- Title Associate Professor of Biology; Member, Whitaker Cardiovascular Institute
- Education PhD, Baylor College of Medicine, 1997
- Email email@example.com
- Phone 617-353-2469
- Area of Interest Cardiac development and disease, muscle regeneration, muscular dystrophy, mouse developmental biology, gene regulation
Our lab focuses on gene regulatory networks in muscle development and disease. Defining these networks in differentiation and homeostasis can yield insight into the mechanisms that drive pathological gene expression in cardiac and skeletal muscle diseases. Our lab has addressed this problem by focusing on gene programs regulated by the mammalian MEF2 transcription factor family, an evolutionarily conserved and core transcription factor in muscle gene regulation. We have used a systems-level approach to reveal that the four related, mammalian MEF2 family members regulate overlapping but distinct gene programs in cardiac and skeletal myocytes. We are investigating the transcriptional mechanisms that establish gene regulatory specificity and how these may be altered in muscle disease.
Another area of investigation relates to the role of noncoding RNAs in muscular dystrophy and cardiovascular disease. Long (lncRNAs) and small (miRNAs) noncoding RNAs are now recognized as key components in gene regulatory networks. Recently, we have identified a noncoding RNA locus (Gtl2-Dio3) involved in skeletal muscle differentiation and regeneration, and in cardiomyocyte proliferation. We have also shown that expression of the Gtl2-Dio3 locus is dysregulated in cardiac and skeletal myopathies. We are investigating the epigenetic role of the noncoding RNAs expressed from this locus in cardiac and skeletal muscle homeostasis and disease.
- Medrano JL, Naya FJ (2017) The transcription factor MEF2A fine-tunes gene expression in the atrial and ventricular chambers of the adult heart. J Biol Chem. Oct 20 [Epub ahead of print].
- Desjardins CA, Naya FJ (2017) Antagonistic regulation of cell cycle and differentiation gene programs in neonatal cardiomyocytes by homologous MEF2 transcription factors. J Biol Chem. 292(25): 10613-10629.
- Desjardins CA, Naya FJ (2016) The Function of the MEF2 Transcription Factor Family in Cardiac Development, Cardiogenomics, and Direct Reprogramming. J Cardiovasc Dev Dis. 3(3): 26.
- Clark AL, Maruyama S, Sano S, Accorsi A, Girgenrath M, Walsh K, and Naya FJ (2016) miR-410 and miR-495 are dynamically regulated in diverse cardiomyopathies and their inhibition attenuates pathological hypertrophy. PLoS One. 11(3): e0151515.
- Estrella NL, Clark AL, Desjardins CA, Nocco SE, Naya FJ (2015) MEF2D Deficiency in Neonatal Cardiomyocytes Triggers Cell Cycle Re-entry and Programmed Cell Death in vitro. J Biol Chem. 2015 August 20. 290(40): 24367-80.
- Clark AL, Naya FJ (2015) MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2. J Biol Chem. 2015 August 3. 290(38): 23162-72.
- Estrella NL, Desjardins CA, Nocco SE, Clark AL, Maksimenko Y, Naya FJ (2015) MEF2 transcription factors regulate distinct gene programs in mammalian skeletal muscle differentiation. J Biol Chem. 290(2): 1256-68.
- Snyder CM, Rice AL, Estrella NL, Held A, Kandarian SC, Naya FJ (2013) MEF2A regulates the Gtl2-Dio3 microRNA mega-cluster to modulate Wnt signaling in skeletal muscle regeneration. Development. 140(1): 31-42.
- BI 213 Intensive Cell Biology
- BI 553 Molecular Biology 2