Publications by authors named "Junyeop D Roh"
Article Synopsis
- * Mice with a specific human mutation in Dyrk1a (Dyrk1a-I48K) exhibit serious issues like microcephaly, social and cognitive deficits, and altered brain signaling patterns.
- * Treatment with lithium in newborn mutant mice helps reverse some of these problems, improving brain volume and behavior, suggesting early intervention can have lasting benefits.
Article Synopsis
- * Research on Arid1b-happloinsufficient mice indicates that they exhibit behaviors similar to autism and have reduced excitatory synaptic density during both juvenile and adult stages.
- * Chronic fluoxetine treatment in Arid1b mice during early postnatal weeks prevents these deficits, leading to positive transcriptomic changes that regulate synaptic protein expression, suggesting early intervention can have lasting benefits.
Article Synopsis
- * Research on mutant mice (both heterozygous and homozygous) shows distinct behavioral differences in areas like movement, repetitive actions, and memory.
- * The study also reveals varying gene expression changes related to synapses and neurological conditions, indicating that different genetic mutations lead to specific behavioral and molecular outcomes.
Article Synopsis
- mTOR signaling, specifically through mTORC1 and mTORC2 complexes, is essential for neural development and is linked to various brain disorders, but upstream regulators of this signaling in neurons are not fully understood.
- This study highlights Tanc2, a neurodevelopmental adaptor protein, as a direct inhibitor of mTOR, with experiments showing that mice lacking Tanc2 exhibit severe developmental issues, while those with reduced Tanc2 levels show mTOR hyperactivity and related behavioral problems that can be reversed with the drug rapamycin.
- Tanc2 specifically inhibits mTOR in different stages of neuron development and in human neural progenitor cells, suggesting its significant role in regulating mTOR activity during neurodevelopment.
Glycine transporters (GlyT1 and GlyT2) that regulate levels of brain glycine, an inhibitory neurotransmitter with co-agonist activity for NMDA receptors (NMDARs), have been considered to be important targets for the treatment of brain disorders with suppressed NMDAR function such as schizophrenia. However, it remains unclear whether other amino acid transporters expressed in the brain can also regulate brain glycine levels and NMDAR function. Here, we report that SLC6A20A, an amino acid transporter known to transport proline based on in vitro data but is understudied in the brain, regulates proline and glycine levels and NMDAR function in the mouse brain.
View Article and Find Full Text PDFAutism spectrum disorders (ASDs) are four times more common in males than in females, but the underlying mechanisms are poorly understood. We characterized sexually dimorphic changes in mice carrying a heterozygous mutation in Chd8 (Chd8) that was first identified in human CHD8 (Asn2373LysfsX2), a strong ASD-risk gene that encodes a chromatin remodeler. Notably, although male mutant mice displayed a range of abnormal behaviors during pup, juvenile, and adult stages, including enhanced mother-seeking ultrasonic vocalization, enhanced attachment to reunited mothers, and isolation-induced self-grooming, their female counterparts do not.
View Article and Find Full Text PDFNetrin-G ligand 2 (NGL-2)/LRRC4, implicated in autism spectrum disorders and schizophrenia, is a leucine-rich repeat-containing postsynaptic adhesion molecule that interacts intracellularly with the excitatory postsynaptic scaffolding protein PSD-95 and trans-synaptically with the presynaptic adhesion molecule netrin-G2. Functionally, NGL-2 regulates excitatory synapse development and synaptic transmission. However, whether it regulates synaptic plasticity and disease-related specific behaviors is not known.
View Article and Find Full Text PDFArticle Synopsis
- SALM1, also known as LRFN2, is a synaptic adhesion molecule that interacts with PSD-95 and is thought to regulate NMDA receptor clustering, although its functions are not fully understood.
- In mice lacking SALM1, there is a normal density of excitatory synapses but altered synaptic functions, including increased NMDA-dependent transmission and decreased plasticity in the hippocampus, as well as reduced inhibitory synapse development.
- Behaviorally, these SALM1-deficient mice displayed altered communication and startle responses, showcasing the molecule's role in regulating synaptic function and overall neural circuit dynamics.
Copy number variants and point mutations of (also called ) gene encoding an immunoglobulin (Ig) superfamily adhesion molecule have been linked to autism spectrum disorders, intellectual disability and neurocognitive delay associated with Jacobsen syndrome, but the physiological roles of Neph2 in the mammalian brain remain largely unknown. Neph2 is highly expressed in the dentate granule (DG) neurons of the hippocampus and is localized in both dendrites and axons. It was recently shown that Neph2 is required for the formation of mossy fiber filopodia, the axon terminal structure of DG neurons forming synapses with GABAergic neurons of CA3.
View Article and Find Full Text PDFSynaptic adhesion molecules regulate various aspects of synapse development, function and plasticity. These functions mainly involve trans-synaptic interactions and positive regulations, whereas cis-interactions and negative regulation are less understood. Here we report that SALM4, a member of the SALM/Lrfn family of synaptic adhesion molecules, suppresses excitatory synapse development through cis inhibition of SALM3, another SALM family protein with synaptogenic activity.
View Article and Find Full Text PDFSynaptic adhesion molecules regulate synapse development and plasticity through mechanisms that include trans-synaptic adhesion and recruitment of diverse synaptic proteins. We found that the immunoglobulin superfamily member 11 (IgSF11), a homophilic adhesion molecule that preferentially expressed in the brain, is a dual-binding partner of the postsynaptic scaffolding protein PSD-95 and AMPA glutamate receptors (AMPARs). IgSF11 required PSD-95 binding for its excitatory synaptic localization.
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- Synaptic adhesion molecules influence how synapses develop and adapt, and SALM3 specifically promotes the growth of presynaptic connections in nerve cells.
- The study found that SALM3 interacts with LAR family receptor proteins, which are crucial for its role in developing presynaptic structures.
- Mice lacking SALM3 have fewer excitatory synapses but still perform well in learning tests, indicating that SALM3 is key for synapse formation and affects movement behaviors.