Marandel Lucie, Seiliez Iban, Véron Vincent, Skiba-Cassy Sandrine, Panserat Stéphane
Institut National de la Recherche Agronomique (INRA), Nutrition, Metabolism and Aquaculture Unit (UR1067), Saint-Pée-sur-Nivelle, France
Institut National de la Recherche Agronomique (INRA), Nutrition, Metabolism and Aquaculture Unit (UR1067), Saint-Pée-sur-Nivelle, France.
Physiol Genomics. 2015 Jul;47(7):253-63. doi: 10.1152/physiolgenomics.00026.2015. Epub 2015 Apr 21.
The rainbow trout (Oncorhynchus mykiss) is considered to be a strictly carnivorous fish species that is metabolically adapted for high catabolism of proteins and low utilization of dietary carbohydrates. This species consequently has a "glucose-intolerant" phenotype manifested by persistent hyperglycemia when fed a high-carbohydrate diet. Gluconeogenesis in adult fish is also poorly, if ever, regulated by carbohydrates, suggesting that this metabolic pathway is involved in this specific phenotype. In this study, we hypothesized that the fate of duplicated genes after the salmonid-specific 4th whole genome duplication (Ss4R) may have led to adaptive innovation and that their study might provide new elements to enhance our understanding of gluconeogenesis and poor dietary carbohydrate use in this species. Our evolutionary analysis of gluconeogenic genes revealed that pck1, pck2, fbp1a, and g6pca were retained as singletons after Ss4r, while g6pcb1, g6pcb2, and fbp1b ohnolog pairs were maintained. For all genes, duplication may have led to sub- or neofunctionalization. Expression profiles suggest that the gluconeogenesis pathway remained active in trout fed a no-carbohydrate diet. When trout were fed a high-carbohydrate diet (30%), most of the gluconeogenic genes were non- or downregulated, except for g6pbc2 ohnologs, whose RNA levels were surprisingly increased. This study demonstrates that Ss4R in trout involved adaptive innovation via gene duplication and via the outcome of the resulting ohnologs. Indeed, maintenance of ohnologous g6pcb2 pair may contribute in a significant way to the glucose-intolerant phenotype of trout and may partially explain its poor use of dietary carbohydrates.
虹鳟（Oncorhynchus mykiss）被认为是一种严格的肉食性鱼类，其新陈代谢适合高蛋白分解代谢和低膳食碳水化合物利用率。因此，当喂食高碳水化合物饮食时，该物种会表现出“葡萄糖不耐受”表型，表现为持续性高血糖。成年鱼的糖异生作用即使有也很少受碳水化合物调节，这表明该代谢途径与这种特定表型有关。在本研究中，我们假设鲑科鱼类特异性第四次全基因组复制（Ss4R）后重复基因的命运可能导致了适应性创新，对它们的研究可能会为增强我们对该物种糖异生作用和膳食碳水化合物利用不良的理解提供新的线索。我们对糖异生基因的进化分析表明，pck1、pck2、fbp1a和g6pca在Ss4r后作为单拷贝基因保留，而g6pcb1、g6pcb2和fbp1b同源基因对则得以保留。对于所有基因，复制可能导致了亚功能化或新功能化。表达谱表明，在喂食无碳水化合物饮食的虹鳟中，糖异生途径仍然活跃。当虹鳟喂食高碳水化合物饮食（30%）时，除了g6pbc2同源基因对的RNA水平意外升高外，大多数糖异生基因未表达或表达下调。本研究表明，虹鳟中的Ss4R通过基因复制和由此产生的同源基因的结果参与了适应性创新。事实上，同源g6pcb2对的保留可能在很大程度上导致了虹鳟的葡萄糖不耐受表型，并可能部分解释其对膳食碳水化合物的利用不良。
