Viral infection and the antiviral innate immune response are regulated by the RNA modification mA. mA directs nearly all aspects of RNA metabolism by recruiting RNA-binding proteins that mediate the fate of mA-containing RNA. mA controls the antiviral innate immune response in diverse ways, including shielding viral RNA from detection by antiviral sensors and influencing the expression of cellular mRNAs encoding antiviral signaling proteins, cytokines, and effector proteins.
View Article and Find Full Text PDFIn excitatory hippocampal pyramidal neurons, integrin β3 is critical for synaptic maturation and plasticity in vitro. Itgb3 is a potential autism susceptibility gene that regulates dendritic morphology in the cerebral cortex in a cell-specific manner. However, it is unknown what role Itgb3 could have in regulating hippocampal pyramidal dendritic morphology in vivo, a key feature that is aberrant in many forms of autism and intellectual disability.
View Article and Find Full Text PDFBackground: Pyramidal neurons throughout hippocampal CA3 are diverse in their dendritic morphology, and CA3 is not homogenous in its structure or function. Nonetheless, few structural studies have captured the precise 3D somatic position and the 3D dendritic morphology of CA3 pyramidal neurons simultaneously.
New Method: Here, we present a simple approach to reconstruct the apical dendritic morphology of CA3 pyramidal neurons using the transgenic fluorescent Thy1-GFP-M line.
Modification of the hepatitis C virus (HCV) positive-strand RNA genome by N6-methyladenosine (mA) regulates the viral life cycle. This life cycle takes place solely in the cytoplasm, while mA addition on cellular mRNA takes place in the nucleus. Thus, the mechanisms by which mA is deposited on the viral RNA have been unclear.
View Article and Find Full Text PDFUnlabelled: Modification of the hepatitis C virus (HCV) positive-strand RNA genome by N6-methyladenosine (m A) regulates the viral lifecycle. This lifecycle takes place solely in the cytoplasm, while m A addition on cellular mRNA takes place in the nucleus. Thus, the mechanisms by which m A is deposited on the viral RNA have been unclear.
View Article and Find Full Text PDFBackground: Autism spectrum disorder (ASD) is characterized by repetitive behaviors, deficits in communication, and overall impaired social interaction. Of all the integrin subunit mutations, mutations in integrin β3 (Itgb3) may be the most closely associated with ASD. Integrin β3 is required for normal structural plasticity of dendrites and synapses specifically in excitatory cortical and hippocampal circuitry.
View Article and Find Full Text PDFFragile X syndrome (FXS) is the most common form of intellectual disability that arises from the dysfunction of a single gene-Fmr1. The main neuroanatomical correlate of FXS is elevated dendritic spine density on cortical pyramidal neurons, which has been modeled in Fmr1 mice. However, the cell-autonomous contribution of Fmr1 on cortical dendritic spine density has not been assessed.
View Article and Find Full Text PDFDysfunctional dendritic arborization is a key feature of many developmental neurological disorders. Across various human brain regions, basal dendritic complexity is known to increase along a caudal-to-rostral gradient. We recently discovered that basal dendritic complexity of layer II/III cortical pyramidal neurons in the mouse increases along a caudomedial-to-rostrolateral gradient spanning multiple regions, but at the time, no molecules were known to regulate that exquisite pattern.
View Article and Find Full Text PDFArchitectonic heterogeneity in neurons is thought to be important for equipping the mammalian cerebral cortex with an adaptable network that can organize the manifold totality of information it receives. To this end, the dendritic arbors of supragranular pyramidal neurons, even those of the same class, are known to vary substantially. This diversity of dendritic morphology appears to have a rostrocaudal configuration in some brain regions of various species.
View Article and Find Full Text PDFCell-autonomous neuronal functions of genes can be revealed by causing loss or gain of function of a gene in a small and sparse population of neurons. To do so requires generating a mosaic in which neurons with loss or gain of function of a gene are surrounded by genetically unperturbed tissue. Here, we combine the Cre-lox recombination system with in utero electroporation in order to generate mosaic brain tissue that can be used to study the cell-autonomous function of genes in neurons.
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