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Published online before print May 18, 2006, 10.1261/rna.84406
RNA (2006), 12:1149-1153. Published by Cold Spring Harbor Laboratory Press. Copyright © 2006 RNA Society.
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HYPOTHESIS

The potential role of ribosomal frameshifting in generating aberrant proteins implicated in neurodegenerative diseases

Norma M. Wills1 and John F. Atkins1,2

1 Department of Human Genetics, University of Utah, Salt Lake City, Utah 84112-5330, USA
2 Biosciences Institute, University College Cork, Cork, Ireland

Aberrant forms of proteins ubiquitin B and ß-amyloid precusor protein, UBB+1 and APP+1, are implicated in human neurodegenerative diseases. They have their carboxyl-terminal regions derived from an alternative reading frame. Transcription slippage has been invoked to explain the production of these proteins from abnormal mRNA. However, ribosomal frameshifting on wild-type mRNA may account for the great majority of the aberrant protein. Ribosomal frameshifting may also be involved in the progression of triplet expansion diseases such as Huntington's and spinocerebellar ataxias. In a particular spinocerebellar ataxia, SCA3, Toulouse and colleagues recently discovered –1 frameshifting in a transcript containing an expanded CAG-repeat. Antibiotics that affect mammalian ribosomes may have complex effects on frameshifting and disease progression.

Keywords: ribosomal frameshifting; Alzheimer's disease; molecular misreading; UBB+1; APP+1; polyglutamine disease

Received March 10, 2006 ; accepted April 12, 2006.


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