About Dr. Galko
Dr. Galko obtained his Ph.D. with Dr. Marc Tessier-Lavigne at the University of California San Francisco. His graduate studies focused on molecular and cellular mechanisms of axon guidance and his work demonstrated that guidance receptors are shed by metalloproteases as a functional guidance mechanism. Dr. Galko performed his postdoctoral studies with Dr. Mark Krasnow, at the Stanford University School of Medicine where he developed a novel genetically tractable system to study epidermal wound healing using fruit fly (Drosophila melanogaster) larvae. This system has led to the identification of conserved cellular and molecular mechanisms of wound healing. During his postdoctoral studies Dr. Galko was funded by fellowships from the American Heart Association and the Arnold and Mabel Beckman Foundation. Dr. Galko has run his research lab at the MD Anderson Cancer Center since late 2005. His lab is focused on understanding how organisms respond to tissue injury. About half of his research effort is devoted to understanding cellular and molecular mechanisms of wound-induced epithelial repair and accompanying inflammatory processes. A second more recent behavioral focus is on identifying the cellular and molecular mechanisms by which animals become locally hypersensitive to sensory stimuli following injury. The work in Dr. Galko’s lab is helping to identify conserved genes that control diverse organismal responses to injury. Dr. Galko’s lab has been funded by the American Heart Association, the March of Dimes, multiple grants from the National Institutes of Health (NINDS and NIGMS), and he was one of the initial MD Anderson R. Lee Clark Fellows in Basic Research.
Visit Dr. Galko's Lab Website.
Director, Genes and Development Graduate Program, The University of Texas MD Anderson Cancer Center, Houston, TX
Associate Professor, Department of Genetics, Division of Basic Science Research, The University of Texas MD Anderson Cancer Center, Houston, TX
Director, Division of Genes and Development Graduate Program, The University of Texas MD Anderson Cancer Center, Houston, TX
Drosophila genetics Tissue repair Pain sensitization Cell migration
Cellular and genetic analysis of epidermal wound closure responses: 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 screening for the complement of Drosophila genes that are required for various steps of epidermal healing (Genetics, 2010). We also identified a conserved receptor tyrosine kinase and ligand (Current Biology, 2009), related to the Vascular Endothelial Growth Factor Receptor signaling cassette, that are required for healing. Our genetic screen is an ongoing effort and we continue to identify new genes (Journal of Cell Science, 2013) as well as characterize the mechanism of action of genes that we have previously identified. In a relatively new effort we have begun to look at the epigenetic regulation of wound closure (Regeneration, 2014).
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 escape 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). Since this initial demonstration that nociceptive sensitization can be modeled in Drosophila we have been using the full genetic power of this system to identify new assays (JoVE, 2012) and new genes (Current Biology, 2011) that regulate nociceptive sensitization. Our most interesting finding to date is that the Hedgehog signaling pathway, which regulates diverse aspects of patterning and cell fate specification during development, also plays a conserved role in regulating the responses of sensory neurons to painful stimuli (Current Biology, 2011). We are continuing to study the mechanisms of TNF- and Hh-induced sensitization, to screen for new genetic regulators of thermal allodynia and hyperalgesia, and to develop new assays for how Drosophila larvae respond to noxious cold, harsh mechanical touch, chemicals, and chemotherapy drugs (MD Anderson Clark Fellowship Project). View a complete list of Dr. Galko's publications in PubMed. View Dr. Galko's SciVal research profile. View Dr. Galko's ResearchGate profile.
Visit Dr. Galko's Lab Website.
|1999||University of California at San Francisco, Mentor Dr. Marc Tessier-Lavigne, San Francisco, CA, USA, PHD, Cell Biology|
|1991||University of Texas at Austin, Austin, TX, USA, BS, Biology|
|2000-2005||Research Fellowship, with Dr. Mark Krasnow, Stanford University School of Medicine, Stanford, CA|
- Im SH, Takle K, Jo J, Babcock DT, Ma Z, Xiang Y, Galko MJ. Tachykinin acts upstream of autocrine Hedgehog signaling during nociceptive sensitization in Drosophila. eLife 17(4):e10735, 2015. PMID: 26575288.
- Wang Y, Antunes M, Anderson, A E, Kadrmas J, Jacinto, A, and Galko MJ. Integrin adhesions suppress syncytium formation in the Drosophila larval epidermis. Curr Biol 25(17):2215-27, 2015. e-Pub 2015. PMID: 26255846.
- Anderson AE and Galko MJ. Rapid clearance of epigenetic protein reporters from wound edge cells in Drosophila larvae does not depend on the JNK or PDGFR/VEGFR signaling pathways. Regeneration 1(2):11-25, 2014. PMID: 25114797.
- Scherfer C, Han VC, Wang Y, Anderson AE, Galko MJ. Autophagy drives epidermal deterioration in a Drosophila model of tissue aging. Aging (Albany NY) 5(4):276-87, 2013. PMID: 23599123.
- Brock AR, Wang Y, Berger S, Renkawitz-Pohl R, Han VC, Wu Y, Galko MJ. Transcriptional regulation of Profilin during wound closure in Drosophila larvae. J Cell Sci 125(Pt 23):5667-76, 2012. e-Pub 2012. PMID: 22976306.
- Chattopadhyay A, Gilstrap AV, Galko MJ. Local and global methods of assessing thermal nociception in Drosophila larvae. J Vis Exp(63), 2012. e-Pub 2012. PMID: 22643884.
- Babcock DT, Shi S, Jo J, Shaw M, Gutstein HB, Galko MJ. Hedgehog signaling regulates nociceptive sensitization. Curr Biol 21(18):1525-33, 2011. e-Pub 2011. PMID: 21906949.
- 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, 2010. e-Pub 2010. PMID: 20813879.
- 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, 2009. e-Pub 2009. PMID: 19646875.
- Babcock DT, Landry C, Galko MJ. Cytokine signaling mediates UV-induced nociceptive sensitization in Drosophila larvae. Curr Biol 19(10):799-806, 2009. e-Pub 2009. PMID: 19375319.
- 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, 2008. e-Pub 2008. PMID: 18632567.
- Galko MJ, Tessier-Lavigne M. Biochemical characterization of netrin-synergizing activity. J Biol Chem 275(11):7832-8, 2000. PMID: 10713098.