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Background   CDK5R1  plays a central role in neuronal migration and differentiation during central nervous system development.  CDK5R1  has been implicated in neurodegenerative disorders and proposed as a candidate gene for mental retardation. The remarkable size of  CDK5R1  3'-untranslated region (3'-UTR) suggests a role in post-transcriptional regulation of  CDK5R1  expression.    Results  The bioinformatic study shows a high conservation degree in mammals and predicts several AU-Rich Elements (AREs). The insertion of  CDK5R1  3'-UTR into luciferase 3'-UTR causes a decreased luciferase activity in four transfected cell lines. We identified 3'-UTR subregions which tend to reduce the reporter gene expression, sometimes in a cell line-dependent manner. In most cases the quantitative analysis of luciferase mRNA suggests that CDK5R1 3'-UTR affects mRNA stability. A region, leading to a very strong mRNA destabilization, showed a significantly low half-life, indicating an accelerated mRNA degradation. The 3' end of the transcript, containing a class I ARE, specifically displays a stabilizing effect in neuroblastoma cell lines. We also observed the interaction of the stabilizing neuronal RNA-binding proteins ELAV with the CDK5R1 transcript in SH-SY5Y cells and identified three 3'-UTR sub-regions showing affinity for ELAV proteins.    Conclusion  Our findings evince the presence of both destabilizing and stabilizing regulatory elements in  CDK5R1  3'-UTR and support the hypothesis that  CDK5R1  gene expression is post-transcriptionally controlled in neurons by ELAV-mediated mechanisms. This is the first evidence of the involvement of 3'-UTR in the modulation of  CDK5R1  expression. The fine tuning of  CDK5R1  expression by 3'-UTR may have a role in central nervous system development and functioning, with potential implications in neurodegenerative and cognitive disorders.

The 3' untranslated region of human Cyclin-Dependent Kinase 5 Regulatory subunit 1 contains regulatory elements affecting transcript stability