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Title: Sequence elements surrounding the acceptor site suppress alternative splicing of the sarco/endoplasmic reticulum Ca2+-ATPase 2 gene transcript
Authors: Van Den Bosch, Ludo ×
Mertens, Luc
Gijsbers, Sofie
Ver Heyen, Mark
Wuytack, Frank
Eggermont, Jan #
Issue Date: May-1997
Series Title: The Biochemical journal. vol:322 ( Pt 3) pages:885-91
Abstract: Expression of the muscle-specific 2a isoform of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2) requires activation of an inefficient optional splice process at the 3' end of the primary gene transcript. The sequence elements required for this regulated splice event were studied by modifying a minigene containing the 3' end of the SERCA2 gene. An important requirement appears to be a strong muscle-specific acceptor site, as replacing it by a weak one prevented the induction of muscle-type splicing during myogenic differentiation. The induction of muscle-type splicing did not depend on positive cis-active sequences in the muscle-specific exon. On the other hand, replacement of a broad region around the acceptor site dramatically deregulated the expression pattern, as this modification strongly induced muscle-type splicing in undifferentiated muscle cells and in fibroblasts. This cis-active region is also involved in the suppression of the neuronal type of splicing. Furthermore selective replacement of the acceptor site as well as deletions or replacements in the muscle-specific exon induced muscle-type splicing to various extents in undifferentiated myogenic cells. Therefore sequence elements in the distal part of the optional intron and in the muscle-specific exon contribute to the suppression of muscle-specific SERCA2 splicing.
URI: 
ISSN: 0264-6021
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Physiology Section (-)
Research Group Experimental Neurology
Laboratory of Virology and Chemotherapy (Rega Institute)
Laboratory for Neurobiology (Vesalius Research Center)
Laboratory of Cellular Transport Systems
× corresponding author
# (joint) last author

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