Sign in to edit your profile (add interests, mentoring, photo, etc.)
    Keywords
    Last Name
    Institution

    Yicktung T Ip PhD

    TitleProfessor
    InstitutionUniversity of Massachusetts Medical School
    DepartmentProgram in Molecular Medicine
    AddressUniversity of Massachusetts Medical School
    373 Plantation Street
    Worcester MA 01605
    Phone508-856-5136
      Other Positions
      InstitutionUMMS - School of Medicine
      DepartmentBiochemistry and Molecular Pharmacology

      InstitutionUMMS - School of Medicine
      DepartmentCell and Developmental Biology

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentCell Biology

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentInterdisciplinary Graduate Program

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentMD/PhD Program

      InstitutionUMMS - Programs, Centers and Institutes
      DepartmentProgram in Cell Dynamics

        Overview 
        Narrative

        Academic background

        Tony Ip received his BS from the National Defense Medical Center, Taipei, ROC in 1984 and his PhD from the University of Iowa in 1989. He was a Hoffmann-LaRoche Fellow of the Life Sciences Research Foundation from 1991-1994 at the University of California at San Diego. In 1994, he joined the University of Massachusetts Medical Center as assistant professor in the Program in Molecular Medicine. He was a recipient of a Scholar Award of the Leukemia Society of America in 1996-2001.

        Intestinal stem cells and tissue regeneration in Drosophila

        Dr. Tony Ip

        Humans and fruit flies do not look alike, yet many physiological processes in these two organisms share homologous molecules.We use Drosophila melanogaster, the common fruit fly, as a model organism to study the mechanisms by which intestinal stem cells respond to injury and initiate tissue repair. Around 1% of the US population experience inflammatory diseases of the intestine. Prolonged inflammation and tissue injury has also been proposed to potentiate gastrointestinal (GI) cancer. To understand how cells in the GI tract interact with wide varieties of microbes and pathogenic substances is important for developing therapeutic strategies that alleviate intestinal diseases. The human gastrointestinal tract is the major nutrient absorption organ that also has immune and endocrine function. It is also a major site for interaction with commensal bacteria and pathogenic substances. However, the human gastrointestinal tract is a relatively under-explored organ due to the complexity of the organ and the difficulty in experimental manipulation. Stem cell-mediated tissue repair is a promising approach for intestinal diseases. A major problem in intestinal stem cell research is that specific markers that can unambiguously identify these stem cells remain rare and the functions of these markers remain difficulty to study.

        My laboratory focuses on understanding how Drosophila intestinal stem cells mediate repair after tissue damage. Drosophila has emerged as a powerful tool for analyzing the function of human disease genes, either as fly homologues or by expressing in transgenic flies the mutated forms of human genes. Drosophila midgut is only 1 cm long and has a relatively simple cellular organization. Midgut intestinal stem cells have recently been identified that function to replenish the different cell types. We have demonstrated that these Drosophila intestinal stem cells can increase their division rate in response to tissue damage. Using this newly established system, we also show that intestinal stem cell division requires insulin signaling, a mechanism not yet shown in mammals thus suggesting that new information can be obtained from this system. To analyze how insulin and other regulatory pathways control intestinal stem cell division is our ongoing research direction. We have identified by transgenic expression assays and RNAi-based genetic screens a number of genes that are essential for damage-induced intestinal stem cell division. By studying the mechanisms of tissue damage-induced stem division in the genetically amenable Drosophila system, important insights will hopefully be obtained that can help to understand human stem cell-mediated tissue repair, intestinal inflammatory diseases and cancer progression.

        Figure1

        Figure Legend

        Cellular organization in adult Drosophila midgut. Left panel is DAPI staining for DNA in midgut. Right panel is a confocal image of midgut cross section. Phalloidin stains smooth muscle cells at the basal side and brush border of enterocytes at the lumenal side. Intestinal stem cells are some of the small cells located near the basal side. In adult Drosophila midgut, intestinal stem cell is the only cell type that divides and gives rise to all other cell types. We want to understand how the stem cell division is regulated, how the damaged epithelium is repaired, and how differentiation into various cell types is determined.




        Rotation Projects

        Rotation Projects

        Project #1: Mechanistic study of isolated mutants that show abnormal intestinal stem cell division phenotypes.

        Project #2:Perform transgenic RNAi-based genetic screen for genes required for intestinal stem cell response to tissue damage.



        Post Docs

        A postdoctoral position is available to study in this laboratory. Contact Dr. Ip for additional details.

