Publications by authors named "Michael Soutschek"

Article Synopsis
  • A subset of circular RNAs (circRNAs) and linear RNAs can block microRNA activity, with some RNAs leading to microRNA degradation via a process called Target RNA-Directed MicroRNA Degradation (TDMD).
  • In this study, researchers explored how the shape (circular vs. linear) of RNA targets impacts TDMD, finding that the circular RNA Cdr1as protects the microRNA miR-7, while an artificial linear version promotes its degradation.
  • The findings suggest that RNA circularity significantly affects TDMD dynamics, influencing the stability and activity of specific microRNAs beyond just their nucleotide sequences.
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The brain constantly adapts to changes in the environment, a capability that underlies memory and behavior. Long-term adaptations require the remodeling of neural circuits that are mediated by activity-dependent alterations in gene expression. Over the last two decades, it has been shown that the expression of protein-coding genes is significantly regulated by a complex layer of non-coding RNA (ncRNA) interactions.

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In adult patients with obsessive-compulsive disorder (OCD), altered DNA methylation has been discerned in several candidate genes, while DNA methylation on an epigenome-wide level has been investigated in only one Chinese study so far. Here, an epigenome-wide association study (EWAS) was performed in a sample of 76 OCD patients of European ancestry (37 women, age ± SD: 33.51 ± 10.

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MicroRNAs (miRNAs) are small non-coding RNAs that are among the main post-transcriptional regulators of gene expression. A number of data collections and prediction tools have gathered putative or confirmed targets of these regulators. It is often useful, for discovery and validation, to harness such collections to perform target enrichment analysis in given transcriptional signatures or gene-sets in order to predict involved miRNAs.

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The proper development and function of neuronal circuits rely on a tightly regulated balance between excitatory and inhibitory (E/I) synaptic transmission, and disrupting this balance can cause neurodevelopmental disorders, for example, schizophrenia. MicroRNA-dependent gene regulation in pyramidal neurons is important for excitatory synaptic function and cognition, but its role in inhibitory interneurons is poorly understood. Here, we identify as a regulator of short-term memory and inhibitory synaptic transmission in the mouse hippocampus.

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Motivation: microRNAs are important post-transcriptional regulators of gene expression, but the identification of functionally relevant targets is still challenging. Recent research has shown improved prediction of microRNA-mediated repression using a biochemical model combined with empirically-derived k-mer affinity predictions; however, these findings are not easily applicable.

Results: We translate this approach into a flexible and user-friendly bioconductor package, scanMiR, also available through a web interface.

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Synaptic scaling is a form of homeostatic plasticity which allows neurons to adjust their action potential firing rate in response to chronic alterations in neural activity. Synaptic scaling requires profound changes in gene expression, but the relative contribution of local and cell-wide mechanisms is controversial. Here we perform a comprehensive multi-omics characterization of the somatic and process compartments of primary rat hippocampal neurons during synaptic scaling.

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SYNCRIP, a member of the cellular heterogeneous nuclear ribonucleoprotein (hnRNP) family of RNA binding proteins, regulates various aspects of neuronal development and plasticity. Although SYNCRIP has been identified as a component of cytoplasmic RNA granules in dendrites of mammalian neurons, only little is known about the specific SYNCRIP target mRNAs that mediate its effect on neuronal morphogenesis and function. Here, we present a comprehensive characterization of the cytoplasmic SYNCRIP mRNA interactome using iCLIP in primary rat cortical neurons.

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Aberrant synaptic function is thought to underlie social deficits in neurodevelopmental disorders such as autism and schizophrenia. Although microRNAs have been shown to regulate synapse development and plasticity, their potential involvement in the control of social behaviour in mammals remains unexplored. Here, we show that deletion of the placental mammal-specific miR379-410 cluster in mice leads to hypersocial behaviour, which is accompanied by increased excitatory synaptic transmission, and exaggerated expression of ionotropic glutamate receptor complexes in the hippocampus.

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