Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata

Victoria A. Sleight; Lloyd S. Peck; Elisabeth A. Dyrynda; Valerie J. Smith; Melody S. Clark

doi:10.1007/s12192-018-0910-5

Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata

Victoria A. Sleight^* (Corresponding Author), Lloyd S. Peck, Elisabeth A. Dyrynda, Valerie J. Smith, Melody S. Clark

^*Corresponding author for this work

Aberdeen Centre For Environmental Sustainability

Research output: Contribution to journal › Article › peer-review

18 Citations (Scopus)

6 Downloads (Pure)

Abstract

Acclimation, via phenotypic flexibility, is a potential means for a fast response to climate change. Understanding the molecular mechanisms underpinning phenotypic flexibility can provide a fine-scale cellular understanding of how organisms acclimate. In the last 30 years, Mya truncata populations around the UK have faced an average increase in sea surface temperature of 0.7 °C
and further warming of between 1.5 and 4 °C, in all marine regions adjacent to the UK, is predicted by the end of the century. Hence, data are required on the ability of M. truncata to acclimate to physiological stresses, and most notably, chronic increases in temperature. Animals in the present study were exposed to chronic heat-stress for 2 months prior to shell damage and subsequently, only 3, out of 20 damaged individuals, were able to repair their shells within 2 weeks. Differentially expressed genes (between control and damaged animals) were functionally enriched with processes relating to cellular stress, the immune
response and biomineralisation. Comparative transcriptomics highlighted genes, and more broadly molecular mechanisms, that are likely to be pivotal in this lack of acclimation. This study demonstrates that discovery-led transcriptomic profiling of animals during stress-response experiments can shed light on the complexity of biological processes and changes within organisms that
can be more difficult to detect at higher levels of biological organisation.

Original language	English
Pages (from-to)	1003-1017
Number of pages	15
Journal	Cell Stress & Chaperones
Volume	23
Early online date	12 May 2018
DOIs	https://doi.org/10.1007/s12192-018-0910-5
Publication status	Published - Sept 2018

Bibliographical note

Acknowledgements
VAS was funded by a NERC DTG studentship (Project Reference: NE/J500173/1) to the British Antarctic Survey. MSC and LSP were financed by NERC core funding to the British Antarctic Survey. We would like to thank Elizabeth M. Harper for advice on M. truncata distributions, shell structure and repair processes; the dive team, and many associated helpers, at the NERC National Facility for
Scientific Diving at Oban for animal collection; both Andrew Mogg and Kim Last at the Scottish Association of Marine Sciences for kindly overseeing animal husbandry during animal holding and acclimation.

Keywords

mollusc
bivalve
transcriptomics
reactive oxygen species
immunology
biomineralisation
Heat shock proteins

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Final published version, 3.32 MBLicence: CC BY

Cite this

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title = "Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata",

abstract = "Acclimation, via phenotypic flexibility, is a potential means for a fast response to climate change. Understanding the molecular mechanisms underpinning phenotypic flexibility can provide a fine-scale cellular understanding of how organisms acclimate. In the last 30 years, Mya truncata populations around the UK have faced an average increase in sea surface temperature of 0.7 °Cand further warming of between 1.5 and 4 °C, in all marine regions adjacent to the UK, is predicted by the end of the century. Hence, data are required on the ability of M. truncata to acclimate to physiological stresses, and most notably, chronic increases in temperature. Animals in the present study were exposed to chronic heat-stress for 2 months prior to shell damage and subsequently, only 3, out of 20 damaged individuals, were able to repair their shells within 2 weeks. Differentially expressed genes (between control and damaged animals) were functionally enriched with processes relating to cellular stress, the immuneresponse and biomineralisation. Comparative transcriptomics highlighted genes, and more broadly molecular mechanisms, that are likely to be pivotal in this lack of acclimation. This study demonstrates that discovery-led transcriptomic profiling of animals during stress-response experiments can shed light on the complexity of biological processes and changes within organisms thatcan be more difficult to detect at higher levels of biological organisation.",

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note = "Acknowledgements VAS was funded by a NERC DTG studentship (Project Reference: NE/J500173/1) to the British Antarctic Survey. MSC and LSP were financed by NERC core funding to the British Antarctic Survey. We would like to thank Elizabeth M. Harper for advice on M. truncata distributions, shell structure and repair processes; the dive team, and many associated helpers, at the NERC National Facility for Scientific Diving at Oban for animal collection; both Andrew Mogg and Kim Last at the Scottish Association of Marine Sciences for kindly overseeing animal husbandry during animal holding and acclimation.",

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N2 - Acclimation, via phenotypic flexibility, is a potential means for a fast response to climate change. Understanding the molecular mechanisms underpinning phenotypic flexibility can provide a fine-scale cellular understanding of how organisms acclimate. In the last 30 years, Mya truncata populations around the UK have faced an average increase in sea surface temperature of 0.7 °Cand further warming of between 1.5 and 4 °C, in all marine regions adjacent to the UK, is predicted by the end of the century. Hence, data are required on the ability of M. truncata to acclimate to physiological stresses, and most notably, chronic increases in temperature. Animals in the present study were exposed to chronic heat-stress for 2 months prior to shell damage and subsequently, only 3, out of 20 damaged individuals, were able to repair their shells within 2 weeks. Differentially expressed genes (between control and damaged animals) were functionally enriched with processes relating to cellular stress, the immuneresponse and biomineralisation. Comparative transcriptomics highlighted genes, and more broadly molecular mechanisms, that are likely to be pivotal in this lack of acclimation. This study demonstrates that discovery-led transcriptomic profiling of animals during stress-response experiments can shed light on the complexity of biological processes and changes within organisms thatcan be more difficult to detect at higher levels of biological organisation.

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Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata

Abstract

Bibliographical note

Keywords

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Victoria Sleight

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Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata

Abstract

Bibliographical note

Keywords

UN SDGs

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Victoria Sleight

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