        Bibliographic 
        selected publications
        List All   |   Timeline
        1. Nirala NK, Rahman M, Walls SM, Singh A, Zhu LJ, Bamba T, Fukusaki E, Srideshikan SM, Harris GL, Ip YT, Bodmer R, Acharya UR. Survival Response to Increased Ceramide Involves Metabolic Adaptation through Novel Regulators of Glycolysis and Lipolysis. PLoS Genet. 2013 Jun; 9(6):e1003556.
          View in: PubMed
        2. Amcheslavsky A, Ip YT. Be a Good Neighbor: Organ-to-Organ Communication during the Innate Immune Response. Cell Host Microbe. 2012 Apr 19; 11(4):323-4.
          View in: PubMed
        3. Kaneko S, Chen X, Lu P, Yao X, Wright TG, Rajurkar M, Kariya K, Mao J, Ip YT, Xu L. Smad inhibition by the Ste20 kinase Misshapen. Proc Natl Acad Sci U S A. 2011 Jul 5; 108(27):11127-32.
          View in: PubMed
        4. Amcheslavsky A, Ito N, Jiang J, Ip YT. Tuberous sclerosis complex and Myc coordinate the growth and division of Drosophila intestinal stem cells. J Cell Biol. 2011 May 16; 193(4):695-710.
          View in: PubMed
        5. Tanji T, Yun EY, Ip YT. Heterodimers of NF-kappaB transcription factors DIF and Relish regulate antimicrobial peptide genes in Drosophila. Proc Natl Acad Sci U S A. 2010 Aug 17; 107(33):14715-20.
          View in: PubMed
        6. Chatterjee M, Ip YT. Pathogenic stimulation of intestinal stem cell response in Drosophila. J Cell Physiol. 2009 Sep; 220(3):664-71.
          View in: PubMed
        7. Amcheslavsky A, Jiang J, Ip YT. Tissue damage-induced intestinal stem cell division in Drosophila. Cell Stem Cell. 2009 Jan 9; 4(1):49-61.
          View in: PubMed
        8. Xu L, Yao X, Chen X, Lu P, Zhang B, Ip YT. Msk is required for nuclear import of TGF-{beta}/BMP-activated Smads. J Cell Biol. 2007 Sep 10; 178(6):981-94.
          View in: PubMed
        9. Tanji T, Hu X, Weber AN, Ip YT. Toll and IMD pathways synergistically activate an innate immune response in Drosophila melanogaster. Mol Cell Biol. 2007 Jun; 27(12):4578-88.
          View in: PubMed
        10. Chen HB, Shen J, Ip YT, Xu L. Identification of phosphatases for Smad in the BMP/DPP pathway. Genes Dev. 2006 Mar 15; 20(6):648-53.
          View in: PubMed
        11. Yagi Y, Ip YT. Helicase89B is a Mot1p/BTAF1 homologue that mediates an antimicrobial response in Drosophila. EMBO Rep. 2005 Nov; 6(11):1088-94.
          View in: PubMed
        12. Ganguly A, Jiang J, Ip YT. Drosophila WntD is a target and an inhibitor of the Dorsal/Twist/Snail network in the gastrulating embryo. Development. 2005 Aug; 132(15):3419-29.
          View in: PubMed
        13. Tanji T, Ip YT. Regulators of the Toll and Imd pathways in the Drosophila innate immune response. Trends Immunol. 2005 Apr; 26(4):193-8.
          View in: PubMed
        14. Ashraf SI, Ganguly A, Roote J, Ip YT. Worniu, a Snail family zinc-finger protein, is required for brain development in Drosophila. Dev Dyn. 2004 Oct; 231(2):379-86.
          View in: PubMed
        15. Bettencourt R, Asha H, Dearolf C, Ip YT. Hemolymph-dependent and -independent responses in Drosophila immune tissue. J Cell Biochem. 2004 Jul 1; 92(4):849-63.
          View in: PubMed
        16. Hu X, Yagi Y, Tanji T, Zhou S, Ip YT. Multimerization and interaction of Toll and SpƤtzle in Drosophila. Proc Natl Acad Sci U S A. 2004 Jun 22; 101(25):9369-74.
          View in: PubMed
        17. Hemavathy K, Hu X, Ashraf SI, Small SJ, Ip YT. The repressor function of snail is required for Drosophila gastrulation and is not replaceable by Escargot or Worniu. Dev Biol. 2004 May 15; 269(2):411-20.
          View in: PubMed
        18. Bettencourt R, Ip YT. Learning the codes of fly immunity. Mol Cell. 2004 Jan 16; 13(1):1-2.
          View in: PubMed
