Skip to content

Research at St Andrews

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

Research output: Contribution to journalArticle

Standard

Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata. / Sleight, Victoria A.; Peck, Lloyd S.; Dyrynda, Elisabeth A.; Smith, Valerie J.; Clark, Melody S.

In: Cell Stress and Chaperones, Vol. First Online, 12.05.2018.

Research output: Contribution to journalArticle

Harvard

Sleight, VA, Peck, LS, Dyrynda, EA, Smith, VJ & Clark, MS 2018, 'Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata' Cell Stress and Chaperones, vol. First Online. https://doi.org/10.1007/s12192-018-0910-5

APA

Sleight, V. A., Peck, L. S., Dyrynda, E. A., Smith, V. J., & Clark, M. S. (2018). Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata. Cell Stress and Chaperones, First Online. https://doi.org/10.1007/s12192-018-0910-5

Vancouver

Sleight VA, Peck LS, Dyrynda EA, Smith VJ, Clark MS. Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata. Cell Stress and Chaperones. 2018 May 12;First Online. https://doi.org/10.1007/s12192-018-0910-5

Author

Sleight, Victoria A. ; Peck, Lloyd S. ; Dyrynda, Elisabeth A. ; Smith, Valerie J. ; Clark, Melody S. / Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata. In: Cell Stress and Chaperones. 2018 ; Vol. First Online.

Bibtex - Download

@article{76784c1ab93a43de959b84ad2d7ed670,
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 °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.",
keywords = "Mollusc, Bivalve, Transcriptomics, Heat shock proteins, Reactive oxygen species , Immunology, Biomineralisation",
author = "Sleight, {Victoria A.} and Peck, {Lloyd S.} and Dyrynda, {Elisabeth A.} and Smith, {Valerie J.} and Clark, {Melody S.}",
note = "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.",
year = "2018",
month = "5",
day = "12",
doi = "10.1007/s12192-018-0910-5",
language = "English",
volume = "First Online",
journal = "Cell Stress and Chaperones",
issn = "1355-8145",
publisher = "Springer",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Cellular stress responses to chronic heat shock and shell damage in temperate Mya truncata

AU - Sleight, Victoria A.

AU - Peck, Lloyd S.

AU - Dyrynda, Elisabeth A.

AU - Smith, Valerie J.

AU - Clark, Melody S.

N1 - 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.

PY - 2018/5/12

Y1 - 2018/5/12

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 °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.

AB - 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.

KW - Mollusc

KW - Bivalve

KW - Transcriptomics

KW - Heat shock proteins

KW - Reactive oxygen species

KW - Immunology

KW - Biomineralisation

U2 - 10.1007/s12192-018-0910-5

DO - 10.1007/s12192-018-0910-5

M3 - Article

VL - First Online

JO - Cell Stress and Chaperones

T2 - Cell Stress and Chaperones

JF - Cell Stress and Chaperones

SN - 1355-8145

ER -

Related by journal

  1. Theiler's murine encephalomyelitis virus infection induces a redistribution of heat shock proteins 70 and 90 in BHK-21 cells, and is inhibited by novobiocin and geldanamycin

    Mutsvunguma, L. Z., Moetlhoa, B., Edkins, A. L., Luke, G. A., Blatch, G. L. & Knox, C., Sep 2011, In : Cell Stress and Chaperones. 16, 5, p. 505-515 11 p.

    Research output: Contribution to journalArticle

  2. Hsp30, the integral plasma membrane heat shock protein of Saccharomyces cerevisiae, is a stress-inducible regulator of plasma membrane H+-ATPase.

    Piper, P., Ortiz-Calderon, C., Holyoak, C., Coote, P. J. & Cole, M., Mar 1997, In : Cell Stress and Chaperones. 2, 1, p. 12-24 13 p.

    Research output: Contribution to journalArticle

ID: 253159402