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Publication : Establishment of a mouse stock heterozygous and homozygous for a new reciprocal translocation T(7;17)3Bkm

First Author  Benova D Year  1990
Journal  Mouse News Lett Volume  87
Pages  100-2 Mgi Jnum  J:28998
Mgi Id  MGI:76536 Citation  Benova D, et al. (1990) Establishment of a mouse stock heterozygous and homozygous for a new reciprocal translocation T(7;17)3Bkm. Mouse News Lett 87:100-2
abstractText  Full text of MNL contribution: S O F I A Institute of Nuclear Medicine, Radiobiology and Radiation Hygiene: D. Benova and M. Koleva; and National Ontological Centre, Medical Academy, Sofia: Y. Manolova. Received: 1st December, 1989. ESTABLISHMENT OF A MOUSE STOCK HETEROZYGOUS AND HOMOZYGOUS FOR A NEW RECIPROCAL TRANSLOCATION T(7;17)3BKM. The present paper describes a new mouse reciprocal translocation induced by radiation and its establishment as a stock of translocation heterozygotes and homozygotes. Development of a mouse stock with a reciprocal translocation. Male mice from the strain C57BL, aged 16 weeks, with proven fertility, were given an acute whole body irradiation with a dose of 8,5 Gy<137>Cs gamma rays at a dose rate of 1,26 Gy/min. Immediately after the irradiation each male was mated to three non-irradiated females during 7 days. The females were from the same strain, aged 14-16 weeks and most of them had littered once. The offspring was numbered individualy at weaning and was mated upon reaching sexual maturity. Translocation heterozygosity was determined by studying the germ cells of F>l< and F>2< males after they had reproduced. Cytogenetic analysis of spermatocytes in diakinesis-metaphases I was performed according to the method of Evans et al.(1). The translocation T3BKM was first detected in one of the sons of a female carrier conceived by a normal mother and a father with irradiated mature spermatozoa. This female carrier had been mated to a cytogenetically proven normal partner. She had 5 litters in all, consisting of 12 viable offsprings and one had died soon after birth. Heterozygosity was ascertained in three sons of this female carrier. One of them is the ancestor of the stock. After mating with two normal females and one female-carrier/his daughter/ he gave a generation of 24 viable individuals, 12 of them being translocation heterozygotes. The translocation was maintained mainly by intercrossing; in rare occasion backcrossing was performed. Analysis of conventionally stained metaphase spreads of bone-marrow cells from the translocation carriers revealed a marker chromosome. This facilitated the recognition of heterozygosity in both sexes. Subsequent intercrosses produced mice homozygous for the T3BKM with normal reproductive performance. At present the established mouse stock consists of translocation heterozygotes, translocation homozygotes as well as their normal litter-mates. There are no discernible phenotype differences between them. Identification of the exchanged chromosome segments. G-banded chromosomes from bone-marrow cells of normal mice, translocation heterozygotes and translocation homozygotes were karyotyped. Early metaphase chromosome preparations from bone-marrow cells were obtained by introducing some modifications in the method of Ford and Woollam(2) - 5 min. in vivo colchicine action and 45 min. hypotonic treatment. The G-banding technique was applied after adapting several methods/4,5,7/. The translocation is reciprocal, with exchange of segments of chromosome 7 and 17. According to the classification of Nesbitt and Francke(4) the translocation should be classified as T(7;17) (F4;B1). Our attention was drawn by the existence of a more complex banding pattern at the site of the rearrangement in marker 7, as well as in the normal number 7 chromosomes in an earlier metaphase. The banding pattern of the normal chromosome 7 revealed, that the minor band indicated as F4 by Nesbitt and Francke actually consists of two G-positive bands-proximal relatively wide and intensely stained, and distal-very narrow and paler, separated by a G-negative band. Thus in a more precise representation of the translocation, the specified subbands should be designated as F4, F5 and F6. In this case the breakpoint in chromosome 7 is at the G-negative subband F5, part of which and the G-positive F6 are translocated to the deleted G-negative band B1 chromosome 17. The precise formula of the translocation is T(7;17)(F5;Bl). Retention of the differentiation in an early phase of contraction at the site of rearrangement in a marker chromosome/prosomisation/, like the presented one in marker 7, was first described by one of us in the Burkitts lymphoma(3). From the genetic maps of mouse chromosome given by Searle et al.(6) it can be seen that the translocated segment maybe comprises a very interesting part of the mouse genome, namely t-complex. ACKNOWLEDGEMENTS The authors are grateful to Professor A.T.Natarajan for his encouragement and reading of the manuscript and to Drs. P.De Boer and E.Evans for their help in the identification of the breakpoints of the translocation. REFERENCES 1. Evans,E., C.Breckon, C.Ford: An air-method for meiotic preparations from mammalian testes, Cytogenetics, 3,289-294,1964. 2. Ford,E., D.Woollam: A study of the mitotic chromosomes of mice of the strong A line, Exp. Cell Res., 32,320-326,1963. 3. Manolova,Y., G.Manolov, J.Kieler, A.Levan: Genesis of the 14q<+> marker in Burkitts lymphoma, Hereditas, 90,5-10,1979. 4. Nesbitt,M., U.Francke: A system of nomenclature for band patterns of mouse chromosome, Chromosoma(Berl.), 41,145-158,1973. 5. Seabright,M.: A rapid banding technique for human chromosomes, The Lancet, II, 971-972,1971. 6. Searle,A., J.Peters, M.Lyon, E.Evans, J.Edwards, V.Buckle: Chromosome maps of man and mouse, III, Genomics, 1, 3-18,1987. 7. Sumner,A., H.Evans, R.Buckland: New technique for distinguishing between human chromosomes, Nature, New Biol., 232,31-32,1971.
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