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Biomedical subjects

N Takagi

Publications and source records attributed to N Takagi.

At least 307 records · Page 17Linked to original sources

Cytologic evidence for preferential inactivation of the paternally derived X chromosome in XX mouse blastocysts.

A total of 941 mouse blastocysts obtained from two types of crosses in which one of parents carried Cattanach's X/autosome translocation was studied cytogenetically by quinacrine mustard fluorescence. The rearranged X (Xt) and the normal X (Xh) were distinguished by size. Karyotype analysis was successful in 721 embryos, of which 205 were heterozygous for Cattanach's translocation. A single heterochromatic and brightly fluorescent X chromosome was identified in 154 metaphase spreads from 89 blastocysts consisting of 32--96 cells. The paternally derived X chromosome (Xp) was heterochromatic in 87% and 88% of the informative cells from the crosses XnXn x XtY and XtXn x XnY, respectively. This preferential choice of Xp at the blastocyst stage might have an important bearing upon the preponderance of cells with an inactive Xp in the chorion and yolk-sac splanchnopleure.

Animals↗

Chromosomal characteristics of six cultured lymphoblastoid cell lines originating from Marek's disease lymphomas.

Cytogenetic observations were made on 6 cell lines (MOB-1, MOB-2, MOB-3, MSB-1, HPRS Line 1, HPRS Line2) originating from Marek's disease lymphomas and 2 clones (1104-B, 1104-X-5) of a cell line established from an avian lymphoid leukosis tumor. The modal chromosome number was within the diploid range in all the lines except HPRS Line 1 and HPRS Line 2, both of which had a mode at about 60. Karyotypes were grossly abnormal in 4 cell lines: trisomy for No. 1 in MOB-2; the heteromorphic No. 1 pair in MSB-1, and marker chromosomes derived from rearrangements involving No. 3 or No. 5 and unidentified elements in HPRS Lines 1 and 2. The MOB-1 line which had been characterized by cells with an apparently normal karyotype was completely taken over by cells with a heteromorphic No. 1 pair morphologically similar to the one found in MSB-1 by the 95th day of continuous growth in vitro. BUdR-acridine orange differential staining technique revealed, however, different banding patterns in these abnormal chromosomes.

Acridines↗

Stability of X chromosome differentiation in mouse embryos. Reversal may not be responsible for the extreme X-inactivation mosaicism in extraembryonic membranes.

By means of a double labeling method with H3-thymidine and 5-bromodeoxyuridine, it was found that the X chromosome showed no sign of change from an allocyclic to an isocyclic state, or vice vers in 6.5- and 7.5-day mouse embryos. Thus, reversal of allocycly may not account for the predominance of cells with the paternally derived X chromosome inactive in the yolk sac and the chorion of the mouse embryo.

Animals↗

Meiotic disjunction in t(14;15)6ca heterozygotes and fate of chromosomally unbalanced gametes in embryonic development.

In heterozygous carriers of the mouse reciprocal translocation T(14;15)6Ca, the frequency of nondisjunction involving the minute marker chromosome was 4.4% in the male and 22.2% in the female. The fate of gametes with unbalanced genomes derived from normal as well as abnormal meiotic disjunction in T6 heterozygotes was investigated on the basis of chromosome counts at metaphase II and karyotype analyses in early postimplantation embryos produced by backcrossing with chromosomally normal animals. Results obtained indicate that meiotic, gametic, and zygotic selection attributable to specific types of chromosomal imbalances is minimal, if any, by the late blastocyst stage. All zygotes with unbalanced genomes, except those with 20 normal pairs plus the minute marker, however, die off in the latter half of pregnancy. Therefore, the increased incidence of translocation trisomics among progeny of female as compared with male heterozygotes reflects the higher incidence of nondisjunction in primary oocytes than in spermatocytes.

Animals↗