Mapping Data

Experiment

• Experiment
  TEXT
• Chromosome
  9
• Reference
  J:36671 Jongmans W, et al., The defect in the AT-like hamster cell mutants is complemented by mouse chromosome 9 but not by any of the human chromosomes. Mutat Res. 1996 Oct 18;364(2):91-102
• ID
  MGI:47806

Genes

Gene	Assay Type	Description
Atm	Southern analysis	Atm cDNA3

Notes

• Experiment
  Authors conducted experiments to attempt to determine which human chromosome complements X-ray sensitivity of ataxia telangiectasia (AT)-like hamster cell mutants. Results of these experiments did not identify a human chromosome; however, the results didsuggest that a co-introduced mouse chromosome could be responsible for the observed complementation found in the X-ray resistant hybrid clones. A screen of the X-ray resistant hybrid clones using mouse chromosome specific SSRs identified the presence of mouse Chromosome 9 in all of the X-ray resistant hybrid clones. This finding was confirmed through Southern blot analysis using a Ldlr probe (Ldlr was previously shown to map to mouse Chromosome 9). Futher experiments using Southern blot analysis and in situ hybridization confirmed that mouse Chromsome 9, not human Chromosome 4 (which also contained in a majority of X-ray resistant clones), was responsible for the observed complementation of the X-ray sensitivity in the AT-like hamster mutants. Southern blot analysis of the AT-like hamster cell mutant hybrids and A9 mouse genomic DNA using Atm cDNA3 indicates that Atm maps to mouse Chromosome 9.