NMDA induces post-transcriptional regulation of α2-guanylyl-cyclase-subunit expression in cerebellar granule cells

被引:14
|
作者
Jurado, S
Rodríguez-Pascual, F
Sánchez-Prieto, J
Reimunde, FM
Lamas, S
Torres, M [1 ]
机构
[1] Univ Complutense, Fac Vet, Dept Bioquim, E-28040 Madrid, Spain
[2] CSIC, CIB, E-28040 Madrid, Spain
关键词
AUF1; cerebellar granule cells; mRNA decay; NO-sensitive guanylyl cyclase; N-methyl; D-aspartate;
D O I
10.1242/jcs.02867
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Activation of N-methyl-D-aspartate (NMDA) glutamate receptors commonly affects gene expression in different neurons. We reported previously that chronic treatment of rat cerebellar granule cells with NMDA ( 24 hours) upregulates the expression of mRNA encoding the alpha(2) subunit of the nitric-oxide-sensitive guanylyl cyclase. However, the molecular mechanisms involved in this process remained to be elucidated. Here, we have performed mRNA-decay experiments using the transcriptional inhibitor actinomycin D, providing evidence that the half-life of alpha(2) mRNA is significantly prolonged in cells exposed to NMDA. The role of the 3' untranslated region of the alpha(2) transcripts in NMDA-induced mRNA stabilisation was examined and an association between the RNA-binding proteins AUF1 and ELAV-like protein 1 (HuR/HuA), and endogenous alpha(2) mRNA was demonstrated in vivo, as revealed by coimmunoprecipitation experiments with specific antibodies against AUF1 and HuR. Further studies indicated that stimulation of the NMDA receptor induces a downregulation in AUF1 levels stabilising the alpha(2) mRNA transcripts. These events are triggered through a mechanism that depends on formation of nitric oxide, and on the subsequent activation of guanylyl cyclase and cGMP dependent protein kinases.
引用
收藏
页码:1622 / 1631
页数:10
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