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FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus.

Abstract：

:Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels.

journal_name

Mol Neurobiol

journal_title

Molecular neurobiology

authors

Weise SC,Arumugam G,Villarreal A,Videm P,Heidrich S,Nebel N,Dumit VI,Sananbenesi F,Reimann V,Craske M,Schilling O,Hess WR,Fischer A,Backofen R,Vogel T

doi

10.1007/s12035-018-1444-7

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

5188-5201

issue

7

eissn

0893-7648

issn

1559-1182

pii

10.1007/s12035-018-1444-7

journal_volume

56

pub_type

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