        19. Bettencourt R, Tanji T, Yagi Y, Ip YT. Toll and Toll-9 in Drosophila innate immune response. J Endotoxin Res. 2004; 10(4):261-8.
          View in: PubMed
        20. Ip YT, Gridley T. Cell movements during gastrulation: snail dependent and independent pathways. Curr Opin Genet Dev. 2002 Aug; 12(4):423-9.
          View in: PubMed
        21. Ooi JY, Yagi Y, Hu X, Ip YT. The Drosophila Toll-9 activates a constitutive antimicrobial defense. EMBO Rep. 2002 Jan; 3(1):82-7.
          View in: PubMed
        22. Ashraf SI, Ip YT. The Snail protein family regulates neuroblast expression of inscuteable and string, genes involved in asymmetry and cell division in Drosophila. Development. 2001 Dec; 128(23):4757-67.
          View in: PubMed
        23. Hemavathy K, Ashraf SI, Ip YT. Snail/slug family of repressors: slowly going into the fast lane of development and cancer. Gene. 2000 Oct 17; 257(1):1-12.
          View in: PubMed
        24. Hemavathy K, Guru SC, Harris J, Chen JD, Ip YT. Human Slug is a repressor that localizes to sites of active transcription. Mol Cell Biol. 2000 Jul; 20(14):5087-95.
          View in: PubMed
        25. Ashraf SI, Hu X, Roote J, Ip YT. The mesoderm determinant snail collaborates with related zinc-finger proteins to control Drosophila neurogenesis. EMBO J. 1999 Nov 15; 18(22):6426-38.
          View in: PubMed
        26. Han ZS, Ip YT. Interaction and specificity of Rel-related proteins in regulating Drosophila immunity gene expression. J Biol Chem. 1999 Jul 23; 274(30):21355-61.
          View in: PubMed
        27. Meng X, Khanuja BS, Ip YT. Toll receptor-mediated Drosophila immune response requires Dif, an NF-kappaB factor. Genes Dev. 1999 Apr 1; 13(7):792-7.
          View in: PubMed
        28. Ashraf SI, Ip YT. Transcriptional control: repression by local chromatin modification. Curr Biol. 1998 Sep 24; 8(19):R683-6.
          View in: PubMed
        29. Han ZS, Enslen H, Hu X, Meng X, Wu IH, Barrett T, Davis RJ, Ip YT. A conserved p38 mitogen-activated protein kinase pathway regulates Drosophila immunity gene expression. Mol Cell Biol. 1998 Jun; 18(6):3527-39.
          View in: PubMed
        30. Ip YT, Davis RJ. Signal transduction by the c-Jun N-terminal kinase (JNK)--from inflammation to development. Curr Opin Cell Biol. 1998 Apr; 10(2):205-19.
          View in: PubMed
        31. Hemavathy K, Meng X, Ip YT. Differential regulation of gastrulation and neuroectodermal gene expression by Snail in the Drosophila embryo. Development. 1997 Oct; 124(19):3683-91.
          View in: PubMed
        32. Ip YT, Hemavathy K. Drosophila development. Delimiting patterns by repression. Curr Biol. 1997 Apr 1; 7(4):R216-8.
          View in: PubMed
        33. Sluss HK, Han Z, Barrett T, Goberdhan DC, Wilson C, Davis RJ, Ip YT. A JNK signal transduction pathway that mediates morphogenesis and an immune response in Drosophila. Genes Dev. 1996 Nov 1; 10(21):2745-58.
          View in: PubMed
        34. Ip YT. Transcriptional regulation. Converting an activator into a repressor. Curr Biol. 1995 Jan 1; 5(1):1-3.
          View in: PubMed
        For assistance with using Profiles, please refer to the online tutorials or contact UMMS Help Desk or call 508-856-8643.
        Yicktung's Networks
        Click the "See All" links for more information and interactive visualizations!
        Concepts
        _
        Co-Authors
        _
        Similar People
        _
        Same Department
        Physical Neighbors
        _

        This is an official Page/Publication of the University of Massachusetts Worcester Campus
        Office of the Vice Provost for Research, 55 Lake Ave North, Worcester, Massachusetts 01655
        Questions or Comments? Email: publicaffairs@umassmed.edu Phone: 508-856-1572