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Michael J Galko, Ph.D.

Present Title & Affiliation

Primary Appointment

Associate Professor, Department of Biochemistry and Molecular Biology, Division of Basic Science Research, The University of Texas MD Anderson Cancer Center, Houston, TX

Bio Statement

 Overview of Research Interests  Multicellular organisms have evolved a variety of tissue repair responses to cope with tissue damage.  Some of these responses (wound closure) are aimed at restoring structure and function to the damaged tissue(s) while others (inflammation and nociceptive sensitization) are aimed at protecting the organism from further infection or injury. My laboratory is interested in identifying the elusive signals that initiate and terminate different aspects of the organismal tissue repair response, as well as the genes that are required to execute each specific response.  Ultimately, we wish to understand in molecular detail how the activities of diverse damage-responsive cell types are coordinated in space and time to give a functional tissue repair program. To pursue these interests we have developed a variety of tissue repair/response assays in the highly genetically tractable model organism, Drosophila melanogaster and are focusing our efforts on three critical responses: epidermal wound closure, inflammation (recruitment of blood cells to the site of injury), and nociceptive sensitization (lowering of the threshold for sensing painful stimuli following injury).  Given that tissue repair responses are an ancient survival mechanism of multicellular animals, we expect that the functional importance of many of these genes we identify will be conserved between flies and vertebrates. Below is a summary of some of the projects ongoing in the lab. 

Research Interests

 Cellular and genetic analysis of epidermal wound closure and wound-induced epidermal cell-cell fusion: To study epidermal healing we developed wound healing assays using Drosophila larvae (PloS Biology, 2004) and showed that epidermal repair proceeds by a similar sequence of steps and involves functionally equivalent cell types to those in vertebrates. Some of the hallmarks of the Drosophila repair process include recruitment of 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 developed transgenic larvae that allow live visualization of epidermal wound responses and enable the performance of large-scale genetic screens designed to identify the complement of Drosophila genes that are required for various steps of epidermal healing. These screens are ongoing.

 Cellular and genetic analysis of wound-induced inflammation (blood cell recruitment):   Circulating blood cells are rapidly recruited to epidermal wound in Drosophila larvae (PNAS, 2008). Remarkably, this recruitment occurs through a similar cellular mechanism (adhesive capture) as in vertebrates. We have created transgenic larvae that permit simultaneous live monitoring of the epidermal wound and circulating blood cells and we are now using these larvae to perform a genetic screen for blood cell factors required for proper adhesion to the wound site. We are hopeful that this approach will allow us to identify adhesion proteins responsible for binding of blood cells to damaged tissue- these factors may represent pattern-recognition receptors for “altered self” tissue.

 Establishment of a genetically tractable model of tissue damage-induced nociceptive sensitization: Local alterations in nociception (pain sensation) are a hallmark of tissue damage in vertebrate organisms. Nociceptive sensitization can involve a lowering of the pain threshold such that previously non-noxious stimuli are perceived as painful (allodynia), as well as a faster or exaggerated response to supra-threshold stimuli (hyperalgesia).  Sensitization serves to foster behaviors that protect sites of tissue damage while they heal.  We have shown that both hyperalgesia and allodynia develop following UV irradiation in Drosophila larvae and that allodynia depends on a conserved tumor necrosis factor (TNF)-like cytokine that is produced by the irradiated epidermal cells and on a TNF receptor-like protein present on nociceptive sensory neurons (Current Biology, 2009). We are currently using genetic and cell biological approaches to define the molecular consequences of activating the TNF-receptor in sensory neurons so that we can understand how tissue damage leads to adaptive alterations in the behavioral response threshold of nociceptive sensory neurons.

