Bruce L. Patton earned his Ph.D. at the California Institute of Technology (Caltech) in 1991, under the direction of Dr. Mary B. Kennedy. Patton did postdoctoral research, in the laboratory of Dr. Joshua R. Sanes at Washington University in St. Louis. He became Assistant Scientist at the CROET, at Oregon Health & Science University, in 1999. Patton did his undergraduate studies at Brandeis University, where he was introduced to neurobiology in the laboratory of Dr. Irwin B. Levitan.

The wiring of the nervous system during development is coordinated by a web of molecular signals exchanged between neurons, the target cells they innervate, and the glial cells which ensheath them. The Patton lab is studying signals exchanged by motor neurons, skeletal muscle fibers, and Schwann cells, which coordinate development in the neuromuscular system. Current research is focused on a series of specialized extracellular matrix proteins, isoforms of laminin, co-discovered by Drs. Patton, Jeffrey Miner (Washington University), Arlene Chiu, and Joshua Sanes (Harvard). Patton's group has found these proteins play several key roles in neuromuscular development. Two isoforms of laminin control myelination in developing nerves, by controlling both Schwann cell proliferation and differentiation. In addition, three synapse-specific forms of laminin made by muscle fibers organize nerve-terminal formation by motor axons. Finally, an extrasynaptic form of laminin prevents new muscle fibers from "popping" when they begin contractions. Loss of this type of laminin is the primary cause of Congenital Muscular Dystrophy in humans, and a similar disorder in dogs and cats. Continuing work is aimed at understanding how laminin-derived signals intersect with other signaling pathways to coordinate the temporal schedule of cellular differentiation in nerve and muscle. We are also asking whether functional redundancy may allow synaptic laminins to prevent muscular dystrophy in children lacking extrasynaptic laminins. Approaches include mammalian genetic manipulation in vivo, cell-biological response studies in vitro, and nanotechnology applications to manipulate cell:surface contacts. Clinical motivations include nerve regeneration, myasthenia, muscular dystrophy, and dysmyelinating neuropathy.

Miner, J.H., Go, G., Cunningham, J., Patton, B.L., and Jarad, G. (2006) Transgenic isolation of skeletal muscle and kidney defects in lamiin β2 mutant mice: Implications for Pierson syndrome. Development 133:967-75. Abstract

Shannon, M.B., Patton, B.L., Harvey, S.J., Miner, J.H. (2006) A Hypomorphic Mutation in the Mouse Laminin α5 Gene Causes Polycystic Kidney Disease. J. Am. Soc. Nephrology 17:1913-1922. Abstract

Yang, D., Bierman, J., Tarumi, Y.S., Zhong, Y-P., Rangwala, R., Proctor, T.M., Miyagoe-Suzuki, Y., Takeda, S., Miner, J.H., Sherman, L.S., Gold, B.G., and Patton, B.L. (2005) Coordinate control of axon defasciculation and myelination by laminin-2 and -8. J Cell Biol. Feb 14;168(4):655-66. Abstract

Patton, B.L. and Burgess, R. W. (2005) Synaptogenesis. In Developmental Neurobiology, 4th Ed. (Editors M.S. Rao and M. Jacobson), Kluwer Academic/Plenum Publishers, New York.

Yurchenco, P.D., Amenta, P.S., and Patton, B.L. (2004) Basement membrane assembly, stability, and activities seen through a developmental lens. Matrix Biol. 22(7):521-38. Abstract

Patton, B.L. (2003) Basal lamina and the organization of neuromuscular synapses. J. Neurocytol. 32(5-8):883-903. Abstract

Patton, B.L., Cunningham, J.M., Thyboll, J., Kortes-maa, J., Westerblad, H., Edstrom, L., Tryggvason, K., and Sanes, J.R. (2001) Properly formed but improperly localized synaptic specializations in the absence of laminin a4. Nature Neuroscience 4, 597-604. Abstract

Patton, B.L., Connolly, A.M., Martin, P.T., Cunningham, J.M., Shobhna, M., Pestronk, A., Miner, J.H., and Sanes, J.R. (1999) Distribution of ten laminin chains in dystrophic and regenerating muscles. Neuromuscular Disorders 9, 423-433. Abstract

Patton, B.L., Chiu, A.Y., and Sanes, J.R. (1998) Synaptic laminin prevents glial entry into the synaptic cleft. Nature 393, 698-701. Abstract