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Functional genomics of the seasonal responses of the camel hypothalamo-neurohypophysial system to dehydration: anticipation and adaptation.

The one-humped Arabian camel (Camelus dromedarius) has a remarkable capacity to survive extended periods of water deprivation. Whereas other mammals would die from circulatory failure when water loss reaches 12% of body weight, the camel can tolerate up to 30%. This is achieved by minimal evaporative cooling, low urinary output, water extraction from undigested food residues, and an increase in body temperature from 34C to 42C. The mammalian brain regulates water balance through the synthesis and secretion of the antidiuretic hormone vasopressin (VP) by the hypothalamo-neurohypophyseal system (HNS). VP is synthesised in HNS neurones which project axons to terminals located in the neural lobe (NL) of the pituitary, where mature VP is stored until released into the circulation in response to electrical activity evoked by physiological cues. VP acts on the kidney to provoke water reabsorption. Interestingly, the ultrastructure of the camel HNS changes according to season, suggesting that in the arid conditions of summer, the dromedary’s HNS is in a state of permanent activation, in preparation for the likely prospect of water deprivation. We have recently sequenced the genome of Camelus dromedarius. Based on this unique resource, we are now using a multi-disciplinary functional genomic approach combining state-of-the-art transcriptomic (RNAseq) and proteomic technologies to comprehensively describe, at the molecular level, the seasonal adaptations of the camel brain, and the responses to chronic dehydration. Camels will be subjected to comprehensive physiological and morphological investigation. HNS transcriptome and neuropeptidome datasets will be compared to existing rodent data sets, and subject to bioinformatic analyses to reveal nodal target genes. The functions of prioritized gene targets will be tested in vivo in rodent established models by HNS injection of viral vectors that over-express or knockdown target genes.

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