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♀&#...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.展开更多
基金supported by the National Natural Science Foundation of China(32002382,32293252,U19A2040,32293254)the National Key Research and Development Program of China(2023YFD2400202)+5 种基金the Natural Science Foundation of Hunan Province(2021JJ40339)the Training Program for Excellent Young Innovators of Changsha(kq2209013)the Earmarked Fund for Agriculture Research System of China(CARS-45)the Laboratory of Lingnan Modern Agriculture Project(NT2021008)the 111 Project(D20007)Special Science Found of Nansha-South China Agricultural University Fishery Research Institute,Guangzhou。
文摘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.
