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.
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References
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: 146–149
Arendt T (2002) Dysregulation of neuronal differentiation and cell cycle control in Alzheimer’s disease. J Neural Transm [Suppl] 62: 77–85
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: 68–70
Cairns NJ (1999) Neuropathology. J Neural Transm [Suppl] 57: 61–74
Capone GT (2001) Down syndrome: advances in molecular biology and the neurosciences. Dev Behav Ped 22: 40–59
Engidawork E, Lubec G (2003) Molecular changes in fetal Down syndrome brain. J Neurochem 84: 895–904
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: 1–9
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: 843–848
Hernandez D, Fisher EMC (1996) Down syndrome genetics: unravelling a multifactorial disorder. Hum Mol Genet 5: 1411–1416
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: 1347–1356
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: 1286–1290
Prusa A-R, Hengstschläger M (2002) Amniotic fluid cells and human stem cell research — a new connection. Med Sci Monit 8: 253–257
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: 649–656
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: 4904–4909
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: 156–163
Wegner R-D (1999) Diagnostic cytogenetics. Springer, Berlin Heidelberg New York Tokyo
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: 628–633
Zetterberg A, Larsson O, Wiman KG (1995) What is the restriction point? Curr Opin Cell Biol 7: 835–842
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© 2003 Springer-Verlag
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Rosner, M., Kowalska, A., Freilinger, A., Prusa, AR., Marton, E., Hengstschläger, M. (2003). Cell cycle and cell size regulation in Down Syndrome cells. In: Lubec, G. (eds) Advances in Down Syndrome Research. Journal of Neural Transmission Supplement 67, vol 67. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6721-2_4
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DOI: https://doi.org/10.1007/978-3-7091-6721-2_4
Publisher Name: Springer, Vienna
Print ISBN: 978-3-211-40776-9
Online ISBN: 978-3-7091-6721-2
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