Beth L. Pruitt
Dr. Beth Pruitt graduated from the Massachusetts Institute of Technology (MIT) with an S.B. in mechanical engineering. She was supported by a Navy ROTC fellowship at MIT where she learned sailing, leadership, and perseverance. She earned an M.S. in Manufacturing Systems Engineering from Stanford University before serving as an officer in the U.S. Navy. Her first tour was at the engineering headquarters of the Navy nuclear program providing engineering review and oversight to refueling operations. Her second tour was as at the U.S. Naval Academy as an instructor teaching Systems Engineering during the academic year and offshore sailing in the summer. She earned her Ph.D. in Mechanical Engineering at Stanford University where she specialized in MEMS and small-scale metrologies for electrical contacts and was supported by a Hertz Foundation Fellowship. She was a postdoctoral researcher at the Swiss Federal Institute of Technology Lausanne (EPFL) where she worked on polymer MEMS. Dr. Pruitt founded and led the Microsystems Lab at Stanford for 15 years, with research focused on small-scale metrologies for interdisciplinary micromechanics problems in mechanobiology, biomechanics and sensing. She was a visiting professor in Prof. Viola Vogel's Lab for Applied Mechanobiology in the Department of Health Sciences and Technology at ETH, Zurich in 2012. Dr. Pruitt moved to UC Santa Barbara in 2018 to help launch a biological engineering degree program and department. She has been Director of the Center for Bioengineering since 2019. She is an elected Fellow of BMES, AIMBE, and ASME and Senior Member of IEEE. She has been recognized by the NSF CAREER Award, DARPA Young Faculty Award, Denice Denton Leadership Award.
Research [video overview]
I am interested in the biophysics and mechanisms of mechanobiology, i.e., the role of mechanical force in the evolution of structure and function in human pluripotent stem cell derived cardiomyocytes (hPSC-CMs) including related topics of cell adhesion, downstream signaling and mechanoresponse. Our lab has developed technologies to enhance maturity in hiPSC-CMs and make quantitative measurements of cell responses to drugs or in the presence of disease mutations. Our research interests span from custom microtechnologies for small-scale mechanical measurements to questions of how mechanics mediate biological signaling. Normal force sensing, remodeling and load bearing by cells are essential for basic life processes. For example, we study signaling, and mechanisms and forces of cell adhesion in coordinating cell behavior and response to mechanical changes, as well as the development and response of stem cells and cardiac myocytes to mechanical loading. We design and fabricate most of our own tools and sensors and are interested in reliable and quantitative measurements of fundamental biophysics to answer novel questions in the areas of physiology, cardiology, stem cells, cell biology, and neuroscience.
Hart, K. C., Sim, J. Y., Hopcroft, M. A., Cohen, D. J., Tan, J., Nelson, W. J., & Pruitt, B. L. (2021). An Easy-to-Fabricate Cell Stretcher Reveals Density-Dependent Mechanical Regulation of Collective Cell Movements in Epithelia. Cellular and Molecular Bioengineering. doi:10.1007/s12195-021-00689-6
Chirikian, O., Goodyer, W. R., Dzilic, E., Serpooshan, V., Buikema, J. W., McKeithan, W., . . . Wu, S. M. (2021). CRISPR/Cas9-based targeting of fluorescent reporters to human iPSCs to isolate atrial and ventricular-specific cardiomyocytes. Scientific Reports (Nature Publisher Group), 11(1). doi:10.1038/s41598-021-81860-x
Vander Roest, A. S., Liu, C., Morck, M. M., Kooiker, K. B., Jung, G., Song, D., . . . Bernstein, D. (2021). Hypertrophic cardiomyopathy β-cardiac myosin mutation (P710R) leads to hypercontractility by disrupting super relaxed state. Proceedings of the National Academy of Sciences, 118(24), e2025030118. doi:10.1073/pnas.2025030118
