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Regulation and Mechanism of cpg15 Expression by HuD

Author: WangZhongHui
Tutor: ChenXianHua
School: Fudan University
Course: Medical Neurobiology
Keywords: epg15 HuD 3'UTR ARE Expression regulation
CLC: R363
Type: Master's thesis
Year: 2010
Downloads: 22
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Abstract

The HuD to adjust cpg15 express their mechanisms of neural plasticity related gene cpg15 play an important role in neurite outgrowth and synapse maturation promoting nerve cells, regulating synaptic circuit formation, nerve cell regeneration and plasticity. Many physiological and pathological stimuli such as light stimulation, nerve injury or ischemia and hypoxia will induced cpgl5 expression. Study cpgl5 induced expression of the mechanism, we first cpg15 mRNA sequence analysis and found that the presence of the 3 'untranslated region (3'UTR) AU enriched sequence (AU-rich elements, ARES), the latter is an RNA binding protein (RNAbinding proteins, RBPs) play the main target post-transcriptional regulation. HuD protein is a neuron-specific the RBPs, aspects of the first-mRNA alternative splicing, RNA transport, stability and translation and other post-transcriptional regulation of target gene expression, which play in the development and maintenance of neurons important role. Our previous studies found that after the mouse transient global cerebral ischemia and reperfusion, the hippocampus cpg15mRNA protein expression was phased upward trend in decline for 14 days after the 21 days to return to normal levels. Of HuD protein also appears to change with the cpg15 the same pattern, and are prompted to the HuD protein possible and cpgl5 express there is some connection. For the HuD cpg15 is involved in the regulation of expression of this problem, we HuD overexpression impact on cpg15 expression analysis in cell culture system. The results showed that HuD overexpression cells, cpg15mRNA and protein are upregulated, indicating the existence of regulation and the regulation of the relationship between the HuD and cpgl5 of synchronization expression change. But HuD inhibit the expression of cell, cpgl5 expression did not appear significant change may be due to inhibition of HuD effect caused by Hu protein family members compensatory. In order to study the nucleotide sequence ARE cpg15 gene regulation in HuD role cpgl5 expression, we analyzed HuD contain cpg15 regulatory sequences ARE reporter gene expression. The results showed, HuD overexpression significant the elevated the expression of the reporter gene containing the 3'UTR, but can not increase the reporter gene expression in the missing ARE sequences. The ARE sequence deletions, cpg15 mRNA and protein expression are not subject to HuD expression. These results described the ARE to play an important role in the HuD adjusting cpgl5 expression. We then immunoprecipitation studies of The ARE sequence mediated the cpg15 mRNA and the HuD protein binding of the importance of the results found that the ARE sequence cpg15 mRNA mediated the HuD protein binding, but not the only sequence. We also explore the the impact the HuD domain of cpgl5 expression. Whether mRNA stability RRM1 and RRM2 (RNA-recognition motifs), deletions, or in combination with poly (A) and the translation initiation the Hinge region with RRM3 the deletion, are weakened a HuD increase the ability of the expression of GFP-CPG15 Hinge region RRM3 deletion of the GFP-CPG15 induced expression inhibition, mRNA stability and translation the regulation involved cpg15 expression regulation. Based on the above results, the results of this thesis, describes the HuD the ARE sequence by cpg15 mRNA3'UTR area adjustment cpg15 gene expression, and this process with HuD to participate in cpg15 mRNA stability and translation adjustment related to

Regulation and Mechanism of cpg15 Expression by HuD

Abstract

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