Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 52, Pages 14349-14357Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2969-07.2007
Keywords
fMRP; fragile X; phosphorylation; mGluR; synaptic plasticity; PP2A
Categories
Funding
- NCI NIH HHS [R01 CA057327, CA57327] Funding Source: Medline
- NICHD NIH HHS [HD20521, HD41591, HD24064] Funding Source: Medline
- NINDS NIH HHS [NS051127] Funding Source: Medline
Ask authors/readers for more resources
Fragile X syndrome is a common form of inherited mental retardation and is caused by loss of fragile X mental retardation protein (FMRP), a selective RNA-binding protein that influences the translation of target messages. Here, we identify protein phosphatase 2A (PP2A) as an FMRP phosphatase and report rapid FMRP dephosphorylation after immediate group I metabotropic glutamate receptor (mGluR) stimulation (< 1 min) in neurons caused by enhanced PP2A enzymatic activity. In contrast, extended mGluR activation (1-5 min) resulted in mammalian target of rapamycin (mTOR)-mediated PP2A suppression and FMRP rephosphorylation. These activity-dependent changes in FMRP phosphorylation were also observed in dendrites and showed a temporal correlation with the translational profile of select FMRP target transcripts. Collectively, these data reveal an immediate-early signaling pathway linking group I mGluR activity to rapid FMRP phosphorylation dynamics mediated by mTOR and PP2A.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available