozoa viability-related genes such as alp and ldh. Estradiol 17β-dehydrogenase 8-like (17βde8) may contain a critical SNP site at exon 544, the bases of this site were “G” in cold-tolerant crayfish and “A” in cold-sensitive crayfish. Above all, our results reveal that lipid metabolism is the main factor affecting cold tolerance in crayfish and reveal the key loci for cold tolerance, providing a reference for cold tolerance breeding.
Published Version
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