Summary
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1.
Tail-kinks (tk/tk) in the mouse is clue to a simple autosomal recessive gene with regular manifestation and full viability under laboratory conditions.
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The major effects of the tail-kinks gene are confined to the axial skeleton. This is grossly affected in the cervical and upper thoracic and again in the caudal region; the intervening region is almost normal. Ribs are often involved and the manubrium sterol is usually fused to the next sternebra.
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The distribution of abnormalities over the vertebral column is such that the small vertebrae at both ends are severely affected while the large ones in the middle are almost immune.
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The abnormalities of the osseous skeleton are preformed in cartilage and are visible to the full extent as soon as chondrification sets in.
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The abnormalities of the cartilaginous skeleton are preceded by defects in the membranous skeleton. These can be traced back to the 10-day stage (C.R..L. 4–5 mm.) when in the normal embryo the cervical sclerotomes have differentiated into anterior and posterior sclerotome halves which differ in tissue density whiletk/tk embryos do not yet show any signs of this differentiation. No differences have been discovered in 9-day embryos (C.R.L. about 3 mm.).
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This paper is dedicated to Prof. Alfred Kühn on the occasion of his 70th birthday (22 April 1955).
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Grüneberg, H. Genetical studies on the skeleton of the mouse xvi. Tail-kinks. J Genet 53, 536–550 (1955). https://doi.org/10.1007/BF02981673
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DOI: https://doi.org/10.1007/BF02981673