Genome-wide analysis of transcriptional changes in the thoracic muscle of the migratory locust, Locusta migratoria, exposed to hypobaric hypoxia

Hypobaric hypoxia has both beneficial and detrimental effects on living organisms in high altitude regions. The impact of hypobaric hypoxia has been investigated in numerous vertebrates. However, it is still not well characterized how invertebrates respond to hypobaric hypoxia. In this study, we examined the transcriptional profiles of locust thoracic muscles using microarrays to disclose their strategies to cope with hypobaric hypoxia. We found that hypoxia-inducible factor (HIF) and its target genes did not respond significantly to hypobaric hypoxia. As with severe, normobaric hypoxia, mitochondrial activities were systemically suppressed, mainly involving in energy production and mitochondrial biogenesis. The surveillance processes, involving in clearance of dysfunctional proteins in endoplasmic reticulum, were activated, e.g. endoplasmic reticulum-associated degradation, protein glycosylation, and protein folding. In contrast to severe, normobaric hypoxia, glycolysis was suppressed and the pentose phosphate pathway strengthened. Our data suggested that hypobaric hypoxia induced an oxidative stress rather than an energy crisis in locust thoracic muscles. Our research provides a different perspective of biological responses to hypoxia, complementing the well-studied biological responses to extreme, normobaric hypoxia.

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► Locust physiology and gene expression were affected by hypobaric hypoxia.
► HIF system did not play a major role in response to hypobaric hypoxia.
► Mitochondrial genes in energy production were systemically suppressed.
► ER functions were enhanced, e.g. ERAD, glycosylation and protein folding.
► Three glucose-sourced pathways were under different regulation.