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Single copy probes derived from CpG-rich island clones from Eag I and Not I linking libraries and nine rare-cutter restriction endonucleases were used to investigate the methylation status of CpG-rich islands on the inactive and active X chromosomes (Chr) of the mouse. Thirteen of the 14 probes used detected CpG-rich islands in genomic DNA. The majority of island CpGs detected by rare-cutter restriction endonucleases were methylated on the inactive X Chr and unmethylated on the active X Chr, but some heterogeneity within the cell population used to make genomic DNA was detected. The CpG-rich islands detected by two putative pseudoautosomal probes remained unmethylated on both the active and inactive X Chrs. Otherwise, distance from the X Chr inactivation center did not affect the methylation profile of CpG-rich islands. We conclude that methylation of CpG-rich islands is a general feature of X Chr inactivation.

Type

Journal article

Journal

Mamm Genome

Publication Date

1991

Volume

1

Pages

78 - 83

Keywords

Animals, Base Sequence, Deoxyribonucleases, Type II Site-Specific, Dosage Compensation, Genetic, Female, Heterochromatin, Male, Methylation, Mice, Mice, Inbred BALB C, Molecular Sequence Data, X Chromosome