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Mus musculus

ABSTRACT: Hippocampus CA1 pyramidal cells Transcriptomic profile in WT and Fmr1 KO mice, using Wfs1-CreERT2:RiboTag:Frm1 knockout and wildtype mice

PROVIDER: PRJNA371470 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5231470.fastq.gz	Fastqsanger.gz
	SRR5231471.fastq.gz	Fastqsanger.gz
	SRR5231472.fastq.gz	Fastqsanger.gz
	SRR5231473.fastq.gz	Fastqsanger.gz
	SRR5231474.fastq.gz	Fastqsanger.gz

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Project description:Excessive mRNA translation downstream of group I metabotropic glutamate receptors (mGlu1/5) is a core pathophysiology of fragile X syndrome (FX), however the differentially translating mRNAs that contribute to altered neural function are not known. We used Translating Ribosome Affinity Purification (TRAP) and RNA-seq to identify mistranslating mRNAs in CA1 pyramidal neurons of the FX mouse model (Fmr1-/y) hippocampus, which exhibit exaggerated mGlu1/5-induced long-term synaptic depression (LTD). In these neurons, we find the Chrm4 transcript encoding muscarinic acetylcholine receptor 4 (M4) is excessively translated, and synthesis of M4 downstream of mGlu5 activation is mimicked and occluded. Surprisingly, enhancement rather than inhibition of M4 activity normalizes core phenotypes in the Fmr1-/y, including excessive protein synthesis, exaggerated mGluR-LTD, and audiogenic seizures. These results suggest that not all excessively translated mRNAs in the Fmr1-/y brain are detrimental, and some may be candidates for enhancement to correct pathological changes in the FX brain.

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