RESEARCH ARTICLE Open Access Molecular pathology of vertebral deformities in hyperthermic Atlantic salmon (Salmo salar)

Background: Hyperthermia has been shown in a number of organisms to induce developmental defects as a result of changes in cell proliferation, differentiation and gene expression. In spite of this, salmon aquaculture commonly uses high water temperature to speed up developmental rate in intensive pr...

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Main Authors: Elisabeth Ytteborg, Grete Baeverfjord, Jacob Torgersen, Kirsti Hjelde, Harald Takle
Other Authors: The Pennsylvania State University CiteSeerX Archives
Format: Text
Language:English
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Online Access:http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.319.5650
http://www.biomedcentral.com/content/pdf/1472-6793-10-12.pdf
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Summary:Background: Hyperthermia has been shown in a number of organisms to induce developmental defects as a result of changes in cell proliferation, differentiation and gene expression. In spite of this, salmon aquaculture commonly uses high water temperature to speed up developmental rate in intensive production systems, resulting in an increased frequency of skeletal deformities. In order to study the molecular pathology of vertebral deformities, Atlantic salmon was subjected to hyperthermic conditions from fertilization until after the juvenile stage. Results: Fish exposed to the high temperature regime showed a markedly higher growth rate and a significant higher percentage of deformities in the spinal column than fish reared at low temperatures. By analyzing phenotypically normal spinal columns from the two temperature regimes, we found that the increased risk of developing vertebral deformities was linked to an altered gene transcription. In particular, down-regulation of extracellular matrix (ECM) genes such as col1a1, osteocalcin, osteonectin and decorin, indicated that maturation and mineralization of osteoblasts were restrained. Moreover, histological staining and in situ hybridization visualized areas with distorted chondrocytes and an increased population of hypertrophic cells. These findings were further confirmed by an up-regulation of mef2c and col10a, genes involved in chondrocyte hypertrophy.