Thermal range and physiological tolerance mechanisms in two shark species from the northwest Atlantic

• Published in: The Biological Bulletin
• Main Authors: Bockus, Abigail B, Labreck, Christopher J., Camberg, Jodi L., Collie, Jeremy S., Seibel, Brad A.
• Format: Text
• Language: unknown
• Published: DigitalCommons@URI 2020
• Subjects: Northwest Atlantic; spiny dogfish; Squalus acanthias
• Online Access: https://digitalcommons.uri.edu/cmb_facpubs/181; https://doi.org/10.1086/708718

Spiny dogfish (Squalus acanthias) and smoothhound (Mustelus canis) sharks in the northwestAtlantic undergo seasonal migrations driven by changes in water temperature. However, the recognized thermal habitats of these regional populations are poorly described. Here, we report the thermal range, catch frequency with bottom temperature, and catch frequency with time of year for both shark species in Narragansett Bay, Rhode Island. Additionally, we describe levels of two thermal stress response indicators, heat-shock protein 70 and trimethylamine N-oxide, with an experimental increase in water temperature from 15 7C to 21 7C. Our results show that S. acanthias can be found in this region year-round and co-occurs with M. canis from June to November. Further, adult S. acanthias routinely inhabits colder waters than M. canis (highest catch frequencies at bottom temperatures of 10 7C and 21 7C, respectively), but both exhibit similar upper thermal ranges in this region (bottom temperatures of 22-23 7C). Additionally, acute exposure to a 6 7C increase in water temperature for 72 hours leads to a nearly threefold increase in heat-shock protein 70 levels in S. acanthias but not M. canis. Therefore, these species display differences in their thermal tolerance and stress response with experimental exposure to 21 7C, a common summer temperature in Narragansett Bay. Further, in temperature-stressed S. acanthias there is no accumulation of trimethylamine N-oxide. At the whole-organism level, elasmobranchs’ trimethylamine N-oxide regulatory capacity may be limited by other factors. Alternatively, elasmobranchs may not rely on trimethylamine N-oxide as a primary thermal protective mechanism under the conditions tested. Findings from this study are in contrast with previous research conducted with elasmobranch cells in vitro that showed accumulation of trimethylamine N-oxide after thermal stress and subsequent suppression of the heat-shock protein 70 response.