Hostname: page-component-586b7cd67f-r5fsc Total loading time: 0 Render date: 2024-11-20T07:17:37.709Z Has data issue: false hasContentIssue false
  • English
  • Français

On the dynamics of activation of mammalian X chromosomes

Published online by Cambridge University Press:  14 April 2009

N. Mukunda ,
H. Sharat Chandra ,
Madhav Gadgil ,
A. K. Rajagopal  and
E. C. G. Sudarshan
N. Mukunda
Affiliation:
Centre for Theoretical StudiesIndian Institute of ScienceBangalore 560 012, India
H. Sharat Chandra
Affiliation:
Centre for Theoretical StudiesIndian Institute of ScienceBangalore 560 012, India Microbiology Cell Biology LaboratoryIndian Institute of Science, Bangalore 560 012, India
Madhav Gadgil
Affiliation:
Centre for Theoretical StudiesIndian Institute of ScienceBangalore 560 012, India
A. K. Rajagopal
Affiliation:
Centre for Theoretical StudiesIndian Institute of ScienceBangalore 560 012, India
E. C. G. Sudarshan
Affiliation:
Centre for Theoretical StudiesIndian Institute of ScienceBangalore 560 012, India
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

We have investigated a mathematical model of the process of activation of the X chromosomes in eutherian mammals. The model assumes that the activation is brought about over some definite time interval T by the complete saturation of N receptor sites on an X chromosome by M activating molecules (or multiples of M). The probability λ of a first hit on the receptor site is considered to be very much lower than that of subsequent hits; that is, we assume strong co-operative binding. Assuming further that an incomplete saturation of receptor sites is malfunctional, we can show that for proper activation of X chromosomes in normal diploid males and females, we must have λMT ≥ 3 and 0·96 ≤ N/M ≤ 1. An extension of this analysis for the triploid cases shows that under these conditions, we cannot explain the activation of two X's if the number of activating molecules is fixed at M. This suggests that there must be two classes of triploid embryos differing from each other in a step-wise manner in the number of activating molecules. In other words, triploids with two active X chromosomes would require 2M activating molecules as opposed to M molecules in triploids with a single active X. This interpretation of the two classes of triploids would be consistent with differing imprinting histories of the parental contributions to the triploid zygote.

Type
Research Article
Information
Genetics Research , Volume 28 , Issue 2 , October 1976 , pp. 147 - 162
Copyright
Copyright © Cambridge University Press 1976

References

REFERENCES

Brown, S. W. & Chandra, H. S. (1973). Inactivation system of the mammalian X chromosome. Proceedings of the National Academy of Sciences, U.S.A. 70, 195–199.Google Scholar
Cattanach, B. M. (1975). Control of chromosome inactivation. Annual Review of Genetics 9, 1–18.Google Scholar
Chandra, H. S. & Brown, S. W. (1975). Chromosome imprinting and the mammalian X chromosome. Nature 253, 165–168.Google Scholar
Drews, U., Blecher, S. R., Owen, D. A. & Ohno, S. (1974). Genetically directed preferential X-activation seen in mice. Cell 1, 3–8.CrossRefGoogle Scholar
Lyon, M. F. (1961). Gene action in the P-chromosome of the mouse (Mus musculus L.). Nature 190, 372–373.Google Scholar
Lyon, M. F. (1974). Mechanisms and evolutionary origins of variable X chromosome activity in mammals. Proceedings of the Royal Society, London B 187, 243–268.Google Scholar
Ohno, S. (1973). Conservation of ancient linkage groups in evolution and some insight into the genetic regulatory mechanism of X-inactivation. Cold Spring Harbor Symposia on Quantitative Biology 38, 155–164.CrossRefGoogle Scholar
Pernis, B., Chiappino, G., Kelus, A. S. & Gell, P. G. H. (1965). Cellular localization of immunoglobulins with different allotypic specificities in rabbit lymphoid tissues. Journal of Experimental Medicine 122, 853–875.Google Scholar
Weiler, E. (1965). Differential activity of allelic γ-globulin genes in antibody-producing cells. Proceedings of the National Academy of Sciences, U.S.A. 54, 1765–1772.CrossRefGoogle ScholarPubMed