10.6084/M9.FIGSHARE.9912854
Simona Capponi
Simona
Capponi
Nadja Stöffler
Nadja
Stöffler
Manuel Irimia
Manuel
Irimia
Frederik M.A. Van Schaik
Frederik M.A.
Van Schaik
Mercedes M. Ondik
Mercedes M.
Ondik
Martin L. Biniossek
Martin L.
Biniossek
Lisa Lehmann
Lisa
Lehmann
Julia Mitschke
Julia
Mitschke
Marit W. Vermunt
Marit W.
Vermunt
Menno P. Creyghton
Menno P.
Creyghton
Ann M. Graybiel
Ann M.
Graybiel
Thomas Reinheckel
Thomas
Reinheckel
Oliver Schilling
Oliver
Schilling
Benjamin J. Blencowe
Benjamin J.
Blencowe
Jill R. Crittenden
Jill R.
Crittenden
H. Th. Marc Timmers
H. Th. Marc
Timmers
Neuronal-specific microexon splicing of <i>TAF1</i> mRNA is directly regulated by SRRM4/nSR100
<p>Neuronal microexons represent the most highly conserved class of alternative splicing events and their timed expression shapes neuronal biology, including neuronal commitment and differentiation. The six-nt microexon 34ʹ is included in the neuronal form of <i>TAF1</i> mRNA, which encodes the largest subunit of the basal transcription factor TFIID. In this study, we investigate the tissue distribution of <i>TAF1-34ʹ</i> mRNA and protein and the mechanism responsible for its neuronal-specific splicing. Using isoform-specific RNA probes and antibodies, we observe that canonical TAF1 and TAF1-34ʹ have different distributions in the brain, which distinguish proliferating from post-mitotic neurons. Knockdown and ectopic expression experiments demonstrate that the neuronal-specific splicing factor SRRM4/nSR100 promotes the inclusion of microexon 34ʹ into <i>TAF1 </i>mRNA, through the recognition of UGC sequences in the poly-pyrimidine tract upstream of the regulated microexon. These results show that SRRM4 regulates temporal and spatial expression of alternative <i>TAF1</i> mRNAs to generate a neuronal-specific TFIID complex.</p>
Cell Biology
Genetics
Molecular Biology
Neuroscience
Mental Health
Taylor & Francis
2019
2019-09-27
2024-03-22
Journal contribution
1761425 Bytes
10.1080/15476286.2019.1667214
CC BY 4.0