Laurie A. Boyer

Laurie A. Boyer

Professor of Biology and Biological Engineering; Co-Undergraduate Officer

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

lboyer@mit.edu

Email

Building 68 - Koch Biology Building

Location

Lab Website
Valerie Corapi

Assistant

617-324-4036

Assistant Phone

Education

  • PhD, 2001, University of Massachusetts Medical School
  • BS, 1990, Biomedical Science, Framingham State University

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. Learn More

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. Correction: Metabolic modulation to improve MSC expansion and therapeutic potential for articular cartilage repair. Tee, CA, Roxby, DN, Othman, R, Denslin, V, Bhat, KS, Yang, Z, Han, J, Tucker-Kellogg, L, Boyer, LA. 2024. Stem Cell Res Ther 15, 403.
    doi: 10.1186/s13287-024-04048-wPMID:39511618
  2. Metabolic modulation to improve MSC expansion and therapeutic potential for articular cartilage repair. Tee, CA, Roxby, DN, Othman, R, Denslin, V, Bhat, KS, Yang, Z, Han, J, Tucker-Kellogg, L, Boyer, LA. 2024. Stem Cell Res Ther 15, 308.
    doi: 10.1186/s13287-024-03923-wPMID:39285485
  3. Expansion of human bone marrow-derived mesenchymal stromal cells with enhanced immunomodulatory properties. Neo, SH, Her, Z, Othman, R, Tee, CA, Ong, LC, Wang, Y, Tan, I, Tan, J, Yang, Y, Yang, Z et al.. 2023. Stem Cell Res Ther 14, 259.
    doi: 10.1186/s13287-023-03481-7PMID:37726837
  4. HiExM: high-throughput expansion microscopy enables scalable super-resolution imaging. Day, JH, Santina, CMD, Maretich, P, Auld, AL, Schnieder, KK, Shin, T, Boyden, ES, Boyer, LA. 2024. bioRxiv , .
    doi: 10.1101/2023.02.07.527509PMID:36798312
  5. A dual role for H2A.Z.1 in modulating the dynamics of RNA polymerase II initiation and elongation. Mylonas, C, Lee, C, Auld, AL, Cisse, II, Boyer, LA. 2021. Nat Struct Mol Biol 28, 435-442.
    doi: 10.1038/s41594-021-00589-3PMID:33972784
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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
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