Soluble mouse major histocompatibility complex class II molecules produced inDrosophila cells

1995 ◽  
Vol 25 (5) ◽  
pp. 1262-1266 ◽  
Author(s):  
Hans-Joachim Wallny ◽  
Giuseppina Sollami ◽  
Klaus Karjalainen
1998 ◽  
Vol 18 (8) ◽  
pp. 4433-4443 ◽  
Author(s):  
Donald Macleod ◽  
Robin R. Ali ◽  
Adrian Bird

ABSTRACT Nonmethylated CpG islands are generally located at the 5′ ends of genes, but a CpG island in the mouse major histocompatibility complex class II I-Aβ gene is remote from the promoter and covers exon 2. We have found that this CpG island includes a novel intronic promoter that is active in embryonic and germ cells. The resulting transcript potentially encodes a severely truncated protein which would lack the signal peptide and external β1 domains. The functional significance of the internal CpG island may be to facilitate gene conversion, thereby sustaining the high level of polymorphism seen at exon 2. Deletions of the I-Aβ CpG island promoter reduce transcription and frequently lead to methylation of the CpG island in a transgenic mouse assay. These and other results support the idea that all CpG islands arise at promoters that are active in early embryonic cells.


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