1. Human and mouse SYBL1 gene structure and expression
- Author
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Maria Giuseppina Miano, Marcella Vacca, Maria Strazzullo, Grazia Mercadante, Maria R. Matarazzo, Michele D'Urso, Anna Curci, Monica Cuccurese, Alfredo Ciccodicola, Massimo Cocchia, Anna Torino, and Maurizio D'Esposito
- Subjects
Chloramphenicol O-Acetyltransferase ,Male ,Transcription, Genetic ,Recombinant Fusion Proteins ,Molecular Sequence Data ,Pseudoautosomal region ,Gene Expression ,Regulatory Sequences, Nucleic Acid ,Biology ,R-SNARE Proteins ,Mice ,Exon ,Sequence Homology, Nucleic Acid ,Genetics ,Transcriptional regulation ,Animals ,Humans ,Gene silencing ,Tissue Distribution ,RNA, Messenger ,Promoter Regions, Genetic ,Gene ,Binding Sites ,Base Sequence ,Gene Expression Regulation, Developmental ,Membrane Proteins ,DNA ,Exons ,Sequence Analysis, DNA ,General Medicine ,Blotting, Northern ,Introns ,Genes ,Regulatory sequence ,DNA methylation ,SYBL1 ,HeLa Cells - Abstract
SYBL1 is a gene in the 320 kb human pseudo-autosomal region at the terminus of Xq and Yq. In contrast to other pseudoautosomal genes, SYBL1 is inactivated on one X in every female cell, and is also inactive on the Y of male cells. Hypermethylation of the CpG island associated with the human gene is involved in this phenomenon. In an attempt to further examine its regulation, the genomic organization of the X-linked mouse Sybl1 homolog was analyzed and compared with the human gene. Human and mouse show the same exon number, exon–intron junctions and a highly conserved basal promoter. The structural and functional conservation of basal regulatory regions suggests that inactivation is imposed by similar auxiliary epistatic regulatory mechanism.
- Published
- 1999
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