Chang, A. C. Y., Pardon, G., Chang, A. C. H., Wu, H., Ong, S.-G., Eguchi, A., . . . Blau, H. M. (2021). Increased tissue stiffness triggers contractile dysfunction and telomere shortening in dystrophic cardiomyocytes. Stem Cell Reports, 16(9), 2169-2181. doi:10.1016/j.stemcr.2021.04.018
Castillo, E. A., Lane, K. V., & Pruitt, B. L. (2020). Micromechanobiology: Focusing on the Cardiac Cell–Substrate Interface. Annual Review of Biomedical Engineering, 22(1), 257-284. doi:10.1146/annurev-bioeng-092019-034950
Wilson, R. E., Denisin, A. K., Dunn, A. R., & Pruitt, B. L. (2020). 3D Microwell Platforms for Control of Single Cell 3D Geometry and Intracellular Organization. Cellular and Molecular Bioengineering. doi:10.1007/s12195-020-00646-9
Blair, C. A., & Pruitt, B. L. (2020). Mechanobiology Assays with Applications in Cardiomyocyte Biology and Cardiotoxicity. Adv Healthc Mater, 9(8), e1901656. doi:10.1002/adhm.201901656
Dainis, A., Zaleta-Rivera, K., Ribeiro, A., Chang, A. C. H., Shang, C., Lan, F., . . . Ashley, E. (2020). Silencing of MYH7 ameliorates disease phenotypes in human iPSC-cardiomyocytes. Physiological Genomics, 52(7), 293-303. doi:10.1152/physiolgenomics.00021.2020
Nekimken, A. L., Pruitt, B. L., & Goodman, M. B. (2020). Touch-induced mechanical strain in somatosensory neurons is independent of extracellular matrix mutations in Caenorhabditis elegans. Molecular Biology of the Cell, 31(16), 1735-1743. doi:10.1091/mbc.E20-01-0049
Garcia, M. A., Sadeghipour, E., Engel, L., Nelson, W. J., & Pruitt, B. L. (2020). MEMS Device for Applying Shear and Tension to an Epithelium Combined with Fluorescent Live Cell Imaging. Journal of Micromechanics and Microengineering. Retrieved from doi:10.1088/1361-6439/abb12c
Engel, L., Gaietta, G., Dow, L. P., Swif, M. F., Pardon, G., Volkmann, N.; Weis, W. I.; Hanein, D.;, B. L. (2019). Extracellular matrix micropatterning technology for whole cell cryogenic electron microscopy studies. Journal of Micromechanics and Microengineering, 29(11), 115018. doi:10.1088/1361-6439/ab419a
Moeller J,* Denisin AK*, Sim JY, Wilson RE, Ribeiro AJS, Pruitt BL. Controlling cell shape on hydrogels using lift-off protein patterning. PLoS One. 2018 Jan 3;13(1): e0189901. doi:10.1371/journal.pone.0189901
Ribeiro, A. J. S., Schwab, O., Mandegar, M. A., Ang, Y. S., Conklin, B. R., Srivastava, D., & Pruitt, B. L. (2017). Multi-Imaging Method to Assay the Contractile Mechanical Output of Micropatterned Human iPSC-Derived Cardiac Myocytes. Circ Res, 120(10), 1572-1583. doi:10.1161/circresaha.116.310363
Benham-Pyle, B. W., Sim, J. Y., Hart, K. C., Pruitt, B. L., & Nelson, W. J. (2016). Increasing β-catenin/Wnt3A activity levels drive mechanical strain-induced cell cycle progression through mitosis. Elife, 5, e19799. doi:10.7554/eLife.19799
Ribeiro, A. J., Ang, Y. S., Fu, J. D., Rivas, R. N., Mohamed, T. M., Higgs, G. C., Srivastava, D., & Pruitt, B. L. (2015). Contractility of single cardiomyocytes differentiated from pluripotent stem cells depends on physiological shape and substrate stiffness. Proc Natl Acad Sci U S A, 112(41), 12705-12710. doi:10.1073/pnas.1508073112
Benham-Pyle, B. W., Pruitt, B. L., & Nelson, W. J. (2015). Mechanical strain induces E-cadherin–dependent Yap1 and β-catenin activation to drive cell cycle entry. Science, 348(6238), 1024-1027. doi:10.1126/science.aaa4559
Sim, J. Y., Moeller, J., Hart, K. C., Ramallo, D., Vogel, V., Dunn, A. R., Nelson, W. J., & Pruitt, B. L. (2015). Spatial distribution of cell–cell and cell–ECM adhesions regulates force balance while maintaining E-cadherin molecular tension in cell pairs. Molecular Biology of the Cell, 26(13), 2456-2465. doi:10.1091/mbc.E14-12-1618
B. W. Benham-Pyle, J. Y. Sim, K. C. Hart, B. L. Pruitt, and W. J. Nelson, "Increasing β-catenin/Wnt3A activity levels drive mechanical strain-induced cell cycle progression through mitosis," eLife, vol. 5, p. e19799, 2016/10/26 2016.