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Shaojun Du, PhD

Academic Title:


Primary Appointment:

Biochemistry and Molecular Biology

Additional Title:



Columbus Center, 3039

Phone (Primary):

(410) 234-8854


(410) 234-8896

Education and Training

  • Shandong University, BS, Biology, 1983
  • Institute of Oceanography, Chinese Academy of Sciences, MS, Cell and Developmental Biology, 1986
  • University of Toronto, Ph.D, Biochemistry and Molecular Biology, 1993 
  • Howard Hughes Medical Institute, University of Washington, Post-Doctoral Fellow, Genetics, 1993-1997


Dr. Du received his Ph.D. in molecular biology and biochemistry from the Department of Biochemistry, University of Toronto, Canada, and then completed his postdoctoral training in developmental biology and genetics at Howard Hughes Medical Institute, University of Washington. In 1997, Dr. Du joined the faculty of Center of Marine Biotechnology, University of Maryland Biotechnology Institute as a tenure-track Assistant Professor and was promoted to Associate Professor with tenure in 2003.  In 2010, Dr. Du joined University of Maryland Baltimore.  Currently, Dr. Du is a professor at Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine.  Dr. Du is also a faculty member at Institute of Marine and Environmental Technology, University of Maryland.

Dr. Du’s major scientific expertise and research achievements lie in using transgenic and genetic approaches to elucidate the molecular regulation of embryonic development and muscle cell differentiation, and the application of transgenic technology in aquaculture.  His current research centers on the following foci:

  • Genetic and epigenetic regulation of skeletal and cardiac muscle development, growth and repair.
  • The roles of posttranslational modification and molecular chaperones in muscle protein folding, stability and assembly during muscle cell differentiation and maturation.
  • Zebrafish as a model of neuromuscular diseases.

Research/Clinical Keywords

Genetic and epigenetic regulation of gene expression, muscle, bone and adipocyte cell differentiation, molecular chaperones and protein stability, zebrafish models, gene transfer and genome editing.

Highlighted Publications

Luo Z., Shi J., Pandey P., Ruan ZR., Lu Y., Sevdali M., Ye B., Du SJ and Chen EH (2022). The cellular architecture and molecular determinants of the zebrafish fusogenic synapse. Developmental Cell, 57 (13):1582-1597.

Xu R. and Du SJ. (2021). Overexpression of Lifeact-GFP disrupts F-Actin organization in cardiomyocytes and impairs cardiac function.  Front. Cell Dev. Biol. 9: 3028.

Jiao S., Xu R. and Du SJ. (2021). Smyd1 is essential for myosin expression and sarcomere organization in craniofacial, extraocular and cardiac muscles. Journal of Genetics and Genomics, 48(3): 208-218

Li H., Yu H., Du SJ., Li, Q. (2021). CRISPR/Cas9 mediated high efficiency knockout of myosin essential light chain gene in the Pacific Oyster (Crassostrea Gigas). Marine Biotechnology, 23(2): 215–224.

Li H., Li Q., Yu H., Du SJ. (2021). Characterization of paramyosin protein structure and gene expression during myogenesis in Pacific oyster (Crassostrea gigas). Comparative Biochemistry and Physiology Part - B: Biochemistry and Molecular Biology, 255: 110594.

Li SP, Wen HS, Du SJ. (2020) Defective sarcomere organization and reduced larval locomotion and fish survival in slow muscle heavy chain 1 (smyhc1) mutants.  FASEB J. 34(1): 1378-1397.

Feng D, Li Q, Yu H, Liu SK, Kong LF & Du SJ. (2020). Integrated analysis of microRNA and mRNA expression profiles in Crassostrea gigas to reveal functional miRNA and miRNA-targets regulating shell pigmentation. Sci Rep. 10, 20238.

Cai M, Han L, Liu L, He F, Chu W, Zhang J, Tian Z and Du SJ. (2019).  Defective sarcomere assembly in smyd1a and smyd1b zebrafish mutants.  FASEB. J. 33(5):6209-6225.  

Si Y, Wen H, Du SJ. (2019). Genetic mutations in jamb, jamc, and myomaker revealed different roles on myoblast fusion and muscle growth.  Mar Biotechnol. (NY). 21 (1): 111-123.

Yu H, Li HJ, LI Q, Xu R, Yue CY, Du SJ. (2019). Targeted gene disruption in pacific oyster based on CRISPR/Cas9 ribonucleoprotein complexes. Mar Biotechnol (NY). 21(3): 301–309.

Shi J, Cai M, Si Y, Zhang J, Du SJ.  (2018). Knockout of myomaker results in defective myoblast fusion, reduced muscle growth and increased adipocyte infiltration in zebrafish skeletal muscle.  Hum Mol Genet. 27(20):3541-3554. 

Cai M, Si Y, Zhang J, Tian Z, Du SJ.  (2018). Zebrafish Embryonic Slow Muscle Is a Rapid System for Genetic Analysis of Sarcomere Organization by CRISPR/Cas9, but Not NgAgo.  Mar Biotechnol. (NY). 20(2):168-181.

Anderson JL, Mulligan TS, Shen MC, Wang H, Scahill CM, Tan FJ, Du SJ, Busch-Nentwich EM, Farber SA. (2017). mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay. PLoS Genet. 13(11):e1007105.

