Risa Kitagawa, PhD

Languages Spoken:

• English

Research Center:

• Center for Childhood Cancer

Areas of Interest:

• The spindle assembly checkpoint (SAC) ensures accurate chromosome segregation. Defects in this system cause chromosome instability that can lead to aneuploidy, a hallmark of many cancers. Therefore, studies of the genes that regulate SAC activity are directly relevant to research on cancer and many genetic diseases. Dr. Kitagawa’s research focuses on the characterization of Mad1, a conserved SAC component, and its genetic or physical interactors, using the roundworm C. elegans as a model. Her research addresses the central hypothesis that CeMAD1 is involved in the initial step of the SAC-signaling pathway and that CeMAD1 activity is regulated by multiple pathways that mediate various developmental or environmental cues. Her lab’s goals are to identify and characterize proteins that regulate SAC activity in multicellular organisms and to elucidate the molecular mechanism by which SAC activity is temporally and spatially regulated during development. She is also investigating a molecular link between DNA damage checkpoint and spindle assembly checkpoint. Lab Web Site: http://www.NationwideChildrens.org/R-Kitagawa-Lab

Medical School

• Nagoya University

Medical School

• Nagoya University

2010–present

• Principal Investigator, Center for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio

2005–2010

• Assistant Member, Department of Molecu,lar Pharmacology, St. Jude Children's Research Hospital, Memphis, Tennessee

2001–2005

• Postdoctoral fellow, Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee

1997–2001

• Postdoctoral Fellow. University of British Columbia, School of Medicine, Department of Medical Genetics. Vancouver, British Culumbia

1997–1997

• Postdoctoral Fellow, The Johns Hopkins University, Department of Molecular Biology and Genetics, School of Medicine. Baltimon:. Maryland

1990–1991

• Research Fellow, National Institute of Health Science, Division of Bio-Chem Informatics, Tokyo, Japan

