Regulation of Shootin1 Gene Expression Involves NGF-induced Alternative Splicing during Neuronal Differentiation of PC12 Cells

ArticleAçık Erişim

Özet

Shootin1 is a protein involved in neuronal polarization, and has been shown to be a key molecule for the positive/negative feedback loop for axon induction required during neuronal symmetry breaking. To better understand the molecular basis of shootin1 dynamics, we analysed the regulatory pathways and the expressional status of shootin1 gene during NGF-induced neuronal differentiation. We demonstrated that the isoform-1 and isoform-2 of shootin1 is differentially expressed during neuronal differentiation. By blocking individual downstream pathways of NGF signalling, we found that PI3K/Akt pathway plays a major role in the expression of shootin1 isoform-2. Western blot and RT-PCR results showed that the isoform-1 of shootin1 is constitutively expressed, while the isoform-2 is expressed in a manner that is strictly dependent on NGF-stimulation. Isoform-specific RT-PCR results demonstrated that the differential expression of the isoform-1 and isoform-2 of shootin1 is a consequence of alternative splicing of shootin1 pre-mRNA, in response to NGF-signalling. Collectively these findings provide the first information on the molecular mechanisms regulating the expression of shootin1 gene and represent the first example of NGF-induced alternative splicing process that has a regulatory role in neuritogenesis.

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https://rdlopen.rawdatalibrary.net/r/ebyu/15364Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1038/srep17931Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorErgin, Volkan
dc.contributor.authorErdogan, Mutlu
dc.contributor.authorMenevse, Adnan
dc.date.accessioned2026-10-18T20:30:10.943882321Z
dc.date.available2026-10-18T20:30:10.943882321Z
dc.date.issued2015
dc.description.abstractShootin1 is a protein involved in neuronal polarization, and has been shown to be a key molecule for the positive/negative feedback loop for axon induction required during neuronal symmetry breaking. To better understand the molecular basis of shootin1 dynamics, we analysed the regulatory pathways and the expressional status of shootin1 gene during NGF-induced neuronal differentiation. We demonstrated that the isoform-1 and isoform-2 of shootin1 is differentially expressed during neuronal differentiation. By blocking individual downstream pathways of NGF signalling, we found that PI3K/Akt pathway plays a major role in the expression of shootin1 isoform-2. Western blot and RT-PCR results showed that the isoform-1 of shootin1 is constitutively expressed, while the isoform-2 is expressed in a manner that is strictly dependent on NGF-stimulation. Isoform-specific RT-PCR results demonstrated that the differential expression of the isoform-1 and isoform-2 of shootin1 is a consequence of alternative splicing of shootin1 pre-mRNA, in response to NGF-signalling. Collectively these findings provide the first information on the molecular mechanisms regulating the expression of shootin1 gene and represent the first example of NGF-induced alternative splicing process that has a regulatory role in neuritogenesis.
dc.description.sponsorshipThe authors acknowledge the support from the Scientific and Technological Research Council of Turkey (TÜBİTAK; Grant no: 212T178; Project manager: A.M.). The authors thank to Bryon Ricketts (Cell Signaling Technology, Inc.) for the generous gift of embryonic rat brain lysates. The authors are grateful to Prof. Naoyuki Inagaki and Dr. Michinori Toriyama for the transfer of various biological materials. The authors also thank to Ergin Sahin for the valuable discussions. This study originated from the PhD thesis of V.E. hence the authors thank to Prof. Emine Sevda Menevse (Gazi University) for her remarkable comments on the thesis.
dc.identifier.doi10.1038/srep17931
dc.identifier.issn2045-2322
dc.identifier.pmid26648138
dc.identifier.scopus2-s2.0-84949552418
dc.identifier.startpage17931
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/15364
dc.identifier.volume5
dc.identifier.wosWOS:000366029600001
dc.language.isoen
dc.publisherNature Publishing Group
dc.relation.ispartofScientific Reports
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAlternative Splicing
dc.subjectAnimals
dc.subjectCell Differentiation
dc.subjectGene Expression Regulation
dc.subjectGene Order
dc.subjectNerve Growth Factor
dc.subjectNerve Tissue Proteins
dc.subjectNeurites
dc.subjectNeurons
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectProtein Isoforms
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectRats
dc.subjectRNA Interference
dc.subjectRNA, Messenger
dc.subjectRNA, Small Interfering
dc.subjectisoprotein
dc.subjectmessenger RNA
dc.subjectnerve protein
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectShootin1 protein, rat
dc.subjectsmall interfering RNA
dc.subjectalternative RNA splicing
dc.subjectanimal
dc.subjectcytology
dc.subjectdrug effects
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectnerve cell
dc.titleRegulation of Shootin1 Gene Expression Involves NGF-induced Alternative Splicing during Neuronal Differentiation of PC12 Cells
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus10
rdl.citation.wos10
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)