The key role of myostatin b in somatic growth in fishes derived from distant hybridization

The basic mechanism of heterosis has not been systematically and completely characterized.In previous studies,we obtained three economically important fishes that exhibit rapid growth,WR(WCC♀×RCC♂),WR-Ⅱ(WR♀×WCC♂),and WR-Ⅲ(WR-Ⅱ♀×4nAU♂),through distant hybridization.However,the mechanism underlying this rapid growth remains unclear.In this study,we found that WR,WR-Ⅱ,and WR-Ⅲshowed muscle hypertrophy and higher muscle protein and fat contents compared with their parent species(RCC and WCC).Candidate genes responsible for this rapid growth were then obtained through an analysis of 12 muscle transcriptomes.Notably,the mRNA level of mstnb(myostatin b),which is a negative regulator of myogenesis,was significantly reduced in WR,WR-Ⅱ,and WR-Ⅲcompared with the parent species.To verify the function of mstnb,a mstnb-deficient mutant RCC line was generated using the CRISPR-Cas9 technique.The average body weight of mstnb-deficient RCC at 12 months of age was significantly increased by 29.57%compared with that in wild-type siblings.Moreover,the area and number of muscle fibers were significantly increased in mstnb-deficient RCC,indicating hypertrophy and hyperplasia.Furthermore,the muscle protein and fat contents were significantly increased in mstnb-deficient RCC.The molecular regulatory mechanism of mstnb was then revealed by transcription profiling,which showed that genes related to myogenesis(myod,myog,and myf5),protein synthesis(PI3K-AKT-mTOR),and lipogenesis(pparγand fabp3)were highly activated in hybrid fishes and mstnb-deficient RCC.This study revealed that low expression or deficiency of mstnb regulates somatic growth by promoting myogenesis,protein synthesis,and lipogenesis in hybrid fishes and mstnb-deficient RCC,which provides evidence for the molecular mechanism of heterosis via distant hybridization.

Neuroendocrine regulation of somatic growth in fishes

Growth is a polygenic trait that is under the influence of multiple physiological pathways regulating energy metabolism and muscle growth.Among the possible growth-regulating pathways in vertebrates,components of the somatotropic axis are thought to have the greatest influence.There is growing body of literature focusing on the somatotropic axis and its role regulating growth in fish.This includes research into growth hormone,upstream hypothalamic hormones,insulin-like growth factors,and downstream signaling molecules.Many of these signals have both somatic effects stimulating the growth of tissues and metabolic effects that play a role in nutrient metabolism.Signals of other endocrine axes exhibit profound effects on the function of the somatotropic axis in vivo.In this review we highlight recent advances in our understanding of the teleost fish endocrine somatotropic axis,including emerging research using genetic modified models.These studies have revealed new aspects and challenges associated with regulation of the important steps of somatic growth.

Hyperandrogenism in POMCa-deficient zebrafish enhances somatic growth without increasing adiposity

The endocrine regulatory roles of the hypothalamic-pituitary-adrenocortical axis on anxiety-like behavior and metabolic status have been found throughout animal taxa.However,the precise effects of the balancing adrenal corticosteroid biosynthesis under the influence of adrenocorticotrophic hormone(ACTH),a pro-opiomelanocortin(POMC)-derived peptide,on animal energy expenditure and somatic growth remain unknown.POMC has also been identified as one of the candidate loci for polycystic ovary syndrome,which features hyperandrogenism and some prevalence of obesity in patients.Here we show that zebrafish lacking functional POMCa exhibit similar phenotypes of stress response and body weight gain but not obesity as observed in mammalian models.In contrast with the impaired anorexigenic signaling cascade of melanocyte-stimulating hormones and leptin,which are responsible for their obesity-prone weight gain observed in various pome mutant mammals,analyses with our pomca mutant series indicate that ACTH is the key regulator for the phenotype with enhanced somatic growth without obesity in pomca-deficient zebrafish.Hypocortisolism associated with hyperandrogenism has been observed in the pomca-deficient zebrafish,with enhanced activation of mammalian target of rapamycin complex 1;reutilization of amino acids and fatty acid^-oxidation are observed in the muscle tissue of the pomca-deficient fish.After reducing hyperandrogenism by crossing our pomca mutant fish with a cy p l 7a 1-deficient background,the phenotype of enhanced somatic growth in pomca-deficient fish was no longer observed.Thus,our work also demonstrated that the role of POMCa in stress response seems to be conserved in vertebrates,whereas its effect on adipostasis is unique to teleosts.

Somatic growth of lean children:the potential role of sleep

Background:Despite the current obesity pandemic,childhood malnutrition remains an urgent,public health concern.Similar to the obesity pandemic,childhood malnutrition is influenced by genetic and a number of social,environmental and biological factors.In this study,we investigated the association between sleep duration and somatic growth in lean children.Methods:A stratified,randomly clustered sampling design was used to select fifth grade students from 10 primary schools in Shanghai.Based on a body mass index below the 15th percentile a subsample of 143 lean children aged 10-11 years old was defi ned.Sleep duration and other potential confounders were surveyed through parental or self-report questionnaires.Body measurements were collected and used to calculate the Z score of weight,height,body mass index as well as body fat percentage.Results:Compared with children who slept<9 hours,those who slept for≥10 hours grew taller and gained more weight after adjusting for confounding factors.When children slept 9-10 hours,they had signifi cantly higher Z score of weight and body mass index.Conclusions:Prolonged sleep not only benefi ts weight gain but also improves height in lean children.Our findings might provide important public health advice such that prolonged sleep may be an effective modifi er of nutritional problems in childhood.