Identification and chromosomal localization of a DNA fragment implicated in the partial correction of the Fanconi anemia group D cellular defect.
Fanconi anemia (FA) cells, complementation group D, which had been transfected with mouse genomic DNA were partially corrected for their mitomycin C (MMC) hypersensitivity. A genomic DNA fragment which complements the resistance of FA(D) cells to MMC close to normal level has been cloned; it has no correcting activity in FA group A cells. It contains two highly conserved regions between the mouse and human genome, which flank mouse repeated DNA. This DNA fragment detects a 3.6-4-kb mRNA transcript in human cells. Moreover this fragment maps to chromosome 11q23, a region of particular interest since several genes involved in the control of major cellular functions are located in this area. This DNA fragment may belong to a gene directly or indirectly involved in FA(D) function.
Diatloff-Zito
C
C
Institut Curie-Biologie, CNRS URA 1292, Paris, France.
Duchaud
E
E
Viegas-Pequignot
E
E
Fraser
D
D
Moustacchi
E
E
D000818:Animals; D001483:Base Sequence; D015152:Blotting, Northern; D015139:Blotting, Southern; D002460:Cell Line; D002874:Chromosome Mapping; D002880:Chromosomes, Human, Pair 11; D003001:Cloning, Molecular; D004247:DNA; D004249:DNA Damage; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics*; D005816:Genetic Complementation Test; D006801:Humans; D051379:Mice; D016685:Mitomycin / Q000494:pharmacology; D008969:Molecular Sequence Data; D015183:Restriction Mapping; D014162:Transfection
D016685:Mitomycin; D004247:DNA