• Kitagawa R. 2009. The spindle assembly checkpoint in Caenorhabditis elegans: one who lacks Mad1 becomes mad one.  Cell Cycle (Georgetown, Tex.). Vol. 8, no. 3. (February 1): 338.
• Kitagawa R. 2009. Key players in chromosome segregation in Caenorhabditis elegans.  Frontiers In Bioscience: A Journal And Virtual Library. Vol. 14. (January 1): 1529.
• Kitagawa R. Spindle Assembly Checkpoint in C. elegans. Cell Cycle. 8(3): 1-7, 2009.
• Kitagawa R. Key players in chromosome segregation in Caenorhabditis elegans. Front Biosci 14: 1529-1557, 2009.
• Yamamoto TG; Watanabe S; Essex A; Kitagawa R. 2008. SPDL-1 functions as a kinetochore receptor for MDF-1 in Caenorhabditis elegans.  The Journal Of Cell Biology. Vol. 183, no. 2. (October 20): 187.
• Watanabe S; Yamamoto TG; Kitagawa R. 2008. Spindle assembly checkpoint gene mdf-1 regulates germ cell proliferation in response to nutrition signals in C. elegans.  The EMBO Journal. Vol. 27, no. 7. (April 9): 1085.
• Watanabe S, Yamamoto TG, Kitagawa R. Spindle assembly checkpoint gene mdf-I regulates genn cell proliferation in response to nutrition signals in C. elegans. EMBO J 27(7): I 085-1 096, 2008.
• Yamamoto TG, Watanabe S, Essex A, Kitagawa R. SPDL-l functions as a kinetochore receptor for MDF-J in Caenorhabditis elegans. J Cell Biol 183(2): 187-194, 2008.
• Tarailo M; Kitagawa R; Rose AM. 2007. Suppressors of spindle checkpoint defect (such) mutants identify new mdf-1/MAD1 interactors in Caenorhabditis elegans.  Genetics. Vol. 175, no. 4. (April 1): 1665.
• Tarailo M, Kitagawa R, Rose A. Suppressors of spindle checkpoint derect (such) mutants identify new mdfI/MADI interactors in Cacnorhabditis eiegans. Genetics 175(4):1665-1679, 2007.
• Bekker-Jensen S; Lukas C; Kitagawa R; Melander F; Kastan MB; Bartek J; Lukas J. 2006. Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks.  The Journal Of Cell Biology. Vol. 173, no. 2. (April 24): 195.
• Bekker-Jensen S, Lukas C, Kitagawa R, Melander F, Kastan MB, Bartek J, Lukas J. Spatial organization of the mammalian genome surveillance machinery in respol1se to DNA strand breaks. J Cell Biol 173(2): 195-206, 2006.
• Morales M; Theunissen JW; Kim CF; Kitagawa R; Kastan MB; Petrini JH. 2005. The Rad50S allele promotes ATM-dependent DNA damage responses and suppresses ATM deficiency: implications for the Mre11 complex as a DNA damage sensor.  Genes & Development. Vol. 19, no. 24. (December 15): 3043.
• Kitagawa R, Kastan MB. The ATM-dependent DNA damage signaling pathway. Cold Spring Harb Symp Quant Biol LXX 70:99-109, 2005.
• Kitagawa R; Kastan MB. 2005. The ATM-dependent DNA damage signaling pathway.  Cold Spring Harbor Symposia On Quantitative Biology. Vol. 70. (January 1): 99.
• Morales M, Theunissen JW, Kim CF, Kitagawa R, Kastan MB, Petrini HI. The Rad50S allele promotes ATMdependent DNA damage responses and suppresses A TM deficiency; Implications for the Mre 1 I complex as a DNA damage sensor. Genes Dev 19(24);3043-3054, 2005.
• Kitagawa R; Bakkenist CJ; McKinnon PJ; Kastan MB. 2004. Phosphorylation of SMC1 is a critical downstream event in the ATM-NBS1-BRCA1 pathway.  Genes & Development. Vol. 18, no. 12. (June 15): 1423.
• Kitagawa R, Bakkenist CJ, McKinnon PJ', Kastan MB. Phosphorylation of SMCI is the critical downstream event in the ATM-NBS I-BRCA I pathway Genes Dev 18(12); 1423-1438, 2004.
• Kitagawa R; Law E; Tang L; Rose AM. 2002. The Cdc20 homolog, FZY-1, and its interacting protein, IFY-1, are required for proper chromosome segregation in Caenorhabditis elegans.  Current Biology: CB. Vol. 12, no. 24. (December 23): 2118.
• Kitagawa R, Law t, Tang L, Rose AM. The Cde20 homolog, PlY-I and its interacting protein, IFY-l are required for proper chromosome segregation in Caenorhabditis elegans. Curr Biol 12(24):2118-2123,2002.
• Ozaki T; Kumaki Y; Kitagawa R; Ogawa T. 2001. Anomalous DnaA protein binding to the regulatory region of the Escherichia coli aldA gene.  Microbiology (Reading, England). Vol. 147, no. Pt 1. (January 1): 153.
• Ozaki T, Kumaki Y, Kitagawa R, Ogawa T. Anomalous DnaA protein binding to the regulatory region of the Escherichia coli aidA gene. Microbiology 147 CPt I); 153-159,2001.
• Furuta T; Tuck S; Kirchner J; Koch B; Auty R; Kitagawa R; Rose AM; Greenstein D. 2000. EMB-30: an APC4 homologue required for metaphase-to-anaphase transitions during meiosis and mitosis in Caenorhabditis elegans.  Molecular Biology Of The Cell. Vol. 11, no. 4. (April 1): 1401.
• Furuta T, Tuck S, Kirchner J, Koch B, Auty R, Kitagawa R, Rose AM, Greenstein D. EMB-30: an APC4 homologue required for metaphase-to-anaphase transitions during meiosis and mitosis in Caenorhabditis elegans. Mol Biol Cell 11(4): 140 1-1419, 2000.
• Kitagawa R; Rose AM. 1999. Components of the spindle-assembly checkpoint are essential in Caenorhabditis elegans.  Nature Cell Biology. Vol. 1, no. 8. (December 1): 514.
• Kitagawa R, Rose AM. Components of the spindle-assembly checkpoint are essential in Caenorhabditis elegans. Nat Cell Biol 1(8):514-521 , 1999.
• Kitagawa R; Ozaki T; Moriya S; Ogawa T. 1998. Negative control of replication initiation by a novel chromosomal locus exhibiting exceptional affinity for Escherichia coli DnaA protein.  Genes & Development. Vol. 12, no. 19. (October 1): 3032.
• Kitagawa R, Ozaki T, Moriya S, Ogawa T. Negative control of replication initiation by a novel chromosomal locus exhibiting exceptional affinity for Escherichia coli DnaA protein. Genes Dev 12(19):3032-3043, 1998.
  
