Francisco J. Naya

About

Francisco J. Naya is an Associate Professor of Biology and the Director of Graduate Studies at Boston University. His research focuses on gene regulation in muscle development and disease, utilizing a systems-level approach to investigate complex gene regulatory networks involved in cardiac and skeletal muscle differentiation. His work emphasizes understanding the role of noncoding RNAs, including microRNAs, small nucleolar RNAs, and long noncoding RNAs, in muscle differentiation, regeneration, and disease mechanisms. Naya's research has identified the significance of the Dlk1-Dio3 noncoding RNA locus in skeletal muscle differentiation, regeneration, and cardiomyocyte proliferation. He has demonstrated that the long noncoding RNA Meg3 regulates myoblast plasticity and muscle regeneration through epithelial mesenchymal transition, and that the entire Dlk1-Dio3 ncRNA cluster coordinates mitochondrial metabolism and chromatin structure to maintain proper myogenic cell states. His ongoing investigations utilize genome-wide transcriptomic and genomic approaches to elucidate the multifunctional gene regulatory roles of this imprinted ncRNA locus.

Research topics

• Cell biology
• Biology
• Genetics
• Neuroscience
• Cardiology
• Chemistry
• Medicine
• Physics
• Endocrinology

Selected publications

• The Function of the MEF2 Family of Transcription Factors in Cardiac Development, Cardiogenomics, and Direct Reprogramming

  Journal of Cardiovascular Development and Disease · 2016-08-11 · 106 citations

  articleOpen accessSenior authorCorresponding

  Proper formation of the mammalian heart requires precise spatiotemporal transcriptional regulation of gene programs in cardiomyocytes. Sophisticated regulatory networks have evolved to not only integrate the activities of distinct transcription factors to control tissue-specific gene programs but also, in many instances, to incorporate multiple members within these transcription factor families to ensure accuracy and specificity in the system. Unsurprisingly, perturbations in this elaborate tran…

  PublisherOA PDFDOI

• MEF2 Transcription Factors Regulate Distinct Gene Programs in Mammalian Skeletal Muscle Differentiation

  Journal of Biological Chemistry · 2014-11-22 · 101 citations

  articleOpen accessSenior authorCorresponding

  Skeletal muscle differentiation requires precisely coordinated transcriptional regulation of diverse gene programs that ultimately give rise to the specialized properties of this cell type. In Drosophila, this process is controlled, in part, by MEF2, the sole member of an evolutionarily conserved transcription factor family. By contrast, vertebrate MEF2 is encoded by four distinct genes, Mef2a, -b, -c, and -d, making it far more challenging to link this transcription factor to the regulation of…

  PublisherOA PDFDOI

• MicroRNAs in the Myocyte Enhancer Factor 2 (MEF2)-regulated Gtl2-Dio3 Noncoding RNA Locus Promote Cardiomyocyte Proliferation by Targeting the Transcriptional Coactivator Cited2

  Journal of Biological Chemistry · 2015-08-04 · 62 citations

  articleOpen accessSenior authorCorresponding

  Understanding cell cycle regulation in postmitotic cardiomyocytes may lead to new therapeutic approaches to regenerate damaged cardiac tissue. We have demonstrated previously that microRNAs encoded by the Gtl2-Dio3 noncoding RNA locus function downstream of the MEF2A transcription factor in skeletal muscle regeneration. We have also reported expression of these miRNAs in the heart. Here we investigated the role of two Gtl2-Dio3 miRNAs, miR-410 and miR-495, in cardiac muscle. Overexpression of mi…

  PublisherOA PDFDOI

• Antagonistic regulation of cell-cycle and differentiation gene programs in neonatal cardiomyocytes by homologous MEF2 transcription factors

  Journal of Biological Chemistry · 2017-05-05 · 43 citations

  articleOpen accessSenior authorCorresponding

  Cardiomyocytes acquire their primary specialized function (contraction) before exiting the cell cycle. In this regard, proliferation and differentiation must be precisely coordinated for proper cardiac morphogenesis. Here, we have investigated the complex transcriptional mechanisms employed by cardiomyocytes to coordinate antagonistic cell-cycle and differentiation gene programs through the molecular dissection of the core cardiac transcription factor, MEF2. Knockdown of individual MEF2 proteins…

  PublisherDOI

• Transcriptome Analysis of Cardiac Hypertrophic Growth in MYBPC3-Null Mice Suggests Early Responders in Hypertrophic Remodeling

  Frontiers in Physiology · 2018-10-25 · 39 citations

  articleOpen access

  Rationale– With a prevalence of 1 in 200 individuals, hypertrophic cardiomyopathy (HCM) is thought to be the most common genetic cardiac disease, with potential outcomes that include severe hypertrophy, heart failure, and sudden cardiac death. Though much research has furthered our understanding of how HCM-causing mutations in genes such as cardiac myosin binding protein C (MYBPC3) impair contractile function, it remains unclear how such dysfunction leads to hypertrophy and/or arrhythmias, which…

  PublisherDOI

Recent grants

• MEF2 Function in Cardiac Muscle Development

  NIH · $3.3M · 2003–2016

Frequent coauthors

• Ming‐Jer Tsai

  National Tsing Hua University

  21 shared

• Andrew B. Leiter

  17 shared

• H. Mutoh

  Hokuriku Electric Power Company (Japan)

  9 shared

• Hiroyuki Mutoh

  The University of Tokyo

  8 shared

• Christine Snyder

  7 shared

• Sarah A. McCalmon

  Pacific Biosciences (United States)

  7 shared

• William T. Pu

  Boston Children's Hospital

  7 shared

• Junko Nishitani

  6 shared

Similar researchers at Boston University

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• Jerry Chenh-96
• Richard B. Primackh-83