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Congenital defects as indicators of lifelong abnormal processes

Published online by Cambridge University Press:  14 April 2009

H. Grüneberg,
Jean M. Gray and
Gillian M. Truslove
H. Grüneberg
Affiliation:
Experimental Genetics Research Unit (Medical Research Council), University College London
Jean M. Gray
Affiliation:
Experimental Genetics Research Unit (Medical Research Council), University College London
Gillian M. Truslove
Affiliation:
Experimental Genetics Research Unit (Medical Research Council), University College London
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Congenital defects due to genes are the static end results of abnormal processes in embryonic development. Are these ‘burnt out’ and no longer in operation later in life, or do they continue as active physiological processes? To answer this question, thirteen genes with comparatively trivial morphological effects have been subjected to a screen test. For eight of them (bp, f, Ts, Sd, un, se, Os and Ph) a prima facie case has been established for the existence of continuing processes of one kind or another. For the remaining five genes (dn, Pt, T, vt and Miwh) there is no such evidence though the possibility remains that such processes might be detectable by different means.

Information

Type
Research Article
Information
Genetics Research , Volume 6 , Issue 2 , July 1965, pp. 263 - 283
Copyright
Copyright © Cambridge University Press 1965

References

REFERENCES

Bateman, N. (1961). Simultaneous eradication of three ectoparasitic species from a colony of laboratory mice. Nature, Lond. 191, 721–722.Google Scholar
Deol, M. S. (1961). Genetical studies on the skeleton of the mouse. XXVIII. Tail-short. Proc. roy. Soc., B, 155, 78.Google Scholar
Deol, M. S. & Kocher, W. (1958). A new gene for deafness in the mouse. Heredity, 12, 463–466.Google Scholar
Deol, M. S. & Truslove, G. M. (1957). Genetical studies on the skeleton of the mouse. XX. Maternal physiology and variation in the skeleton of C57BL mice. J. Genet. 55, 288–312.Google Scholar
Dunn, L. C., Gluecksohn-Schoenheimer, S. & Bryson, V. (1940). A new mutation in the mouse affecting spinal column and urogenital system. J. Hered. 31, 343–348.Google Scholar
Falconer, D. S., Latyszewski, M. & Isaacson, J. H. (1964). Diabetes insipidus associated with Oligosyndactyly in the mouse. Genet. Res. 5, 473–488.Google Scholar
Green, E. L. & Green, M. C. (1942). The development of three manifestations of the short ear gene in the mouse. J. Morph. 70, 1–19.Google Scholar
Green, M. C. (1958). Effects of the short ear gene in the mouse on cartilage formation in healing bone fractures. J. exp. Zool. 137, 75–88.Google Scholar
Grüneberg, H. (1942 a). The anaemia of flexed-tailed mice (Mus musculus L.). I. Static and dynamic haematology. J. Genet. 43, 45–68.Google Scholar
Grüneberg, H. (1942 b). The anaemia of flexed-tailed mice (Mus musculus L.). II. Siderocytes. J. Genet. 44, 246–271.Google Scholar
Grüneberg, H. (1950). Genetical studies on the skeleton of the mouse. II. Undulated and its ‘modifiers’. J. Genet. 50, 142–173.Google Scholar
Grüneberg, H. (1952). The Genetics of the Mouse, 2nd ed.The Hague: Martinus Nijhoff. Pp. xiv + 650.Google Scholar
Grüneberg, H. (1954). Genetical studies on the skeleton of the mouse. XII. The development of undulated. J. Genet. 52, 441–455.Google Scholar
Grüneberg, H. (1956). Genetical studies on the skeleton of the mouse. XVIII. Three genes for syndactylism. J. Genet. 54, 113–145.Google Scholar
Grüneberg, H. (1958 a). Genetical studies on the skeleton of the mouse. XXII. The development of Danforth's short-tail. J. Embryol. exp. Morph. 6, 124–148.Google Scholar
Grüneberg, H. (1958 b). Genetical studies on the skeleton of the mouse. XXIII. The development of Brachyury and Anury. J. Embryol. exp. Morph. 6, 424–443.Google Scholar
Grüneberg, H. (1961). Genetical studies on the skeleton of the mouse. XXVII. The development of Oligosyndactylism. Genet. Res. 2, 33–42.Google Scholar
Grüneberg, H. (1963). The Pathology of Development. A Study of Inherited Skeletal Disorders in Animals. Oxford: Blackwell Scientific Publications. Pp. xvi + 309.Google Scholar
Grüneberg, H. & Truslove, G. M. (1960). Two closely linked genes in the mouse. Genet. Res. 1, 69–90.Google Scholar
Hunt, H. R., Mixter, R. & Permar, D. (1933). Flexed tail in the mouse, Mus musculus. Genetics, 18, 335–366.Google Scholar
Landauer, W. (1952). Brachypodism, a recessive mutation of house-mice. J. Hered. 43, 293–298.Google Scholar
Law, L. W. (1938). Studies on size inheritance in mice. Genetics, 23, 399–422.Google Scholar
Lynch, C. J. (1921). Short ears, an autosomal mutation in the house mouse. Amer. Nat. 55, 421–426.CrossRefGoogle Scholar
Morgan, W. C. Jr (1950). A new tail-short mutation in the mouse whose lethal effects are conditioned by the residual genotypes. J. Hered. 41, 208–215.Google Scholar