Graduate Studies Faculty

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Linda Susan. Musil, PhD

Associate Professor
Admin Unit: SOM-Biochemistry & Molecular Biology Department
Phone: 503 494 1300
Lab Phone: 503 494 1301
Fax: 503 494 8393
Office: BSC 7343
Mail Code: L224
Programs:
Biochemistry & Molecular Biology
Cell & Developmental Biology
Program in Molecular & Cellular Biosciences
Research Interests:
gap junctions lens development growth factor signaling membrane protein assembly and degradation ubiquitin; developmental » PubMed Listing
Preceptor Rotations
Dr. Musil has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Musil has not indicated availability as a mentor at this time.
Profile

Lab Research

Folding, transport, assembly, and degradation of gap junction proteins; regulation of lens development and function by growth factors

Gap junctions are aggregations of intercellular channels that mediate the regulated transfer of ions and small molecules between adjoining cells. Present in virtually all animal cells, gap junctions serve to maintain metabolic continuity within, and relay signals between, adjacent cells. In this capacity, gap junctions are essential to the proper function of tissues throughout the body and are involved in the regulation of cellular differentiation, growth control, and embryonic development. Our lab combines biochemical and molecular biology approaches to study gap junction formation and function using both wild-type and disease-causing mutant forms of gap junction proteins (connexins). Our current emphasis is on the processes of gap junction assembly and degradation, both of which are highly regulated and have several unexpected features. For example, we have shown that a large fraction of newly synthesized, wild-type connexins are degraded shortly after synthesis via ERAD (ER-associated degradation). Induction of the cytosolic heat shock response by mild oxidative or thermal stress inhibits this process, leading to a large increase in gap junction formation and function in otherwise gap junction-deficient cell types (VanSlyke and Musil 2002 J. Cell Biol.,157:381-394; selected as an Editors' Choice in Science, 296:1209-1210). A related interest is elucidating the signal transduction pathways whereby gap junctions influence, and are influenced by, other molecules, especially growth factors. One of the systems that we study is the vertebrate lens, an avascular organ that is uniquely dependent on gap junctions to maintain the metabolic homeostasis required for lens transparency (Le and Musil 2001 J. Cell Biol. 154:197-216). The goal of these studies is to understand how gap junction-mediated cell-cell communication is established and how gap junction assembly and degradation (and therefore function) are modulated in physiological and pathophysiological processes as diverse as parturition, early embryonic development, cataract, the peripheral neuropathy X-linked Charcot-Marie-Tooth disease, oxidative stress, and cancer.
 

Recent Publications:

  1. VanSlyke JK, Musil LS. Degradation of connexins from the plasma membrane is regulated by inhibitors of protein synthesis. Cell Commun Adhes. 2003 Jul-Dec;10(4-6):329-33.

  2. VanSlyke JK, Musil LS. Dislocation and degradation from the ER are regulated by cytosolic stress. J Cell Biol. 2002 Apr 29;157(3):381-94. Epub 2002 Apr 29.

  3. Le AC, Musil LS. A novel role for FGF and extracellular signal-regulated kinase in gap junction-mediated intercellular communication in the lens. J Cell Biol. 2001 Jul 9;154(1):197-216.