Laurie A. Boyer

Laurie A. Boyer

Associate Professor of Biology

Laurie A. Boyer investigates the gene regulatory mechanisms that drive heart development and regeneration using embryonic stem cells and mouse models.

617-324-3335

Phone

68-230

Office

Adjovi Koene

Assistant

617-324-4026

Assistant Phone

Education

PhD 2001, University of Massachusetts Medical School

Research Summary

We investigate how complex circuits of genes are regulated to produce robust developmental outcomes particularly during heart development. A main focus is to determine how DNA is packaged into chromatin, and how ATP-dependent chromatin remodelers modify this packaging to control lineage commitment. We are now applying these principles to develop methods to stimulate repair of damaged cardiac tissue (e.g., regeneration). Our ability to combine genomic, genetic, biochemical, and cell biological approaches both in vitro and in vivo as well as ongoing efforts to use tissue engineering to model the 3D architecture of the heart will ultimately allow us to gain a systems level and quantitative understanding of the regulatory circuits that promote normal heart development and how faulty regulation can lead to disease.

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Awards

  • Medicine by Design Distinguished Lecture, 2017
  • Cardiovascular Rising Star Distinguished Lecture, 2017
  • American Heart Association Innovative Research Award, 2013
  • Irvin and Helen Sizer Career Development Award, 2012
  • Smith Family Award for Excellence in Biomedical Science, 2009
  • Massachusetts Life Sciences Center New Investigator Award, 2008
  • Pew Scholars Award in the Biomedical Sciences, 2008
  • Honorary Doctorate, Framingham State College, 2007
  • The Scientific American World’s 50 top leaders in research, business or policy, 2006

Key Publications

  1. A G-Rich Motif in the lncRNA Braveheart Interacts with a Zinc-Finger Transcription Factor to Specify the Cardiovascular Lineage. Xue, Z, Hennelly, S, Doyle, B, Gulati, AA, Novikova, IV, Sanbonmatsu, KY, Boyer, LA. 2016. Mol. Cell 64, 37-50.
    doi: 10.1016/j.molcel.2016.08.010PMID:27618485
  2. Discovery and validation of sub-threshold genome-wide association study loci using epigenomic signatures. Wang, X, Tucker, NR, Rizki, G, Mills, R, Krijger, PH, de Wit, E, Subramanian, V, Bartell, E, Nguyen, XX, Ye, J et al.. 2016. Elife 5, .
    doi: 10.7554/eLife.10557PMID:27162171
  3. H2A.Z.1 Monoubiquitylation Antagonizes BRD2 to Maintain Poised Chromatin in ESCs. Surface, LE, Fields, PA, Subramanian, V, Behmer, R, Udeshi, N, Peach, SE, Carr, SA, Jaffe, JD, Boyer, LA. 2016. Cell Rep 14, 1142-1155.
    doi: 10.1016/j.celrep.2015.12.100PMID:26804911
  4. Braveheart, a long noncoding RNA required for cardiovascular lineage commitment. Klattenhoff, CA, Scheuermann, JC, Surface, LE, Bradley, RK, Fields, PA, Steinhauser, ML, Ding, H, Butty, VL, Torrey, L, Haas, S et al.. 2013. Cell 152, 570-83.
    doi: 10.1016/j.cell.2013.01.003PMID:23352431
  5. Dynamic and coordinated epigenetic regulation of developmental transitions in the cardiac lineage. Wamstad, JA, Alexander, JM, Truty, RM, Shrikumar, A, Li, F, Eilertson, KE, Ding, H, Wylie, JN, Pico, AR, Capra, JA et al.. 2012. Cell 151, 206-20.
    doi: 10.1016/j.cell.2012.07.035PMID:22981692

Recent Publications

  1. A G-Rich Motif in the lncRNA Braveheart Interacts with a Zinc-Finger Transcription Factor to Specify the Cardiovascular Lineage. Xue, Z, Hennelly, S, Doyle, B, Gulati, AA, Novikova, IV, Sanbonmatsu, KY, Boyer, LA. 2016. Mol. Cell 64, 37-50.
    doi: 10.1016/j.molcel.2016.08.010PMID:27618485
  2. Microfluidic device for the formation of optically excitable, three-dimensional, compartmentalized motor units. Uzel, SG, Platt, RJ, Subramanian, V, Pearl, TM, Rowlands, CJ, Chan, V, Boyer, LA, So, PT, Kamm, RD. 2016. Sci Adv 2, e1501429.
    doi: 10.1126/sciadv.1501429PMID:27493991
  3. Discovery and validation of sub-threshold genome-wide association study loci using epigenomic signatures. Wang, X, Tucker, NR, Rizki, G, Mills, R, Krijger, PH, de Wit, E, Subramanian, V, Bartell, E, Nguyen, XX, Ye, J et al.. 2016. Elife 5, .
    doi: 10.7554/eLife.10557PMID:27162171
  4. H2A.Z.1 Monoubiquitylation Antagonizes BRD2 to Maintain Poised Chromatin in ESCs. Surface, LE, Fields, PA, Subramanian, V, Behmer, R, Udeshi, N, Peach, SE, Carr, SA, Jaffe, JD, Boyer, LA. 2016. Cell Rep 14, 1142-1155.
    doi: 10.1016/j.celrep.2015.12.100PMID:26804911
  5. Lncing epigenetic control of transcription to cardiovascular development and disease. Rizki, G, Boyer, LA. 2015. Circ. Res. 117, 192-206.
    doi: 10.1161/CIRCRESAHA.117.304156PMID:26139858
  6. H2A.Z: a molecular rheostat for transcriptional control. Subramanian, V, Fields, PA, Boyer, LA. 2015. F1000Prime Rep 7, 01.
    doi: 10.12703/P7-01PMID:25705384
  7. Integrative analysis of 111 reference human epigenomes. Roadmap Epigenomics Consortium, Kundaje, A, Meuleman, W, Ernst, J, Bilenky, M, Yen, A, Heravi-Moussavi, A, Kheradpour, P, Zhang, Z, Wang, J et al.. 2015. Nature 518, 317-30.
    doi: 10.1038/nature14248PMID:25693563
  8. Polycomb Repressive Complex 2 regulates lineage fidelity during embryonic stem cell differentiation. Thornton, SR, Butty, VL, Levine, SS, Boyer, LA. 2014. PLoS ONE 9, e110498.
    doi: 10.1371/journal.pone.0110498PMID:25333635
  9. Distal enhancers: new insights into heart development and disease. Wamstad, JA, Wang, X, Demuren, OO, Boyer, LA. 2014. Trends Cell Biol. 24, 294-302.
    doi: 10.1016/j.tcb.2013.10.008PMID:24321408
  10. H2A.Z acidic patch couples chromatin dynamics to regulation of gene expression programs during ESC differentiation. Subramanian, V, Mazumder, A, Surface, LE, Butty, VL, Fields, PA, Alwan, A, Torrey, L, Thai, KK, Levine, SS, Bathe, M et al.. 2013. PLoS Genet. 9, e1003725.
    doi: 10.1371/journal.pgen.1003725PMID:23990805
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