Founctional Research Of The Gene Tecrb Of Zebrafish

There are two types of mental retardation(MR),one is syndromic mental retardation(SMR),the patient has mental retardation,can not adapt to society,and is accompanied by obvious physical malformations or other diseases;the other is non-syndromic mental retardation(NSMR),in addition to intelligence,there are no apparent external phenotypic features.According to the existing literature,trans-2,3-enoyl-CoA reductase(TECR)is related to human NSMR.MR is one of the most common diseases in children's growth and development.With the continuous development of science,people are eager to understand the pathological causes and mechanisms that cause MR so as to overcome this disease as soon as possible,so that more patients could get effective treatment.Using zebrafish as a model animal,building disease models has become an important method for studying related diseases.The homologue of the TECR gene in zebrafish is trans-2,3-enoyl-CoA reductase b(tecrb).We knocked out the tecrb gene of the zebrafish and obtained two heterozygous mutants of +14 and-5 bp.There are no homozygous mutants in the heterozygous offspring,so we believe that the tecrb mutation results in the death of homozygous mutants.After research,it was found that the mutant died within 15 days after hatching.In situ hybridization showed that terb was a maternally expressed gene and was highly expressed in the brain,eye and soma of zebrafish during early embryonic development;qPCR showed that it was highly expressed on the 11th day after hatching and then stabilized at a low level;in addition,in adulthood,tecrb have higher expression in brain and eye.qPCR was used to detect the expression of 3-ketoacyl-CoA reductase(KAR),and 3-hydroxyacyl-CoA dehydratase(HACD),key genes in the synthesis of long and very long chain fatty acids,we also detected 5-hydroxytryptamine receptor 1A(5HT1 A),which related to cognition.Compared with the wild type,the homozygous mutants had significantly increased KAR,HACD and 5HT1A expression.HE staining and Nissl's staining of paraffin sections showed that compared with the wild type,the brains of the mutants gradually atrophied with the extension of the development days after hatching,and the neurons in the brain were not well developed;the learning and memory ability of the zebrafish was examined.It was found that although the wild-type zebrafish and heterozygous mutants did not differ significantly,the heterozygous mutants had poorer learning and memory capabilities than the wild-type counterparts,and we speculated that the tecrb mutation may have more impact on learning and genetic capabilities of homozygous.The death of homozygous mutants may be due to the disorder of the synthesis of long-chain and very-long chain fatty acids,neurodevelopmental disabilityor other factors.Through this study,we hope to provide a theoretical basis for studying the role of its homologous genes in humans.