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Cell cycle and cell size regulation in Down Syndrome cells

  • M. Rosner
  • A. Kowalska
  • A. Freilinger
  • A-R. Prusa
  • E. Marton
  • M. Hengstschläger
Part of the Journal of Neural Transmission Supplement 67 book series (NEURAL SUPPL, volume 67)

Summary

Although the neuropathological features typical for Down Syndrome obviously result from deregulation of both, cell cycle control and differentiation processes, so far research focused on the latter. Considering the known similarities between the neuropathology of Down Syndrome and Alzheimer’s disease and the knowledge, that in Alzheimer’s disease neuronal degeneration is associated with the activation of mitogenic signals and cell cycle activation, it is tempting to investigate the consequences of an additional chromosome 21 on mammalian cell cycle regulation. We analysed the distribution of cells in different cell cycle phases on the flowcytometer and the cell size of human amniotic fluid cells with normal karyotypes and with trisomy 21. We could not detect any significant differences suggesting that the presence of an additional copy of the about 225 genes on human chromosome 21 does not trigger cell cycle effects in amniotic fluid cells. These data provide new insights into the cell biology of trisomy 21 cells.

Keywords

Down Syndrome Cell Cycle Control Cell Cycle Phase Additional Chromosome Cell Cycle Activation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Antonarakis SE, Avramopoulos D, Blouin JL, Talbot CC, Schinzel AA (1993) Mitotic errors in somatic cells cause trisomy 21 in about 4.5% of cases and are not associated with maternal age. Nat Genet 3: 146–149PubMedCrossRefGoogle Scholar
  2. Arendt T (2002) Dysregulation of neuronal differentiation and cell cycle control in Alzheimer’s disease. J Neural Transm [Suppl] 62: 77–85Google Scholar
  3. Bernert G, Nemethova M, Herrera-Marschitz M, Cairns N, Lubec G (1996) Decreased cyclin dependent kinase in brain of patients with Down Syndrome. Neurosci Lett 216: 68–70PubMedCrossRefGoogle Scholar
  4. Cairns NJ (1999) Neuropathology. J Neural Transm [Suppl] 57: 61–74Google Scholar
  5. Capone GT (2001) Down syndrome: advances in molecular biology and the neurosciences. Dev Behav Ped 22: 40–59CrossRefGoogle Scholar
  6. Engidawork E, Lubec G (2003) Molecular changes in fetal Down syndrome brain. J Neurochem 84: 895–904PubMedCrossRefGoogle Scholar
  7. Hengstschläger M, Braun K, Soucek T, Miloloza A, Hengstschläger-Ottnad E (1999a) Cyclin-dependent kinases at the G1-S transition of the mammalian cell cycle. Rev Mutat Res 436: 1–9CrossRefGoogle Scholar
  8. Hengstschläger M, Hölzl G, Hengstschläger-Ottnad E (1999b) Different regulation of c-Myc-and E2F-1-induced apoptosis during the ongoing cell cycle. Oncogene 18: 843–848PubMedCrossRefGoogle Scholar
  9. Hernandez D, Fisher EMC (1996) Down syndrome genetics: unravelling a multifactorial disorder. Hum Mol Genet 5: 1411–1416PubMedGoogle Scholar
  10. Kligman D, Hilt CD (1988) The S100 protein family. Trends Biochem Sci 13: 437–443 Lubec G, Engidawork E (2002) The brain in Down syndrome (TRISOMY 21). J Neurol 249: 1347–1356Google Scholar
  11. Nurse P (1975) Genetic control of cell size at cell division in yeast. Nature 256: 547–551 Pardee AB (1974) A restriction point for control of normal animal proliferation. Proc Natl Acad Sci USA 71: 1286–1290Google Scholar
  12. Prusa A-R, Hengstschläger M (2002) Amniotic fluid cells and human stem cell research — a new connection. Med Sci Monit 8: 253–257Google Scholar
  13. Pusch O, Bernaschek G, Eilers M, Hengstschläger M (1997) Activation of c-Myc uncouples DNA replication from activation of G1-cyclin-dependent kinases. Oncogene 15: 649–656PubMedCrossRefGoogle Scholar
  14. Soucek T, Rosner M, Miloloza A, Kubista M, Cheadle J, Sampson J, Hengstschläger M (2001) Tuberous sclerosis causing mutants of the TSC2 gene product affect proliferation and p27 expression. Oncogene 20: 4904–4909PubMedCrossRefGoogle Scholar
  15. Vidal-Taboada J, Lu A, Pique M, Pons G, Gil J, Oliva R (2000) Down Syndrome critical region gene 2: expression during mouse development and in human cell lines indicates a function related to cell proliferation. Biochem Biophys Res Corn 272: 156–163CrossRefGoogle Scholar
  16. Wegner R-D (1999) Diagnostic cytogenetics. Springer, Berlin Heidelberg New York TokyoGoogle Scholar
  17. Yoon PW, Freeman SB, Sherman SL, Taft LF, Gu Y, Pettay D, Flanders WD, Khoury MJ, Hassold TJ (1996) Advanced maternal age and the risk of Down syndrome characterized by the meiotic stage of the chromosomal error: a population-based study. Am J Hum Genet 58: 628–633PubMedGoogle Scholar
  18. Zetterberg A, Larsson O, Wiman KG (1995) What is the restriction point? Curr Opin Cell Biol 7: 835–842PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 2003

Authors and Affiliations

  • M. Rosner
    • 1
  • A. Kowalska
    • 1
  • A. Freilinger
    • 1
  • A-R. Prusa
    • 1
  • E. Marton
    • 1
  • M. Hengstschläger
    • 1
    • 2
  1. 1.Obstetrics and Gynecology, Prenatal Diagnosis and TherapyUniversity of ViennaViennaAustria
  2. 2.Obstetrics and Gynecology, Prenatal Diagnosis and TherapyUniversity of ViennaViennaAustria

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