Nucleic Acids Research, Vol 25, Issue 9 1678-1684, Copyright © 1997 by Oxford University Press
K Savitsky, M Platzer, T Uziel, S Gilad, A Sartiel, A Rosenthal, O Elroy-Stein, Y Shiloh and G Rotman
Mutations in the ATM gene are responsible for the multisystem disorder
ataxia-telangiectasia, characterized by neurodegeneration, immune
deficiency and cancer predisposition. While no alternative splicing was
identified within the coding region, the first four exons of the ATM gene,
which fall within the 5'untranslated region (UTR), undergo extensive
alternative splicing. We identified 12 different 5'UTRs that show
considerable diversity in length and sequence contents. These mRNA leaders,
which range from 150 to 884 nucleotides (nt), are expected to form variable
secondary structures and contain different numbers of AUG codons. The
longest 5'UTR contains a total of 18 AUGs upstream of the translation start
site. The 3'UTR of 3590 nt is contained within a single 3'exon. Alternative
polyadenylation results in 3'UTRs of varying lengths. These structural
features suggest that ATM expression might be subject to complex
post-transcriptional regulation, enabling rapid modulation of ATM protein
level in response to environmental stimuli or alterations in cellular
physiological states.
ARTICLES
Ataxia-telangiectasia: structural diversity of untranslated sequences suggests complex post-transcriptional regulation of ATM gene expression
Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel.
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