Publications by authors named "Yuan-Ju Wu"
Article Synopsis
- Tunneling nanotubes (TNTs) are temporary tubular structures that connect cells for direct communication, influencing both normal processes (like development and tissue repair) and disease conditions (such as cancer and neurodegeneration).
- The Wnt/Ca pathway, which affects the structure of the actin cytoskeleton, is involved in the formation and function of TNTs, particularly through the action of CaMKII, a protein that helps modulate these structures in neurons.
- The study highlights the potential of targeting the Wnt/Ca pathway to develop therapies that could disrupt the harmful spread of pathogens via TNTs among cells.
Congenital microcephaly is highly associated with intellectual disability. Features of autosomal recessive primary microcephaly subtype 3 (MCPH3) also include hyperactivity and seizures. The disease is caused by biallelic mutations in the Cyclin-dependent kinase 5 regulatory subunit-associated protein 2 gene CDK5RAP2.
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- Mutations in the MeCP2 gene lead to Rett syndrome, a neurodevelopmental disorder, where altered MeCP2 levels disrupt neuron growth and synapse formation.
- The study reveals that a BDNF signaling pathway is crucial for the growth and differentiation of glutamatergic neurons, and blocking TrkB receptors mimics the effects of MeCP2 deficiency.
- Reintroducing BDNF can partially rescue the growth deficits caused by MeCP2 loss, indicating its essential role in neuron health and the complexities of Rett syndrome pathology involving both wildtype and mutant neurons.
Article Synopsis
- * Complete loss of function studies for Stx1 have been challenging, but research using Stx1B deletion (with Stx1A absent) reveals that Stx1 is critical for neuronal viability and proper neurotransmitter release.
- * The study indicates that while Stx1 is essential for both neuronal maintenance and neurotransmission, partial SNARE complex formation can support neuronal viability but fails to enable neurotransmitter release, underscoring the importance of
STX1 is a major neuronal syntaxin protein located at the plasma membrane of the neuronal tissues. Rodent STX1 has two highly similar paralogs, STX1A and STX1B, that are thought to be functionally redundant. Interestingly, some studies have shown that the distribution patterns of STX1A and STX1B at the central and peripheral nervous systems only partially overlapped, implying that there might be differential functions between these paralogs.
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- Researchers studied the role of the SNARE protein Syntaxin1 (Stx1) in neurotransmitter release, focusing on how its levels influence synaptic function in mouse hippocampal neurons.
- By reducing Stx1 levels using two methods, they found that while vesicle proximity to the active zone remained mostly unchanged, overall synaptic release efficiency was significantly decreased, indicated by a smaller pool of releasable vesicles and a slower refilling rate.
- The analysis showed that both priming of vesicles and their fusion share similar molecular behaviors, as evidenced by comparable dissociation constant values, suggesting that they are controlled by closely related mechanisms.
Borna disease virus (BDV) is a nonsegmented, negative-stranded RNA virus characterized by noncytolytic persistent infection and replication in the nuclei of infected cells. To gain further insight on the intracellular trafficking of BDV components during infection, we sought to generate recombinant BDV (rBDV) encoding fluorescent fusion viral proteins. We successfully rescued a virus bearing a tetracysteine tag fused to BDV-P protein, which allowed assessment of the intracellular distribution and dynamics of BDV using real-time live imaging.
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- Borna disease virus (BDV) infects neurons in the central nervous system of various hosts, including rats, and is not effectively blocked by the innate immune response in these neurons.
- In studies using rat hippocampal slice cultures, while astrocytes and microglial cells showed an antiviral response by producing Mx proteins, the neurons did not, indicating their susceptibility to BDV infection.
- Interestingly, mouse neurons responded differently to IFN-α treatment, producing Mx proteins and successfully blocking BDV replication, highlighting species-specific differences in immune response.
Article Synopsis
- Newborn rats infected with Borne disease virus (BDV) exhibit degeneration of specific neurons in the dentate gyrus, prompting researchers to investigate genetic resistance in different rat strains.
- While some strains like Lewis (LEW) showed damage to the dentate gyrus, others, such as Sprague-Dawley (SD), remained unaffected despite similar viral replication levels.
- Further genetic analysis identified specific regions on chromosomes linked to resistance and susceptibility, indicating that the degree of BDV-induced neuronal degeneration is influenced by the host's genetic background and protective factors from disease-resistant strains.
Article Synopsis
- The vesicular stomatitis virus (VSV) M protein inhibits the synthesis of type I interferon (IFN) by blocking nuclear transcription and RNA transport, which contributes to the virus's pathogenicity.
- Specific amino acid substitutions in the M protein affect IFN induction, with the M51R mutation leading to IFN production, while combinations of V221F and S226R mutations can also induce IFN by eliminating the M protein's host shut-off activity.
- The study finds that while M-mutant VSV maintains its cytotoxic properties, the G protein's fusion activity plays a key role in its cytotoxicity, highlighting the interaction between M protein and G protein in VSV's overall pathogenic effects.
Article Synopsis
- Granule cells in the dentate gyrus are heavily impacted by Borna disease virus (BDV) in newborn rats, leading to their progressive loss and disconnecting entorhinal fiber connections.
- Despite this loss, recent studies using DiI tracing reveal that entorhinal projections maintain a layered structure even after most granule cells have died off by 9 weeks post-infection.
- There is a temporary increase in synaptic density in the outer molecular layer of remaining granule cells and adjacent neurons at 6 weeks, but by 9 weeks, synaptic density levels return to those seen in uninfected controls, suggesting adaptive changes in neuron connections following the infection.