• Kitagawa R. Inhibition of reinitiation of replication by datA, a novel DnaA-binding locus at 94.7 min on the Escherichia coli chromosome. Ph.D. thesis. Nagoya University, Nagoya, Japan, Mar. 1997.
  
• Kitagawa R; Mitsuki H; Okazaki T; Ogawa T. 1996. A novel DnaA protein-binding site at 94.7 min on the Escherichia coli chromosome.  Molecular Microbiology. Vol. 19, no. 5. (March 1): 1137.
• Kitagawa R, Mitsuki H, Okazaki T, Ogawa T. A novel DnaA protein-binding site at 94.7 min on the Escherichia coli chromosome. Mol Microbiol 19(5):1137-1147, 1996.
• Kitagawa, R; Bakkenist, CJ, Kastan, MB, Presenter. 2005. The role of SMC1 in DNA damage induced signaling pathways. Presented at The Molecular Cellular and Developmental Biology Program. Kansas State University. Manhattan, Kansas. (October 18)
• Kitagawa, R; Bakkenist, CJ, Kastan, MB, Presenter. 2003. The roles of ATM and SMC1 inDNA damage response. Presented at The 20th Radiation Biology Center International Symposium "Genome Repair Dynamics and Human Disease". Kyoto Research Park. Kyoto, Japan. (October 6 - 8)
• Watanabe, S; Yamamoto, TG, Kitagawa, R, Presenter. 2007. Spindle assembly checkpoint gene mdf-1 regulates germ cell proliferation in response to nutrition signals in C. elegans. Presented at The Annual Meeting of Japanese Molecular Biology Society & Biochemical Society. Pacifico Yokohama. Yokohama, Kanagawa, Japan. (December 11 - 15)
• Yamamoto, TG; Watanabe, S; Essex, A; Kitagawa, R, Presenter. 2008. The san-1/MAD3 Synthetic Lethal Screen Identified a Kinetochore Receptor of MDF-1/MAD1 in C. elegans. Presented at C. elegans Development & Evolution Meeting. University of Wisconsin. Madison, WI. (June 11 - 15)
• Kitagawa, R; Rose, AM, Presenter. 1999. Genes, mdf-1 and mdf-2, encoding mitotic checkpoint components are essential in C. elegans. Presented at The 1st Salk Institute Cell Cycle Meeting. Salk Institute. La Jolla, CA. (June 18 - 22)
• Kitagawa, R; Rose, AM, Presenter. 1999. Genes, mdf-1 and mdf-2, encoding mitotic checkpoint components are essential in C. elegans. Presented at The 12th International C. elegans meeting. University of Wisconsin. Madison, WI. (June 2 - 6)
• Kitagawa, R; Bakkenist, CJ, Kastan, MB, Presenter. 2004. The roles of SMC1 in DNA damage induced signaling pathways. Presented at The 95th American Associate of Cancer Research Annual Meeeting. Orange County Convention Center. Orlando, FL. (March 27 - 31)