Cold stress upregulates the expression of heat shock and Frost genes, but the evolution of cold stress resistance is apparently not mediated through either heat shock or Frost genes in the cold stress selected populations of Drosophila melanogaster
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Cold stress upregulates heat shock and Frost gene expression, but cold resistance evolution in selected fly populations is not mediated by these genes.
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Abstract
The ability to thermal adaptation can alter insects’ reproductive traits and physiologic response. A number of studies in Drosophila documented the higher expression levels of heat shock proteins ( Hsps ) and Frost ( Fst ) genes during the recovery phase of cold shock treatment and suggested that higher expression levels of these genes and lipids can protect from cold stress. However, these genes’ expression and cold adaptation have not been well studied. Therefore, understanding the molecular and biochemical basis of cold adaptation, we examined the levels of lipid and expression patterns of Hsp22, Hsp23, Hsp40, Hsp68, Hsp70, Hsp 83 , and Fst genes under the cold stress or benign condition in the populations of Drosophila melanogaster selected for increased resistance to cold shock. We observed the significant up-regulation of Hsp22, Hsp23, Hsp40, Hsp68 , and Fst genes in the FSB and FCB populations during the recovery phase post cold shock compared to the no shock condition. However, there was not a significant change in the transcript levels of these genes between FSB and FCB under both the cold stress or no shock condition. Additionally, we noticed higher total lipid levels in the females from cold shock treatment than those from no shock treatment. This finding suggests that cold selected populations have different mechanisms to sustain cold stress.
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License: CC-BY-NC-ND-4.0