Chu W, Zhang F, Song R, Li Y, Wu P, Chen L, Cheng J, Du SJ, Zhang J. (2017). Proteomic and microRNA Transcriptome Analysis revealed the microRNA-SmyD1 network regulation in Skeletal Muscle Fibers performance of Chinese perch.  Sci Rep. 7(1):16498. 

Suarez-Bregua P, Chien CJ, Megias M, Du SJ, Rotllant J.  (2017). Promoter architecture and transcriptional regulation of musculoskeletal embryonic nuclear protein 1b (mustn1b) gene in zebrafish.  Dev Dyn. 246(12):992-1000.

Suarez-Bregua P, Torres-Nuñez E, Saxena A, Guerreiro P, Braasch I, Prover D, Moran P, Cerda-Reverter J, Du SJ, Adrio F, Power D, Canario A, Postlethwait J, Bronner M, Cañestro C, Rotllant J.  (2017). Pth4, an Ancient Parathyroid Hormone Lost in Eutherian Mammals, Reveals a New Brain-to-Bone Signaling Pathway. FASEB J. 31(2):569-583.

He Q, Liu K, Tian Z and Du SJ (2015). The Effects of Hsp90α1 Mutations on Myosin Thick Filament Organization. PLoS One. 10(11):e0142573.

Li J, Chen Z, Gao LY, Colorni A, Ucko M, Fang S and Du SJ (2015). A transgenic zebrafish model for monitoring xbp1 splicing and endoplasmic reticulum stress in vivo.  Mech Dev. 137:33-44.

Du SJ, Tan, XG and Zhang JS. (2014). Smyd proteins: key regulators in skeletal and cardiac muscle development and function. Anatomical Record, 297:1650-1662.

Li H, Zhong Y, Wang Z, Gao J, Xu J, Chu W, Zhang J and Du SJ (2013).  Smyd1b is required for skeletal and cardiac muscle function in zebrafish. Molecular Biology of the Cell. 24(22):3511-21.

Xu J, Gao J, Li J, Xue L, Clark KJ, Ekker SC and Du SJ (2012).  Functional analysis of slow myosin heavy chain 1 and myomesin-3 in sarcomere organization in zebrafish embryonic slow muscles.  Journal of Genetics and Genomics, 39: 69-80.

Li H, Randall W and Du SJ (2009). skNAC (skeletal Naca), a muscle-specific isoform of Naca (nascent polypeptide-associated complex alpha), is required for myofibril organization. FASEB J. 23 (6):1988-2000.

Du SJ, Li H., Bian YH and Zhong Y (2008). Heat shock protein 90a1 is required for organized myofibril assembly in skeletal muscles of zebrafish embryos. Proc. Natl. Academy. Sci. USA. 105(2):554-559.

Tan XG, Rotllant J, Li H, De Deyne P and Du SJ (2006). SmyD1, a histone methyltransferase, is required for myofibril organization and muscle contraction in zebrafish embryos. Proc. Natl. Academy. Sci. USA. 103:2713-2718.

Du SJ, Devoto S, Westerfield M and Moon RT (1997). Positive and negative regulation of muscle cell identity by members of the hedgehog and TGF-b gene families. J. Cell Biol. 139:145-156.

Du SJ, Purcell SM, Christian JL, McGrew LL and Moon RT (1995). Identification of distinct classes and functional domains of Wnts through expression of wild-type and chimeric proteins in Xenopus embryos. Molecular and Cellular Biology, 15:2625-2634.

Du SJ, Gong Z, Fletcher G, Shears MA, King MJ, Idler DR and Hew CL (1992). Growth enhancement in transgenic Atlantic salmon by the use of an "all fish" chimeric growth hormone gene construct.  Nature Biotechnology, 10:176-181.

Research Interests

The fundamental question that drives the research in Dr. Du’s lab is: "How a single cell, the fertilized egg, develops into an animal with thousands of distinct type of cells - muscle cells, neurons, epidermal cells, blood cells, and so on?" We are particularly interested in the molecular and cellular mechanisms that control the differentiation of skeletal and cardiac muscle cells during embryogenesis. Specifically, we use zebrafish as a model system to uncover novel genetic pathways and gene function involved in muscle development, growth and repair.  We use the genetic approach to carry out gain- and loss-of-function studies using the Tol2 transposon, TALEN and CRISPR technologies.  We have generated over 40 transgenic and mutant zebrafish models focused on muscle structural proteins, transcriptional factors, chaperones, and microRNAs.  Here are few examples of key findings from our previous studies.  1) We have demonstrated that Hedgehog signaling is required for specification of slow muscles that do not fuse (Du et al., 1997).  2) We demonstrated that SmyD1, a muscle-specific protein methyltransferase, is essential for muscle cell differentiation and myofibril assembly in cardiac and skeletal muscles (Tan et al., 2008. Li et al., 2013).  3) We uncovered that Hsp90a1 is absolutely required for sarcomere assembly of myosin in skeletal muscles in vivo (Du et al., 2008). Moreover, post-translational modifications by phosphorylation and acetylation play an important regulatory role in modulating Hsp90a1 function in myosin thick filament organization (He et al., 2015).  

Grants and Contracts

2018-2024: 1R01AR072703-01A1 (NIH)

Title: Molecular regulation of muscle development by Smyd1.