Mice lacking Snrpn expression show normal regulation of neuronal alternative splicing events.
The SmN protein is closely related to the constitutively expressed RNA splicing protein SmB but is expressed only in brain and heart tissue. Mice which lack expression of SmN die shortly after birth suggesting a critical role for this protein possibly in the regulation of neuronal-specific alternative splicing events. We show here however that the neuronal-specific alternative splicing of the RNAs encoding several different classes of protein proceeds normally in mice lacking SmN expression. The potential role of SmN and the reasons for the lethal effect observed in non-expressing mice are discussed.
Department of Molecular Pathology, University College London Medical School, UK.
J D
JD
Huntriss
J A
JA
Barr
D A
DA
Horn
D G
DG
Williams
D S
DS
Latchman
D017398:Alternative Splicing; D000818:Animals; D001324:Autoantigens / Q000235:genetics*; D051379:Mice; D009474:Neurons / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D017411:Ribonucleoproteins, Small Nuclear / Q000235:genetics*; D055517:snRNP Core Proteins
D001324:Autoantigens; D012333:RNA, Messenger; D017411:Ribonucleoproteins, Small Nuclear; C526416:Snrpb protein, mouse; D055517:snRNP Core Proteins