| First Author | Aitken DA | Year | 1979 |
| Journal | Cytogenet Cell Genet | Volume | 25 |
| Pages | 131 (Abstr.) | Mgi Jnum | J:15944 |
| Mgi Id | MGI:64048 | Citation | Aitken DA, et al. (1979) Intrachromosomal assignment of the structural gene for GALT to the short arm of chromosome 9 by gene dosage studies. Cytogenet Cell Genet 25:131 (Abstr.) |
| abstractText | Full text: Complementation studies for Bloom's syndrome with somatic cell hybrids. B. ALHADEFF, W.C. WRIGHT, and M. SINISCALCO; Sloan-Kettering Institute for Cancer Research, New York. The high rate of sister chromatid exchange (SCE), which is characteristic of cultured somatic cells from patients with Bloom's syndrome (BS), was found to be fully corrected in the BS chromosomes retained by somatic cell hybrids between Chinese hamster cells (CHO-YH21) and BS fibroblasts (GM1492), independent of the size and the number of human chromosomes retained. In all of the hybrid lines so far examined, the rodent chromosomes continue to exhibit the parental rate of SCE, while the BS chromosomes have a normal rate of SCE. The Chinese hamster genome has been found to complement the high SCE rate of the BS chromosomes in over 500 metaphases derived from 5 separate primary hybrid clones. Cytogenetic and biochemical studies established that every human chromosome was present in at least 10% of the hybrid cell metaphases analyzed. Thus, we can conclude that the high SCE rate of BS chromosomes is due to a recessive defect which is fully complemented in the hybrid genome. A partial suppression of SCE of about 30% was observed in the BS cells themselves when these were co-cultivated with Chinese hamsterXBloom hybrid cells. In these hybrids the rate of SCE per chromosome (Chinese hamster or human) was unaffected by co-cultivation. The hybridization of BS cells and murine tumor cells (L-A9), which themselves exhibit a significantly higher rate of SCE per murine chromosome, resulted in the correction of the high SCE rate for both murine and BS chromosomes. |
