Advertisement

Chromosome Segregation and Aneuploidy

  • Baldev K. Vig
Part of the NATO ASI Series book series (volume 72)

Abstract

Of all genetic afflictions of man, aneuploidy ranks as the most prevalent. Among liveborn babies aneuploidy exist to the extent of about 0.3%, to about 5% among stillborns and a dramatic 25% among miscarriages. The burden is too heavy to be taken lightly. Whereas cytogeneticists are capable of tracing the origin of the extra or missing chromosome to the contributing parent, it is not certain what factors are responsible for this ‘epidemic’ affecting the human genome. The matter is complicated by the observation that, to the best of our knowledge, all chromosomes do not malsegregate with equal frequency. Chromosome number 16, for example, is the most prevalent among abortuses -one-third of all aneuploid miscarriages are due to trisomy 16 (Chandley, 1987) — yet it never appears in aneuploid constitution among the liveborn. Some chromosomes, number 1, for example, appear only rarely, if at all. In the latter case painstaking efforts have to be made to karyotype very early stages of embryonic development, as early as the 8-cell stage. Even though no convincing data are yet available, it is conceivable that the product of most aneuploid zygotes are lost before implantation.

Keywords

Chromosome Segregation Alpha Satellite Spindle Microtubule Indian Muntjac Centromere Sequence 
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.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Bond D.J. and Chandley, A.C. (1983) Aneuploidy. Oxford University Press.Google Scholar
  2. Chandley, A. C. (1987) Aneuploidy: An introduction. In Aneuploidy, Part A: Incidence and Etiology (B.K. Vig and A.A. Sandberg, Eds) Alan R. Liss, New York, Pp. 1–8.Google Scholar
  3. Dellarco, V.L., Voytek, P.E. and Hollander, A. (1985) Aneuploidy — Etiology and Mechanisms. Plenum Press. New York.Google Scholar
  4. Resnick M. and Vig B. K. (1989) Mechanisms of Chromosome Distribution and Aneuploidy. Alan R. Liss, New York.Google Scholar
  5. Earnshaw WC, Ratrie BE, Mulligan RC (1989) Visualization of centromere proteins CENP-B and CENP-C on a stable dicentric chromosomes in cytological spreads. Chromosoma 98:1–12.PubMedCrossRefGoogle Scholar
  6. Radic, M.Z., Saghbini, M, Elton, T, Reeves, R. and Hamkalo, B. (1992) Hoechst 33258, distamycin A, and high mobility group protein I (HMG-I) compete for binding to mouse satellite DNA. Chromosoma 101: 602–608.PubMedCrossRefGoogle Scholar
  7. Resnick, M.A. and Vig, B. K. (1989) Mechanisms of Chromosome Distribution and Aneuploidy. Alan R. Liss, New York.Google Scholar
  8. Sullivan KF, Glass CA (1991) CENP-B is a highly conserved mammalian centromere protein with homology to the helix-loop-helix family of proteins. Chromosoma 100:360–370.PubMedCrossRefGoogle Scholar
  9. Varma, R.S. and Luke S. (1992) variations in alphoid DNA sequence escape detection of aneuploidy at interphase by FISH technique. Genomics 14: 113–116.CrossRefGoogle Scholar
  10. Vig, B.K. and Sandberg A.A. (1987) Aneuploidy, Part A: Incidence and Etiology. Alan R. Liss, New York.Google Scholar
  11. Vig, B.K. and Sandberg A.A. (1988) Aneuploidy, Part B: Induction and Test Systems. Alan R. Liss, New York.Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1993

Authors and Affiliations

  • Baldev K. Vig
    • 1
  1. 1.Department of BiologyUniversity of NevadaRenoUSA

Personalised recommendations