Peter J McKinnon, Ph.D.

Peter J McKinnon, Ph.D.

Department of Genetics and Tumor
Cell Biology
St. Jude Children's Research Hospital

Affiliated Professor
Department of Anatomy and Neurobiology


St. Jude Children's Research Hospital
Department Genetics & Tumor Cell Biology
262 Danny Thomas Place
Memphis, TN 38105
Phone (901) 595-2700
Fax (901) 525-6035
Email: Peter J McKinnon



Education

  • Ph.D. Institution: The Flinders Universiry of South Australia, Adelaide, Australia
  • Postdoctoral: The Roche Institute of Molecular Biology, Nutley, New Jersey

Link

Research Interests

Our goal is to understand the role of the DNA damage response in the nervous system, and how this functions to prevent disease. The response to genotoxic stress is a prerequisite for development of the nervous system. Mutations in a variety of DNA damage-response factors can lead to human diseases that are characterized by pronounced neuropathology. In many of these syndromes the neurological component is amongst the most deleterious aspects of the disease. Because the nervous system poses a particular challenge in terms of clinical intervention, understanding how DNA repair deficiency impacts the nervous system will be important for design of therapies targeted at ameliorating neuropathology including neurodegeneration and brain tumors. For more information please see: http://www.stjude.org/mckinnon

Representative Publications

  • Shimada M, Dumitrache LC, Russell HR, McKinnon PJ. Polynucleotide kinase-phosphatase enables neurogenesis via multiple DNA repair pathways to maintain genome stability. EMBO J. 2015 Aug 19. pii: e201591363. [Epub ahead of print] PubMed PMID: 26290337.
  • Marjanović M, Sánchez-Huertas C, Terré B, Gómez R, Scheel JF, Pacheco S, Knobel PA, Martínez-Marchal A, Aivio S, Palenzuela L, Wolfrum U, McKinnon PJ, Suja JA, Roig I, Costanzo V, Lüders J, Stracker TH. CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination. Nat Commun. 2015 Jul 9;6:7676. doi: 10.1038/ncomms8676. PubMed PMID: 26158450; PubMed Central PMCID: PMC4499871.
  • Zindy F, Lee Y, Kawauchi D, Ayrault O, Merzoug LB, Li Y, McKinnon PJ, Roussel MF. Dicer Is Required for Normal Cerebellar Development and to Restrain Medulloblastoma Formation. PLoS One. 2015 Jun 19;10(6):e0129642. doi: 10.1371/journal.pone.0129642. eCollection 2015. PubMed PMID: 26091048; PubMed Central PMCID: PMC4474721.
  • Heo J, Li J, Summerlin M, Hays A, Katyal S, McKinnon PJ, Nitiss KC, Nitiss JL, Hanakahi LA. TDP1 promotes assembly of non-homologous end joining protein complexes on DNA. DNA Repair (Amst). 2015 Jun;30:28-37. doi: 10.1016/j.dnarep.2015.03.003. Epub 2015 Mar 17. PubMed PMID: 25841101.
  • Lindsey JC, Kawauchi D, Schwalbe EC, Solecki DJ, Selby MP, McKinnon PJ, Olson JM, Hayden JT, Grundy RG, Ellison DW, Williamson D, Bailey S, Roussel MF, Clifford SC. Cross-species epigenetics identifies a critical role for VAV1 in SHH subgroup medulloblastoma maintenance. Oncogene. 2015 Sep 3;34(36):4746-57. doi: 10.1038/onc.2014.405. Epub 2014 Dec 22. PubMed PMID: 25531316; PubMed Central PMCID: PMC4386991.
  • Carroll J, Page TK, Chiang SC, Kalmar B, Bode D, Greensmith L, Mckinnon PJ, Thorpe JR, Hafezparast M, El-Khamisy SF. Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing. Hum Mol Genet. 2015 Feb 1;24(3):828-40. doi: 10.1093/hmg/ddu500. Epub 2014 Sep 30. PubMed PMID: 25274775; PubMed Central PMCID: PMC4291253.

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