Office Address

The University of Texas MD Anderson Cancer Center
1515 Holcombe Blvd.
Unit Number: 1000
Houston, TX 77030
Room Number: S11.8316A
Phone: 713-792-9182
Fax: 713-834-6291
Email: mjgalko@mdanderson.org

Education & Training

Degree-Granting Education

1999 University of California at San Francisco, Mentor Dr. Marc Tessier-Lavigne, San Francisco, CA, PHD, with Dr. Marc Tessier-Lavigne, Cell Biology
1991 University of Texas at Austin, Austin, TX, BS, Biology

Postgraduate Training

6/2000-11/2005 Research Fellowship, with Dr. Mark Krasnow, Stanford University School of Medicine, Stanford, CA

Experience/Service

Academic Appointments

Assistant Professor, Department of Biochemistry and Molecular Biology, Division of Basic Science Research, The University of Texas MD Anderson Cancer Center, Houston, TX, 12/2005-8/2012

Selected Publications

Peer-Reviewed Original Research Articles

1. Babcock DT, Shi S, Jo J, Shaw M, Gutstein HB, Galko MJ. Hedgehog signaling regulates nociceptive sensitization. Curr Biol 21(18):1525-33, 9/2011. e-Pub 9/2011. PMID: 21906949.
2. Lesch C, Jo J, Wu Y, Fish GS, Galko MJ. A Targeted UAS-RNAi Screen in Drosophila Larvae Identifies Wound Closure Genes Regulating Distinct Cellular Processes. Genetics 186(3):943-57, 11/2010. e-Pub 9/2010. PMCID: PMC2975283.
3. Wu Y, Brock AR, Wang Y, Fujitani K, Ueda R, Galko MJ. A blood-borne PDGF/VEGF-like ligand initiates wound-induced epidermal cell migration in Drosophila larvae. Curr Biol 19(17):1473-7, 9/15/2009. e-Pub 7/30/2009. PMCID: PMC2783944.
4. Babcock DT, Landry C, Galko MJ. Cytokine signaling mediates UV-induced nociceptive sensitization in Drosophila larvae. Curr Biol 19(10):799-806, 5/2009. e-Pub 4/2009. PMID: 19375319.
5. Babcock DT, Brock AR, Fish GS, Wang Y, Perrin L, Krasnow MA, Galko MJ. Circulating blood cells function as a surveillance system for damaged tissue in Drosophila larvae. Proc Natl Acad Sci U S A 105(105):10017-10022, 7/2008. e-Pub 7/2008. PMCID: PMC2474562.
6. Stramer B, Wood W, Galko MJ, Redd MJ, Jacinto A, Parkhurst SM, Martin P. Live imaging of wound inflammation in Drosophila embryos reveals key roles for small GTPases during in vivo cell migration. J Cell Biol 168(4):567-73, 2/14/2005. e-Pub 2/7/2005. PMCID: PMC2171743.
7. Galko MJ, Krasnow MA. Cellular and genetic analysis of wound healing in Drosophila larvae. PLoS Biol 2(8):e239, 8/2004. e-Pub 7/20/2004. PMCID: PMC479041.
8. Galko MJ, Tessier-Lavigne M. Function of an axonal chemoattractant modulated by metalloprotease activity. Science 289(289):1365-1367, 8/25/2000. PMID: 10958786.
9. Galko MJ, Tessier-Lavigne M. Biochemical characterization of netrin-synergizing activity. J Biol Chem 275(11):7832-8, 3/17/2000. PMID: 10713098.
10. Headley V, Hong M, Galko M, Payne SM. Expression of Aerobactin genes by Shigella Flexneri during extracellular and intracellular growth. Infect Immun 65(65):818-821, 2/1997. PMCID: PMC176133.
11. Serafini T, Kennedy TE, Galko MJ, Mirzayan C, Jessell TM, Tessier-Lavigne M. The netrins define a family of axon outgrowth-promoting proteins homologous to C. elegans UNC-6. Cell 78(78):409-424, 8/12/1994. PMID: 8062384.

Invited Articles

1. Babcock DT, Galko MJ. Two sides of the same coin no longer: Genetic separation of nociceptive sensitization responses. Commun Integr Biol 2(6):1-3, 11/2009. PMCID: PMC2829827.
2. Brock AR, Babcock DT, Galko MJ. Active cop, passive cop: developmental stage-specific modes of wound-induced blood cell recruitment in Drosophila. Fly (Austin) 2(6):303-305, Nov-Dec, 11/2008. e-Pub 11/13/2008. PMID: 19077535.

Last updated: 3/17/2014