The left end of rat L1 (L1Rn, long interspersed repeated) DNA which is a CpG island can function as a promoter.
Here we report that the 600 bp promoter-like region at the left end of a newly isolated and characterized rat L1 DNA element can activate the prokaryotic chloramphenicol acyltransferase gene in a rat cell line. Activation only occurs when the promoter region is oriented to the transferase gene as it is to the L1 protein encoding sequences and is 75% inhibited by methylation of just 5 of the 22 CpGs present in the promoter. The G + C rich promoter contains enough CpGs to qualify it as a CpG island, but in contrast to other CpG islands, genomic L1 promoters are fully methylated in both somatic cell and sperm DNA as judged by restriction enzyme analysis. Partial demethylation of the genomic promoters by treatment with 5-azacytidine failed to produce discrete L1 transcripts. The relationship of methylation to the evolutionary history and fate of the rat L1 promoter is discussed.
Nur
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Section on Genomic Structure and Function, National Institute of Diabetes, and Digestive and Kidney Diseases, Bethesda, MD 20892.
Pascale
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Furano
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AV
D000818:Animals; D001374:Azacitidine / Q000494:pharmacology; D001482:Base Composition; D005075:Biological Evolution; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D008745:Methylation; D011401:Promoter Regions, Genetic; D051381:Rats / Q000235:genetics*; D012045:Regulatory Sequences, Nucleic Acid; D012091:Repetitive Sequences, Nucleic Acid; D014158:Transcription, Genetic
D015500:Chloramphenicol O-Acetyltransferase; D001374:Azacitidine