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Rainbow trout (Oncorhynchus mykiss) is one of the most widely cultivated salmonid species in the world, with well developed breeding programmes. Few studies have investigated the feasibility of genetically improving hypoxia tolerance in this highly sensitive species. In the present study, we tested 1320 trout of a commercial line for hypoxia resistance to explore the genetic architecture of this trait and identify the major genome regions (QTLs) involved and associated candidate genes potentially affecting the response to hypoxia. The heritability was estimated to be sufficient (around 0.25) to improve hypoxia tolerance by genetic selection. We clearly identified three QTL, two on chromosome 31, one on chromosome 20, and found two other putative QTL on chromosomes 15 and 28. Each of these QTLs explains only between 0.2% and 0.8% of the genetic variance of the trait, indicating that hypoxia tolerance is due to the expression of very many genes. 

Furthermore, we showed that genomic selection for hypoxia tolerance would lead to a relative increase of ~11% in selection accuracy compared to pedigree-based selection, considering a reference population of 1000 individuals. Finally, fifteen genes (ids, fmr1, arx, lonrf3, commd5, map4k4, smu1, b4galt1, re1, abca1, noa1, igfbp7, noxo1, bcl2a, mylk3) were proposed as functional candidates potentially involved in hypoxia tolerance. Given the large number of candidate genes proposed within the main QTL (6 genes) and the high linkage disequilibrium values existing within this genomic region, we suggest that the complex response to acute hypoxia, i.e. the interplay between behavioural, morphological and physiological responses in rainbow trout, is mainly encoded by a supergene present in this QTL region of chromosome 31. Functional validation of the effects of the genes could help to clarify the biological mechanisms triggering a response to acute hypoxia in rainbow trout.

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• Florence Phocas