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Functional Analysis of Slow Myosin Heavy Chain 1 and Myomesin-3 in sarcomere Organization in Zebrafish Embryonic Slow Muscles

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Journal of Genetics and Genomics 2012年第2期39卷 69-80页

作者： Jin Xu Jie Gao Junling Li Liangyi Xue Kan J. Clark Stephen C. Ekker Shao Jun Du Department of Biochemistry and Molecular Biology University of Maryland School of Medicine Baltimore MD 21202 USA College of Life Science and Biotechnology Ningbo University Ningbo 315211 Zhejiang China Department of Biochemistry ＆ Molecular Biology Mayo Clinic Rochester MN 55905 USA

Myofibrillogenesis, the process of sarcomere formation, requires close interactions of sarcomeric proteins and various components of sarcomere structures. The myosin thick filaments and M-lines are two key components of the sarcomere. It has been suggested that myomesin proteins of M-lines interact with myosin and titin proteins and keep the thick and titin filaments in order. However, the function of myomesin in myofibrillogenesis and sarcomere organization remained largely enigmatic. No knockout or knockdown animal models have been reported to elucidate the role of myomesin in sarcomere organization in vivo. In this study, by using the gene-specific knockdown approach in zebrafish embryos, we carded out a loss-of-function analysis of myomesin-3 and slow myosin heavy chain 1 （smyhcl） expressed specifically in slow muscles. We demonstrated that knockdown of smyhcl abolished the sarcomeric localization of myomesin-3 in slow muscles. In contrast, loss of myomesin-3 had no effect on the sarcomeric organization of thick and thin filaments as well as M- and Z-line structures. Together, these studies indicate that myosin thick filaments are required for M-line organization and M-line localization of myomesin-3. In contrast, myomesin-3 is dispensable for sarcomere organization in slow muscles.

关键词： Myosin Myomesin-3 M-line sarcomere

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

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Journal of Genetics and Genomics 2021年第3期48卷 208-218页

作者： Shuang Jiao Rui Xu Shaojun Du Department of Biochemistry and Molecular Biology Institute of Marine and Environmental TechnologyUniversity of Maryland School of MedicineBaltimoreMD 21202USA Key Laboratory of Experimental Marine Biology Center for Ocean Mega-ScienceInstitute of OceanologyChinese Academy of SciencesQingdao 266071China School of Life Sciences Shandong University of TechnologyZibo 255049China

Skeletal and cardiac muscles are striated myofibers that contain highly organized sarcomeres for muscle *** studies revealed that Smyd1,a lysine methyltransferase,plays a key role in sarcomere assembly in heart and trunk skeletal ***,Smyd1 expression and function in craniofacial muscles are not ***,we analyze the developmental expression and function of two smyd1 paralogous genes,smyd1 a and smyd1 b,in craniofacial and cardiac muscles of zebrafish *** 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 ***,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) *** defects are also observed in cardiac muscles of smyd1b^(sa15678) *** craniofacial and cardiac muscle formation is associated with an upregulation of hsp90α1 and unc45b mRNA expression in smyd1b^(sa15678) and smyd1a^(mb5);smyd1b^(sa15678) ***,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 *** of smyd1b results in muscle-specific stress response.

关键词： Smyd1 Myosin sarcomere Craniofacial muscle Cardiac muscle

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Seeking candidate variants of arrhythmogenic cardiomyopathy in sarcomere genes

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中国循环杂志 2018年第S1期33卷 139-139页

作者： Kai Chen Jiangping Song Man Rao National Center for Cardiovascular Diseases Fuwai HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina

ObjectiveTo seek potential pathogenic variants in sarcomere genes in arrhythmogenic cardiomyopathy(ACM)and describe the *** and Results We performed targeted sequencing of 14sarcomere genes in 118 cases with the clini... 详细信息

关键词： arrhythmogenic cardiomyopathy sarcomere genes family members of the probands

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Importance of genetic evaluation and testing in pediatric cardiomyopathy

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World Journal of Cardiology 2014年第11期6卷 1156-1165页

作者： Muhammad Tariq Stephanie M Ware Department of Pediatrics and Herman B Wells Center for Pediatric Research Indiana University School of Medicine Indianapolis IN 46202 United States

Pediatric cardiomyopathies are clinically heterogeneous heart muscle disorders that are responsible for significant morbidity and mortality. Phenotypes include hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, left ventricular noncompaction and arrhythmogenic right ventricular cardiomyopathy. There is substantial evidence for a genetic contribution to pediatric cardiomyopathy. To date, more than 100 genes have been implicated in cardiomyopathy, but comprehensive genetic diagnosis has been problematic because of the large number of genes, the private nature of mutations, and difficulties in interpreting novel rare variants. This review will focus on current knowledge on the genetic etiologies of pediatric cardiomyopathy and their diagnostic relevance in clinical settings. Recent developments in sequencing technologies are greatly impacting the pace of gene discovery and clinical diagnosis. Understanding the genetic basis for pediatric cardiomyopathy and establishing genotypephenotype correlations may help delineate the molecular and cellular events necessary to identify potential novel therapeutic targets for heart muscle dysfunction in children.

关键词： Pediatric Mutation Exome sequencing sarcomere

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Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy

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World Journal of Diabetes 2015年第7期6卷 943-960页

作者： Mark T Waddingham Amanda J Edgley Hirotsugu Tsuchimochi Darren J Kelly Mikiyasu Shirai James T Pearson Department of Medicine St Vincent’s HospitalUniversity of Melbourne Department of Physiology Monash University Department of Cardiac Physiology National Cerebral and Cardiovascular Center Research Institute Monash Biomedical Imaging Facility Monash University Australian Synchrotron

Diabetes mellitus significantly increases the risk of cardiovascular disease and heart failure in *** of hypertension and coronary artery disease,diabetes is associated with a specific cardiomyopathy,known as diabetic cardiomyopathy(DCM).Four decades of research in experimental animal models and advances in clinical imaging techniques suggest that DCM is a progressive disease,beginning early after the onset of type 1 and type 2 diabetes,ahead of left ventricular remodeling and overt diastolic *** the molecular pathogenesis of early DCM still remains largely unclear,activation of protein kinase C appears to be central in driving the oxidative stress dependent and independent pathways in the development of contractile *** subcellular alterations to the cardiomyocyte are now being highlighted as critical events in the early changes to the rate of force development,relaxation and stability under pathophysiological *** changes include perturbed calcium handling,suppressed activity of aerobic energy producing enzymes,altered transcriptional and posttranslational modification of membrane and sarcomeric cytoskeletal proteins,reduced actin-myosin cross-bridge cycling and dynamics,and changed myofilament calcium *** this review,we will present and discuss novel aspects of the molecular pathogenesis of early DCM,with a special focus on the sarcomeric contractile apparatus.

关键词： Diabetes Prediabetes Insulin resistance Myocardium sarcomere Protein kinase C Rho kinase

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