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MiR-7 controls glutamatergic transmission and neuronal connectivity in a Cdr1as-dependent manner

ABSTRACT: miR-7 controls glutamatergic transmission and neuronal connectivity in a Cdr1as-dependent manner

PROVIDER: PRJNA930025 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23292044.fastq.gz	Fastqsanger.gz
	SRR23292045.fastq.gz	Fastqsanger.gz
	SRR23292046.fastq.gz	Fastqsanger.gz
	SRR23292047.fastq.gz	Fastqsanger.gz
	SRR23292048.fastq.gz	Fastqsanger.gz

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miR-7 controls glutamatergic transmission and neuronal connectivity in a Cdr1as-dependent manner

Project description:To investigate interactions of Cdr1as and miR-7 in mouse neuron, we cultured primary mouse cell in which each target gene has been knocked out from C57BL/6N mouse and overexpression of pri-miR-7a

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miR-7 controls glutamatergic transmission and neuronal connectivity in a Cdr1as-dependent manner

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miR-7 controls glutamatergic transmission and neuronal connectivity in a Cdr1as-dependent manner.

Project description:The circular RNA (circRNA) Cdr1as is conserved across mammals and highly expressed in neurons, where it directly interacts with microRNA miR-7. However, the biological function of this interaction is unknown. Here, using primary cortical murine neurons, we demonstrate that stimulating neurons by sustained depolarization rapidly induces two-fold transcriptional upregulation of Cdr1as and strong post-transcriptional stabilization of miR-7. Cdr1as loss causes doubling of glutamate release from stimulated synapses and increased frequency and duration of local neuronal bursts. Moreover, the periodicity of neuronal networks increases, and synchronicity is impaired. Strikingly, these effects are reverted by sustained expression of miR-7, which also clears Cdr1as molecules from neuronal projections. Consistently, without Cdr1as, transcriptomic changes caused by miR-7 overexpression are stronger (including miR-7-targets downregulation) and enriched in secretion/synaptic plasticity pathways. Altogether, our results suggest that in cortical neurons Cdr1as buffers miR-7 activity to control glutamatergic excitatory transmission and neuronal connectivity important for long-lasting synaptic adaptations.

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Comprehensive transcriptome analysis regarding CDR1AS expression

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Project description:Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of Cerebellar Degeneration Related 1 (CDR1as), a regulator of the microRNA miR-7, as a hallmark of melanoma progression. We find that CDR1as depletion results from epigenetic silencing of its originating lincRNA, and promotes invasion in vitro and metastasis in vivo, through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as levels identify cellular states associated with distinct therapeutic responses. Our study reveals functional, prognostic and predictive roles for CDR1as and expose circRNAs as key players in metastasis.

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Epigenetic silencing of CDR1as drives IGF2BP3-mediated melanoma invasion and metastasis [RIP-Seq]

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CPEB2-activated axonal translation of VGLUT2 mRNA promotes glutamatergic transmission and presynaptic plasticity

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Comprehensive transcriptome analysis regarding CDR1AS expression

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Haploinsufficiency in bromodomain containing 2 (Brd2) gene remodels synaptic transmission in female mouse striatum in a sex-specific manner

Project description:Our previous work showed that Brd2+/- mouse models the sex specific characteristics of juvenile myoclonic epilepsy, a subsyndrome of idiopathic generalized epilepsy. Here, we investigated a role of Brd2 gene in modulating the genomic fabrics responsible for the glutamatergic, GABAergic, dopaminergic, cholinergic and serotonergic transmission in the striatum of female mice. Agilent two-color gene expression arrays and the genomic fabric paradigm were used to determine whether the expression and networking of genes involved in the synaptic transmission differ between Brd2+/- and wildtype mice and whether these differences are sex-specific. As in Brd+/- male mice we found relatively few regulated genes in Brd2+/-female mice with respect to their wildtype counterparts. However, most of the regulated genes were directly related to control of anxiety and seizures, justifying the role of Brd2 upstream control of these traits. Remarkably, the sets of regulated genes in the two sexes did not overlap, supporting the conclusion of sex-specific control of traits by Brd2. Agilent mouse two-color gene expression arrays to profile striata of the prefrontal cortices of wildtype (W) and Brd2+/- (H) mouse female (F) adult C57Bl/6j mice. Differently labeled biological replicates were cohybridized with each array. Results of similarly labeled different conditions were compared then averaged for the two fluorescent labels. For instance: FW1 & FW3 were compared with FH1 & FH3, FW2 & FW4 were compared with FH2 & + FH4, and the results of the comparisons averaged. This design uses 100% of the resources, has a better normlaiztion and allows all possible comparisons among the conditions.

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