The effect of thermal stress on whole-body metabolic rate and cellular stress response in the truncate softshell clam, Mya truncata

dc.contributor.authorMiller, Linh
dc.contributor.examiningcommitteeDetwiler, Jillian (Biological Sciences)
dc.contributor.examiningcommitteeNiemi, Andrea (Fisheries and Ocean Canada)
dc.contributor.supervisorAnderson, Gary
dc.date.accessioned2024-09-04T16:36:50Z
dc.date.available2024-09-04T16:36:50Z
dc.date.issued2024-07-29
dc.date.submitted2024-08-15T16:04:41Zen_US
dc.date.submitted2024-08-31T02:54:42Zen_US
dc.date.submitted2024-09-04T05:04:15Zen_US
dc.degree.disciplineBiological Sciences
dc.degree.levelMaster of Science (M.Sc.)
dc.description.abstractRising global temperatures associated with climate change have led to various responses and consequences across aquatic ectotherms. At the whole-body level, temperature governs all physiological and biochemical processes, and an increase in temperature is normally positively correlated to the aerobic respiration rate of an organism. However, at a critical sub-lethal temperature (Tcrit), most organisms are unable to supply sufficient oxygen to meet demand of the tissues, leading to a reliance on anaerobic metabolism. At the cellular level, the heat shock response (HSR) is a primary mechanism driving differences in thermal tolerances of ectotherms through the induction of heat shock proteins (HSPs). At a species-specific onset temperature (Ton) when the HSR is activated, there is increased production of HSPs that is positively correlated with temperature but will reach a maximum capacity (Tpeak). Thus, Tpeak for HSP induction can be one metric used to understand thermal tolerance of a given species. Importantly, the HSR is energetically costly as energy demand increases under a thermal stress event, which leads to a further increase in oxygen consumption. This study aimed to examine the effects of increasing temperature on whole-body metabolic rate and mRNA transcript abundance in truncate softshell clam, Mya truncata. We acutely exposed clams from the Northern (Iqaluit, Nunavut) and Southern (Godbout, Quebec) populations to one of six temperature treatments (10, 13, 16, 19, and 22 ℃, and a control group at 7 ℃) for 2 hours and measured whole-body metabolic rate and transcript abundance of key molecular markers of the HSR. Our findings indicated temperature influenced both oxygen consumption and the transcript abundance of thermal stress-related genes. Although there was no statistical significance, a noticeable trend of increasing oxygen consumption with rising temperatures was observed. The impact of temperature on the HSR was clearly reflected in alterations in the transcript levels of hsp60 and hsp90, which are linked to protein protection, along with citrate synthase (cs), a marker of cellular aerobic metabolism. These results suggest that truncate softshell clam may be able to tolerate acute heat stress under climate change scenarios.
dc.description.noteOctober 2024
dc.description.sponsorshipUniversity of Manitoba Graduate Fellowship The Resilience Results Fund project, “Arctic Marine Ecosystem Resilience and Resistance to Environmental Changes” NSERC Discovery Grant, Fisheries and Oceans Cana-da Ecosystems and Oceans Science Contribution Framework fund University of Manitoba Field Work Support Program Grants
dc.identifier.urihttp://hdl.handle.net/1993/38501
dc.language.isoeng
dc.subjectMya truncata
dc.subjectThermal stress
dc.subjectCellular stress response
dc.subjectWhole-body metabolic rate
dc.titleThe effect of thermal stress on whole-body metabolic rate and cellular stress response in the truncate softshell clam, Mya truncata
local.subject.manitobano
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