Our mission is to elucidate the molecular and cellular mechanisms that regulate muscle development, structure, and contractile function in health and disease, with the goal of advancing therapies for congenital and acquired cardiac and skeletal muscle disorders.

2016 - 2021  Postdoc., Department of Internal Medicine, University of Cincinnati 

2009 - 2015  Ph.D., Department of Kinesiology and Health Education, University of Texas at Austin 

2005 - 2009  M.A., Department of Kinesiology and Health Education, University of Texas at Austin 

1998 - 2004  B.A., Department of Physical Education, Pusan National University, South Korea

Our research is dedicated to understanding how sarcomeric proteins regulate skeletal and cardiac muscle development, structure, function, regeneration, and aging in health and disease. We focus on the Myosin Binding Protein-C (MyBP-C) family (MYBPC1, MYBPC2, and MYBPC3) to define their roles in sarcomere assembly, thick filament regulation, contractility, and muscle homeostasis. Our ultimate goal is to translate these mechanistic discoveries into novel therapies for inherited muscle diseases.

Muscle Function & Contractility 

From Whole Muscle to Single Myocytes

We combine genetically engineered mouse models and human iPSC-derived muscle systems with comprehensive muscle physiology platforms to evaluate contractile performance at multiple levels—from whole muscles and single muscle fibers to individual cardiomyocytes and skeletal myocytes. These approaches allow us to define how sarcomeric protein dysfunction impairs muscle mechanics in genetic diseases.

Structural Biology & Disease Progression

From Sarcomere Architecture to Disease Pathogenesis

Using advanced imaging modalities, including MRI, CT scan, fluorescence microscopy, confocal microscopy, and electron microscopy, we investigate how disease-causing mutations alter musculoskeletal anatomy, sarcomere architecture, muscle fiber composition, tissue remodeling, and disease progression. Our research provides mechanistic insights into the pathogenesis of inherited muscle disorders, including MYBPC1-associated distal arthrogryposis, congenital myopathies, and MYBPC3-associated hypertrophic cardiomyopathy (HCM).

Translational Therapeutics

Mechanism-Guided Therapy Development

Our laboratory combines SRX/DRX analysis, small-angle X-ray diffraction, and multi-omics to uncover the molecular mechanisms underlying inherited muscle diseases. These integrated approaches enable us to identify therapeutic targets and develop small molecules, AAV-mediated gene therapies, and antisense oligonucleotides (ASOs) for MYBPC1-associated distal arthrogryposis, congenital myopathies, and MYBPC3-associated hypertrophic cardiomyopathy (HCM).

3. Akhil Baby, Kalyani Ananthamohan, Brenna N McIntyre, Sankar Natesan, Taejeong Song. Fast Myosin Binding Protein-C is a Vital Regulator in Young and Aged Fast Skeletal Muscle Homeostasis. Journal of Cachexia, Sarcopenia and Muscle (Corresponding author). 2025 Nov 13. doi:org/10.1002/jcsm.70106. 

4. Christofer Calvo, Coalesco Smith, Taejeong Song, Fabian Montecino-Morales, Sakthivel Sadayappan, Douglas P. Millay, Minchul Kim. Loss of Ufsp1 does not cause major changes at the neuromuscular junction. PLOS ONE. 2025 Aug 1:20(8):e03228690. doi: 10.1371/journal.pone.0328690. 

5. Desai D, Song T, Singh RR, Baby A, McNamara J, Green LC, Nabavizadeh P, Ericksen M, Bazrafshan S, Natesan S, Sadayappan S. MYBPC3 D389V Variant Induces Hypercontractility in Cardiac Organoids. Cells. 2024 Nov 19;13(22):1913. doi: 10.3390/cells13221913. 

6. Jiwoong Jang, Yeongmin Kim, Taejeong Song, Sanghee Park, Hee-Joo Kim, Jin-ho Koh, Yoonil Cho, ShiYoung Park, Sakthivel Sadayappan, Hyo-Bum Kwak, Robert R. Wolfe, Il-Young Kim, Cheol Soo Choi. Balanced Free Essential Amino Acid Feeding Improves Endurance Capacity During Strength-Enhancing Resistance Training via DRP1-Dependent Dynamic Remodeling of Mitochondria. Journal of Cachexia, Sarcopenia Muscle. 2024 Oct;15(5):1651-1663. doi:10.1002/jcsm.13519. 

7. Hessel AL, Kuehn M, Han SW, Ma W, Irving TC, Momb BA, Song T, Sadayappan S, Linke WA, Palmer BM. Fast myosin binding protein C knockout in skeletal muscle alters length-dependent activation and myofilament structure. Commun Biol 7, 648 (2024). doi:10.1038/s42003-024-06265-8. 

