Meet Michael Galko, Ph.D.
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. His research is currently supported by a five-year ‘people not projects’ R35 grant from NIGMS.
Visit Dr. Galko's Lab Website.
Professor, Department of Genetics, Division of Basic Science Research, The University of Texas MD Anderson Cancer Center, Houston, TX
Professor, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, 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 ( PNAS, 2008), epidermal cell orientation and fusion ( Currrent Biology, 2015), 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, 2012; Developmental Biology, 2017) required for wound closure and to expand our efforts into epigenetic regulation of wound closure ( Regeneration, 2014) and regulation of cell adhesion dynamics at the wound edge ( Development, 2019).
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. Pain hypersensitivity is a major clinical issue with cancer and cancer treatment.
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; Cell Death and Disease, 2017). Our most interesting finding to date is that the conserved Hedgehog signaling pathway, which regulates diverse aspects of patterning and cell fate specification during both fly and vertebrate development, also plays a conserved role in regulating the responses of sensory neurons to painful stimuli ( Current Biology, 2011; eLife, 2015). We continue to explore the mechanisms of action of these two signaling pathways.
We also continue to develop new assays for how Drosophila larvae respond to noxious cold ( Current Biology, 2016; PLoS One, 2018), harsh mechanical touch ( Journal of Neuroscience, 2019), and chemical exposure ( Philosophical Transactions of the Royal Society, 2019). We have also developed a promising new Drosophila model of diabetes-associated pain ( Disease Models and Mechanisms, 2018) using seed research money awarded through and MD Anderson R. Lee Clark basic science fellowship.
We expect that our efforts on wound closure and pain sensitization, because they focus on biomedically important biology and conserved genes, will eventually lead to clinically actionable insight for human patients.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|
|2017||Nominee, Regent’s Outstanding Teaching Award, The University of Texas System|
|2016||Faculty Educator of the Month, MD Anderson Cancer Center|
|2016||Faculty Recognition for Outstanding Service to Graduate Education, GSBS|
|2014||R. Lee Clark Fellow in Basic Research, MD Anderson Cancer Center|
|2012||MD Anderson Distinguished Faculty Mentor Award, Nominee, MD Anderson Cancer Center|
|2011||Mentor of Genetics Society of America's Larry Sandler Awardee, Daniel Babcock, Ph.D, For Best Graduate Thesis using Drosophila as a Research Tool|
|2010||MD Anderson Distinguished Faculty Mentor Award, Nominee, MD Anderson Cancer Center|
|2007||Basil O'Connor Starter Scholar Research Award, March of Dimes Foundation|
|2007||Cancer Center Support Grant Developmental Funds Trust Recipient, Cancer Center Support Grant|
|2001||Postdoctoral Fellowship Award, American Heart Association|
|2001||Research Fellow Award, Arnold and Mabel Beckman Foundation|
|2000||Lievre Family Fellowship Award, American Heart Association|
|1995||Predoctoral Fellowship Award, American Heart Association|
|1991||Predoctoral Fellowship Award, National Science Foundation|
|1990||Undergraduate Research Award, Howard Hughes Medical Institute|
- Lopez-Bellido R, Galko MJ. An Improved Assay and Tools for Measuring Mechanical Nociception in Drosophila Larvae. J Vis Exp(164), 2020. e-Pub 2020. PMID: 33191934.
- Lopez-Bellido R, Himmel NJ, Gutstein HB, Cox DN, Galko MJ. An assay for chemical nociception in Drosophila larvae. Philos Trans R Soc Lond B Biol Sci 374(1785):20190282, 2019. e-Pub 2019. PMID: 31544619.
- Tsai CR, Galko MJ. Casein kinase 1α decreases β-catenin levels at adherens junctions to facilitate wound closure in Drosophila larvae. Development 146(20), 2019. e-Pub 2019. PMID: 31511254.
- Lopez-Bellido R, Puig S, Huang PJ, Tsai CR, Turner HN, Galko MJ, Gutstein HB. Growth factor signaling regulates mechanical nociception in flies and vertebrates. J Neurosci 39(30):6012-6030, 2019. e-Pub 2019. PMID: 31138657.
- Im SH, Patel AA, Cox DN, Galko MJ. Drosophila Insulin receptor regulates the persistence of injury-induced nociceptive sensitization. Dis Model Mech 11(5), 2018. e-Pub 2018. PMID: 29752280.
- Turner HN, Patel AA, Cox DN, Galko MJ. Injury-induced cold sensitization in Drosophila larvae involves behavioral shifts that require the TRP channel Brv1. PLoS One 13(12):e0209577, 2018. e-Pub 2018. PMID: 30586392.
- Follansbee TL, Gjelsvik KJ, Brann CL, McParland AL, Longhurst CA, Galko, MJ, & Ganter, GK. Drosophila nociceptive sensitization requires BMP signaling via the canonical SMAD pathway. J. Neurosci 37(35):8524-8533, 2017. PMID: 28855331.
- Tsai CR, Anderson AE, Burra S, Jo J, Galko MJ. Yorkie regulates epidermal wound healing in Drosophila larvae independently of cell proliferation and apoptosis. Developmental Biology 427(1):61-71, 2017. e-Pub 2017. PMID: 28514643.
- Jo, J, Im SH, Babcock DT, Iyer SC, Gunawan F, Cox DN & Galko MJ. Drosophila caspase activity is required independently of apoptosis to produce active TNF/Eiger during nociceptive sensitization. Cell Death and Disease 11(8):5, 2017. PMID: 28492538.
- Turner HN, Landry C and Galko MJ. Novel Assay for cold nociception in Drosophila larvae. JoVE(3):122, 2017. PMID: 28448025.
- Turner HN, Armengol K, Patel AA, Himmel NJ, Sullivan L, Iyer SC, Bhattacharya S, Iyer EP, Landry C, Galko MJ, Cox DN. The TRP Channels Pkd2, NompC, and Trpm Act in Cold-Sensing Neurons to Mediate Unique Aversive Behaviors to Noxious Cold in Drosophila. Curr Biol 26(23):3116-3128, 2016. PMID: 27818173.
- 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.