Post-transcriptional control is a finely tuned mechanism regulating RNA expression. Dysfunction of this process defines specific pathologies, as these are linked to genetic and somatic disorders including neurodegeneration and neurodevelopmental disorders (such as Alzheimer’s disease, Amyotrophic lateral sclerosis, Fragile X syndrome, etc.).
This process is regulated by a group of RNA Binding Protein (RBPs) that specifically recognize short RNA binding domains characterized by different target sites consisting of specific sequence elements/motifs regulating their expression.
After a direct or indirect binding with mRNA, they create a highly dynamic ribonucleoprotein complex that works by regulating splicing, editing, polyadenylation, nuclear export, localization, translation, and stability.
Some RBPs can bind mRNA in the cytoplasm, translocate to the synapses, and locally regulate their expression following on-site translational control. This mechanism is important when it comes to defining synaptic strength, function, and dysfunction, affecting dendrites and dendritic spine plasticity, maturity, and morphology, linking to learning and memory processes.
Loss of function or absence of different RBPs may well act and regulate specific genes associated with synaptic plasticity affecting the dendritic spine function. For example, FMRP, an RNA-binding protein, absent in Fragile X Syndrome patients, affects neuronal plasticity and induces the increase of dendritic spines which appear longer, thinner, and less mature. Other RBPs are mainly associated with the main neuronal function and their absence might crucially affect dendritic spine activity.
Most of them are mainly negative or positive regulators of specific mRNA involved in synaptic plasticity. This means that they are able to specifically regulate their expression. The alteration of the physiological status of RBPs affects protein synthesis machinery and this dysregulation induces local malfunctioning at the level of synapses.
The goal of this Research Topic is to provide the grounds for a detailed description and investigation of the underlying general molecular mechanism regulated by RBPs and how these mechanisms impact neuronal function in physiology and pathology.
Focus is required in terms of novel methods’ development and what has been so far applied to investigate, both in vivo and in vitro models applied to the fields of neurobiology, developmental neurobiology, psychiatry, and psychology, describing recent advances in the application of novel methods.
We aim to receive article contributions addressing, but not limited to the following:
1. Description of new technical approaches to identify RBPs function (RNA immunoprecipitation), controlling RNA biology and expression, including RNA stability control, splicing regulation mechanisms, RNA localization, and gene expression regulation
2. Identify how RBPs contribute to RNA expression control
3. Evidence for a common mechanism involving RBPs
4. RBPs role in neurological disorders – characterization
5. Define a general list of possible RBPs in neural disorders
6. Provide an exhaustive collection of RBPs mechanisms in physiological and pathological conditions
This Research Topic will help the scientific community to collect a large-scale and coherent binding map of RBPs allowing for an in-depth description and investigation of mechanisms of action in physiological pathological conditions.
Keywords:
post-transcriptional control, RBPs, RNA stability, splicing regulation, CNS, RNA expression, neurodegeneration, neurodevelopment, AD, ALS, FMRP, mRNA, synaptic dysregulation
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Post-transcriptional control is a finely tuned mechanism regulating RNA expression. Dysfunction of this process defines specific pathologies, as these are linked to genetic and somatic disorders including neurodegeneration and neurodevelopmental disorders (such as Alzheimer’s disease, Amyotrophic lateral sclerosis, Fragile X syndrome, etc.).
This process is regulated by a group of RNA Binding Protein (RBPs) that specifically recognize short RNA binding domains characterized by different target sites consisting of specific sequence elements/motifs regulating their expression.
After a direct or indirect binding with mRNA, they create a highly dynamic ribonucleoprotein complex that works by regulating splicing, editing, polyadenylation, nuclear export, localization, translation, and stability.
Some RBPs can bind mRNA in the cytoplasm, translocate to the synapses, and locally regulate their expression following on-site translational control. This mechanism is important when it comes to defining synaptic strength, function, and dysfunction, affecting dendrites and dendritic spine plasticity, maturity, and morphology, linking to learning and memory processes.
Loss of function or absence of different RBPs may well act and regulate specific genes associated with synaptic plasticity affecting the dendritic spine function. For example, FMRP, an RNA-binding protein, absent in Fragile X Syndrome patients, affects neuronal plasticity and induces the increase of dendritic spines which appear longer, thinner, and less mature. Other RBPs are mainly associated with the main neuronal function and their absence might crucially affect dendritic spine activity.
Most of them are mainly negative or positive regulators of specific mRNA involved in synaptic plasticity. This means that they are able to specifically regulate their expression. The alteration of the physiological status of RBPs affects protein synthesis machinery and this dysregulation induces local malfunctioning at the level of synapses.
The goal of this Research Topic is to provide the grounds for a detailed description and investigation of the underlying general molecular mechanism regulated by RBPs and how these mechanisms impact neuronal function in physiology and pathology.
Focus is required in terms of novel methods’ development and what has been so far applied to investigate, both in vivo and in vitro models applied to the fields of neurobiology, developmental neurobiology, psychiatry, and psychology, describing recent advances in the application of novel methods.
We aim to receive article contributions addressing, but not limited to the following:
1. Description of new technical approaches to identify RBPs function (RNA immunoprecipitation), controlling RNA biology and expression, including RNA stability control, splicing regulation mechanisms, RNA localization, and gene expression regulation
2. Identify how RBPs contribute to RNA expression control
3. Evidence for a common mechanism involving RBPs
4. RBPs role in neurological disorders – characterization
5. Define a general list of possible RBPs in neural disorders
6. Provide an exhaustive collection of RBPs mechanisms in physiological and pathological conditions
This Research Topic will help the scientific community to collect a large-scale and coherent binding map of RBPs allowing for an in-depth description and investigation of mechanisms of action in physiological pathological conditions.
Keywords:
post-transcriptional control, RBPs, RNA stability, splicing regulation, CNS, RNA expression, neurodegeneration, neurodevelopment, AD, ALS, FMRP, mRNA, synaptic dysregulation
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.