8. Jani VP*, Song T*, Gao C, Gong H, Sadayappan S, Kass DA, Irving TC, Ma W. The structural OFF and ON states of myosin can be decoupled from the biochemical super-relaxed and disordered-relaxed states. PNAS NEXUS. (* Co-first author) 2024 Jan 30. doi:10.1093/pnasnexus/pgae039.

9. Brittany A. Gonzalez, Samuel W. Harmeyer, Taejeong Song, Sakthivel Sadayappan, Katherine E. Yutzey. Dynamic changes in mitral valve extracellular matrix, tissue mechanics and function in a mouse model of Marfan syndrome. Matrix Biology. 2024 Jan 5:S0945-053X(24)00001-5. doi: 10.1016/j.matbio.2024.01.001. 

10. Maicon Landim-Vieira, Weikang Ma, Taejeong Song, Hosna Rastegarpouyani, Henry Gong, Isabella Leite Coscarella, Sylvia Bogaards, Stefan Conijn, Coen Ottenheijm, Hyun Seok Hwang, Maria Papadaki, Bjorn Knollmann, Sakthivel Sadayappan, Thomas Irving, Vitold Galkin, P. Bryant Chase, J. Renato Pinto. 3 Cardiac troponin T N-domain variant destabilizes the actin interface resulting in disturbed myofilament function. PNAS. 2023 Jun 6;120(23):e2221244120. doi: 10.1073/pnas.2221244120. 

11. Taejeong Song, Maicon Landim-Vieira, Mustafa Ozdemir, Caroline Gott, Onur Kanisicak, Jose Renato Pinto and Sakthivel Sadayappan. Etiology of genetic muscle disorders induced by mutations in fast and slow skeletal MyBP-C paralogs. Experimental & Molecular Medicine (Corresponding author).2023 Mar;55(3):502-509. doi: 10.1038/s12276-023-00953-x. 

12. Justin Boyer, Jiuzhou Huo, Sarah Han, Julian Havens, Vikram Prasad, Brian Lin, David Kass, Taejeong Song, Ramzi Khairallah, Sakthivel Sadayappan, Christopher Ward, and Jeffery Molkentin. Deletion of skeletal muscle satellite cells attenuates pathology in muscular dystrophy. Nature Communications. 2022 May 26;13(1):2940. doi: 10.1038/s41467-022-30619-7.

Homepage : https://mcrp.med.arizona.edu/research/song-laboratory

Contact :  tjsong@arizona.edu

저희 연구실은 Sarcomere Biology & Physiology에 기반한, 골격근과 심장근의 발생, 구조, 기능, 노화 및 질환의 분자 기전을 규명하는 데 집중하고 있습니다. 특히 Myosin Binding Protein-C (MyBP-C) 단백질군을 중심으로 근육의 수축 조절 기전과 유전성 근육질환의 발병 원인을 연구하고 있으며, 이를 바탕으로 새로운 치료법 개발을 목표로 하고 있습니다.

특히 올해 선정된 NIH R01 연구과제를 기반으로 MYBPC1 유전자 돌연변이에 의해 발생하는 Distal Arthrogryposis의 발병 기전, 질환 진행 과정, 그리고 치료 전략을 활발히 연구하고 있습니다. 

제가 속해 있는 Department of Cell and Molecular Medicine 과 Sarver Heart Center는 골격근과 심장근의 기능을 다양한 수준에서 정밀하게 분석할 수 있는 세계 최고 수준의 연구 인프라를 갖추고 있습니다. Aurora Scientific과 IonOptix의 최신 장비를 이용하여, 전체 근육(whole muscle), 단일 근섬유(single muscle fiber), 개별 근세포(single myocyte)의 기능을 정량적으로 평가할 수 있는 시스템을 구축하고 있습니다.

또한 심장 및 골격근 연구 분야의 세계적인 석학인 Dr. Sakthivel Sadayappan, Dr. Henk Granzier, Dr. Samantha Harris, Dr. Jill Tardiff, Dr. Brett Colson, 그리고 Sarver Heart Center의 센터장인 Dr. Hesham Sadek 연구팀과 긴밀한 공동연구를 수행하고 있으며, 다양한 융합 연구를 통해 새로운 치료 전략 개발에 힘쓰고 있습니다.

앞으로 국내외 연구자들과의 활발한 공동연구를 기대하며, 특히 한국의 관련 연구실들과 긴밀한 협력 관계를 구축하고자 합니다. 또한 학부생, 대학원생, 박사후연구원(Postdoctoral Fellow)은 물론, 단기 연수 및 인턴십을 희망하는 연구자들의 지원을 언제든지 환영합니다. 관심 있는 분들은 부담 없이 연락해 주시기 바랍니다. 

PI contact :  tjsong@arizona.edu