Molecular misreading in non-neuronal cells

+1 Frame-shifted proteins such as amyloid precursor protein(+1) and ubiquit in-B+1 have been identified in the neuropathological hallmarks of Alzheimer 's disease. These frameshifts are caused by dinucleotide deletions in GAGAG motifs of messenger RNA encoded by genes that have maintained the unchange d wild-type DNA sequence. This process is termed 'molecular misreading'. A key question is whether this process is confined to neurons or whether it c ould also occur in non-neuronal cells. A transgenic mouse line (MV-B) carry ing multiple copies of a rat vasopressin minigene as a reporter driven by t he MMTV-LTR promotor was used to screen non-neuronal tissues for molecular misreading by means of detection of the rat vasopressin(+1) protein and mut ated mRNA. Molecular misreading was demonstrated to occur in several organs (e.g., epididymis and the parotid gland) where transgenic vasopressin expr ession is abundant, but its penetrance is variable both between and within tissues. This implies that non-neural tissues too, could be affected by cel lular derangements caused by molecular misreading.