Smyd1 is essential for myosin expression and sarcomere organization in craniofacial,extraocular,and cardiac muscles  

作　　者：Shuang Jiao Rui Xu Shaojun Du 

机构地区：[1]Department of Biochemistry and Molecular Biology,Institute of Marine and Environmental Technology,University of Maryland School of Medicine,Baltimore,MD 21202,USA [2]Key Laboratory of Experimental Marine Biology,Center for Ocean Mega-Science,Institute of Oceanology,Chinese Academy of Sciences,Qingdao 266071,China [3]School of Life Sciences,Shandong University of Technology,Zibo 255049,China

出　　处：《Journal of Genetics and Genomics》2021年第3期208-218,共11页遗传学报（英文版）

基　　金：supported by funding from the U.S.National Institute of Health(NIH)National Institute of Arthritis and Musculoskeletal and Skin Diseases(R01AR072703 to S.Du);supported in part by fellowships from the China Scholarship Council。

摘　　要：Skeletal and cardiac muscles are striated myofibers that contain highly organized sarcomeres for muscle contraction.Recent studies revealed that Smyd1,a lysine methyltransferase,plays a key role in sarcomere assembly in heart and trunk skeletal muscles.However,Smyd1 expression and function in craniofacial muscles are not known.Here,we analyze the developmental expression and function of two smyd1 paralogous genes,smyd1 a and smyd1 b,in craniofacial and cardiac muscles of zebrafish embryos.Our data show that loss of smyd1a(smyd1a^(mb5))or smyd1b(smyd1b^(sa15678))has no visible effects on myogenic commitment and expression of myod and myosin heavy-chain m RNA transcripts in craniofacial muscles.However,myosin heavy-chain protein accumulation and sarcomere organization are dramatically reduced in smyd1b^(sa15678) single mutant,and almost completely diminish in smyd1a^(mb5);smyd1b^(sa15678) double mutant,but not in smyd1a^(mb5) mutant.Similar defects are also observed in cardiac muscles of smyd1b^(sa15678) mutant.Defective craniofacial and cardiac muscle formation is associated with an upregulation of hsp90α1 and unc45b mRNA expression in smyd1b^(sa15678) and smyd1a^(mb5);smyd1b^(sa15678) mutants.Together,our studies indicate that Smyd1b,but not Smyd1a,plays a key role in myosin heavy-chain protein expression and sarcomere organization in craniofacial and cardiac muscles.Loss of smyd1b results in muscle-specific stress response.

关 键 词：Smyd1 MYOSIN SARCOMERE Craniofacial muscle Cardiac muscle 

分 类 号：Q344[生物学—遗传学]