The interplay between prior selection, mild intermittent exposure, and acute severe exposure in phenotypic and transcriptional response to hypoxia

Hypoxia has profound and diverse effects on aerobic organisms, disrupting
oxidative phosphorylation and activating several protective pathways.
Predictions have been made that exposure to mild intermittent hypoxia may
be protective against more severe exposure and may extend lifespan. Both
effects are likely to depend on prior selection on phenotypic and
transcriptional plasticity in response to hypoxia, and may therefore show
signs of local adaptation. Here we report the lifespan effects of chronic,
mild, intermittent hypoxia (CMIH) and short-term survival in acute severe
hypoxia (ASH) in four clones of Daphnia magna originating from either
permanent or intermittent habitats, the latter regularly drying up with
frequent hypoxic conditions. We show that CMIH extended the lifespan in
the two clones originating from intermittent habitats but had the opposite
effect in the two clones from permanent habitats, which also showed lower
tolerance to ASH. Exposure to CMIH did not protect against ASH; to the
contrary, Daphnia from the CMIH treatment had lower ASH tolerance than
normoxic controls. Few transcripts changed their abundance in response to
the CMIH treatment in any of the clones. After 12 hours of ASH treatment,
the transcriptional response was more pronounced, with numerous
protein-coding genes with functionality in mitochondrial and respiratory
metabolism, oxygen transport, and, unexpectedly, gluconeogenesis showing
up-regulation. While clones from intermittent habitats showed somewhat
stronger differential expression in response to ASH than those from
permanent habitats, there were no significant hypoxia-by-habitat of origin
or CMIH-by-ASH interactions. GO enrichment analysis revealed a possible
hypoxia tolerance role by accelerating the molting cycle and regulating
neuron survival through up-regulation of cuticular proteins and
neurotrophins, respectively.