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| Faculty Research Interests | M.D. Anderson | GSBS

MICHAEL GALKO, PH.D.
Assistant Professor

Department of Biochemistry and Molecular Biology
Room: S9.8316A
E-mail: mjgalko@mdanderson.org
Telephone: 713-792-9182 / Fax: 713-792-0346
Lab: 713-792-9132

Research interests

  • molecular genetics of tissue repair
  • Drosophila genetics
  • cell migration
  • cell signaling and signal transduction
 

Wound healing, or the ability to repair damaged tissues, is a fundamental survival mechanism of multicellular organisms. My laboratory is interested in identifying the elusive signals that initiate and terminate different aspects of the wound healing program, as well as the genes that are required to execute the repair program. Proper wound healing following epidermal injury in vertebrates involves the coordinated action of a variety of cell types, including the epidermal cells themselves, underlying dermal fibroblasts, immune-responsive blood cells, and the local vasculature. To study wound healing in a genetically tractable model organism we developed wound healing assays using Drosophila larvae and showed that epidermal repair proceeds by a similar sequence of steps and involves functionally equivalent cell types to those in vertebrates. Ultimately, we wish to understand in molecular detail how the activities of diverse wound-responsive cell types are coordinated in space and time to give a functional tissue repair program. Some of the hallmarks of the Drosophila repair process include rapid hemostasis (scab formation), recruitment of immune-responsive blood cells, epidermal cell orientation and fusion, epidermal activation of the Jun N-terminal kinase (JNK) signaling pathway, JNK-dependent reepithelialization of the wound site, and clearance of cell debris and scab material. Recently, we have developed transgenic larvae that allow live visualization of epidermal wound responses. These larvae enable the performance of large-scale genetic screens designed to identify the complement of Drosophila genes that are required for various steps of the healing process. The sophisticated genetics of Drosophila, as well as complementary genomic and biochemical experiments, will permit detailed analysis of the precise function of these genes. Given that wound healing is an ancient survival mechanism, we expect that the functional importance of many of these genes will be conserved between flies and vertebrates.


Recent publications
  • Babcock, D. T., Brock, A. R., Fish, G. S., Wang, Y., Perrin, L., Krasnow, M. A., and Galko, M. J. (2008). Circulating blood cells function as a surveillance system for damaged tissue in Drosophila larvae. In press at PNAS.

  • Stramer, B. M., Wood, W., Galko, M. J., Redd, M., Jacinto, A., Parkhurst, S. M., and Martin, P. (2005). Live imaging of wound inflammation in Drosophila embryos reveals key roles for small GTPase during in vivo cell migration. J. Cell Biol. 168:567–573.

  • Galko, M. J. and Krasnow, M. A. (2004). Cellular and genetic analysis of wound healing in Drosophila. PLoS Biology 2(8):e239.

    Commentaries on this work:
    - JCB/ASCB meeting review (prepublication)
    - Nature research highlights
    - Faculty of 1000: rated “Exceptional”
    - Howard Hughes Medical Institute (1)

    - Howard Hughes Medical Institute (2)
    - American Scientist magazine

  • Galko, M. J., and Tessier-Lavigne, M. (2000). Function of an axonal chemoattractant modulated by metalloprotease activity. Science 289:1365–1367.

  • Galko, M. J., and Tessier-Lavigne, M. (2000). Biochemical characterization of a netrin-synergizing activity. Journal of Biological Chemistry 275:7832–7838.

  • Serafini, T., Kennedy, T., Galko, M. J., Mirzayan, C., Jessel, T. M., and Tessier-Lavigne, M. (1994). The netrins define a family of axon outgrowth-promoting proteins homologous to C. elegans UNC-6. Cell 78:409–424.


Mailing Address:
Department of Biochemistry and Molecular Biology, Unit 1000
U.T. M.D. Anderson Cancer Center
1515 Holcombe Boulevard
Houston, TX 77030

Last updated 05/21/2008