The ancestory of Koller's subline of the C57BL strain is not known. A study of the minor skeletal variants in this subHne showed that it differs from the other ten sublines of C57BL more than they difier from each other. It appears to have separated from. the rest before the genotypes of the sublines had been fixed by inbreeding. There is enough evidence to show that it is indeed a branch of C57BL strain.The rate of divergence of the sublines of C57BL is surprisingly high. It is reconsidered whether the whole of this divergence can be explained by recent mutations or whether residual heterozygosis has also played a part in it.

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A karyotype of the mitotic chromosomes of the house mouse has been prepared based upon quinacrine fluorescence patterns. All 19 pairs of autosomes and the X and Y chromosomes have been identified. Examination of the chromosomes of the following translocation stocks, T(11;?)lAld, T(3;?)6Ca, T(2;9)138Ca, T(2;12)163H, and T(9;13)19OCa, have led to the tentative assignments of autosomal linkage groups (LG) Meiotic studies of the house mouse, Mus musculus, have been very informative (1), but mitotic studies have been restricted by the limited variation in morphology of the chromosomes, all of which are acrocentric with small gradations in length. The only translocations that could be detected in stained preparations of mitotic chromosomes involved a marked change in length, such as the presence of a minute chromosome in the T6 (2) and one very long and one very short chromosome in the T190 (3), or the formation of a metacentric chromosome, as in the T163 (4). Bennett (3), who gives a brief review of prior cytologic studies, used the secondary constrictions in several chromosomes to help divide the complement into pairs. She was unable to detect any abnormality in T138.It was recently reported that quinacrine and quinacrine mustard are bound to the DNA of human chromosomes in such a highly specific manner that each chromosome can be identified by its pattern of quinacrine fluorescence (5). Furthermore, the fluorescence patterns of chromosomal segments do not appear to be altered by translocation (6).The accuracy of the quinacrine fluorescence technique of chromosome identification, and the availability of numerous potentially overlapping translocations in the house mouse, suggested to us the possibility of assigning the known murine linkage groups (LG) involved in these translocations to their specific chromosomes. MATERIALS AND METHODSStandard inbred and hybrid mice were purchased from The Jackson Laboratory, as were translocation stocks T(3;?)6Ca and T(2;9)138Ca. Translocation stocks T(2;12)163H,T(11;?)-lAld, and T(9;13)19OCa were obtained from the M.R.C. Primary tissue cultures were established from mice by trypsinization of 11-to 13-day embryos in saline-citrate to obtain suspensions of single cells (10). Cells were grown in HEPES-buffered Nutrient Mixture containing 10% calf serum and 5% fetal calf serum. Falcon tissue-culture flasks (75 cm2) were used and each flask was seeded with 10-12 ml of a suspension containing 5 X 105 viable cells/ml. After 2 or 3 days at 370C, cells (including a large proportion in metaphase) were collected by washing the cell surface twice with calcium-and magnesium-free phosphate-buffered saline, followed by a 5-min treatment of the surface with 3 ml per flask of 0.25% Viokase. Cells from 5-7 flasks were pooled, and Colcemid was added to a final concentration of 0.5 ,g/ml. Cells were immediately pelleted by centrifugation at 500 g for 10 min, resuspended in 10 ml of 0.032 M KCl, and incubated at 37°C for 5 min. 0.5 ml of freshly prepared fixative (methyl alcohol-glacial acet...

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Quinacrine-fluorescence karyotypes were prepared on a series of human cell lines. WI-38 karyotypes were indistinguishable from those obtained from cultured XX blood leukocytes. WI-L2 lymphoblastoid cells were 46, XY and pseudodiploid, with a single chromosome 21 and an additional submetacentric marker whose short arm may have been derived from a No. 21. Three HeLa cell lines had several marker chromosomes in common. Three of these marker chromosomes were also present in a D98/AG line, which therefore must have been of HeLa cell origin. Another cell line of presumptive human origin was shown to be a contaminant, of mouse origin.