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Chen, T.-J.

Publications and source records attributed to Chen, T.-J..

4 recordsLinked to original sources

Short-term synaptic plasticity at neuron-OPC synapses in the corpus callosum during postnatal development of mice: experimental and computational study

Neuronal circuits rely on precisely timed synaptic transmission and plasticity, which are established through activity-dependent maturation during development. While these processes are well characterized at neuronal synapses, far less is known about how synaptic communication between neurons and glial cells develops. Pyramidal cortical neurons project axons through white matter where they release glutamate ectopically along their shafts and form glutamatergic synapses with oligodendrocyte precursor cells (OPCs). The functional maturation of these neuron-glia connections remains unknown. Here, using single-cell electrophysiology combined with computational modelling, we show that neuron-OPC synapses in the mouse corpus callosum undergo a pronounced developmental transformation in short-term synaptic plasticity. During the first two postnatal months, these synapses switch from strong synaptic depression to facilitation. This transition is accompanied by a shortening of synaptic delay and a reduction in asynchronous glutamate release, indicating an increase in temporal precision of neurotransmitter signalling in white matter. Computational modelling suggests that both pre- and postsynaptic changes may underlie this functional maturation. Taken together, our findings demonstrate that neuron-OPC synapses in white matter are not static but undergo developmental transition towards facilitation and temporally precise transmission that parallels the maturation trajectory of classical neuronal synapses in cortical grey matter. These results identify neuron-glia synapses in white matter as dynamic elements of developing neural circuits, and suggest that synaptic release machineries at axonal shafts in white matter and synaptic boutons in grey matter mature in a similar fashion.

neuroscience↗

ISPpu10 is a structure-gated bridge RNA recombinase that drives safe, large-scale genomic plasticity

IS110 elements employ bridge RNA to direct target site recognition, yet whether additional layers of specificity exist beyond RNA-DNA base pairing is unknown. Here we identified ISPpu10, an IS110 element in Pseudomonas putida that is associated with >100-kb segmental amplifications during adaptive laboratory evolution. All insertions mapped to multiple identical copies of a single conserved intergenic sequence harboring a GC-rich 5' extension that forms a stem-loop. Systematic mismatch and compensatory substitution scanning revealed a sequence-structure dual-match logic: base pairing between the bridge RNA and target DNA serves as an RNA-guided match, whereas the target-encoded stem-loop provides an additional specificity determinant. Transplanting this stem-loop into Escherichia coli targets improved on-target integration and reduced genome-wide off-target insertion, establishing the stem-loop as a portable structural gate. These findings reveal a structural recognition layer beyond base-pairing, suggesting how bacteria reconcile transposition with genome integrity and offering a strategy for precise genome editing.

microbiology↗

A post-translational regulatory map of chronic antigen-driven human T cell dysfunction.

T cells exposed to persistent antigen in the context of chronic viral infections or cancer lose self-renewal and cytotoxic capacity. Several transcriptional, epigenetic, and metabolic drivers of this process have been identified. However, the post-transcriptional regulatory mechanisms influencing the proteome of dysfunctional T cells are not well understood. Here we present a time-resolved molecular landscape of human T cells during the development of chronic antigen-driven dysfunction. Persistent T cell receptor stimulation significantly remodeled the proteome, including changes in canonical T cell exhaustion-associated proteins and proteins related to mitochondrial function, redox homeostasis, nucleotide metabolism, and cell-cycle progression. Dysfunctional T cells displayed activation of stress response pathways that were recapitulated in vivo; targeting these pathways altered the cytotoxic capacity of T cells during persistent tumor exposure. Our comprehensive proteomic resource reveals unique post-transcriptional changes in dysfunctional T cells and lays the groundwork for novel cysteine-directed therapeutics to enhance cancer immunotherapy.

immunology↗

BMAL1 and MEX3A co-regulate intestinal stem cell succession

Chemotherapeutic agents, such as 5-fluorouracil (5-FU), often induce intestinal mucositis due to toxicity to rapidly dividing intestinal stem cells (ISCs). Drug delivery at different times of day can alter 5-FU toxicity; however, the underlying biology is unclear. We found that homeostasis and succession between two ISC types, fast proliferating Lgr5+ crypt base columnar (CBC) cells and stress-resistant +4 cells (Bmi1+), are controlled by the circadian clock transcription factor BMAL1 and the BMAL1-regulated RNA-binding protein MEX3A via both direct transcriptional regulation and post-transcriptional control of Lgr5 mRNA stability. Bmal1 knockout in Lgr5+ CBCs reduced MEX3A expression and CBC numbers but increased Bmi1 expression in the crypts. Timing 5-FU delivery when crypt cells had low Lgr5 but peak level of Bmi1 protected ISCs from apoptosis. Together, these findings identify a novel role of BMAL1 in ISC homeostasis and provide a biological explanation for chronotherapeutic chemoprotection.

cell biology↗