Beth L. Pruitt

Biography

Dr. Pruitt moved to UC Santa Barbara in 2018 to help launch a biological engineering degree program and our new Bioengineering Department. She has served as the founding chair since 2021. 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. 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.

Research [video overview]

Broadly speaking, we are interested in all things mechanobiology, i.e., the role of mechanical perturbations in the evolution of mechanosignaling, structure and function, including related topics of cell adhesion, cell and matrix remodeling, and downstream changes in genotype and phenotype. Normal force sensing, remodeling and load bearing by cells are essential for basic life processes. To study these processes, our lab develops technologies to enhance maturity in human pluripotent stem cell derived cardiomyocytes (hPSC-CMs), to manipulate hiPSC-CM and other cell types in "micro physiological systems), and to make quantitative measurements of cell responses to drugs, mechanical stimuli like stiffness or stretch, 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. We design and fabricate most of our own tools and  custom analysis methods, 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. 

Selected Publications

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.