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Min, J.-H.

Publications and source records attributed to Min, J.-H..

2 recordsLinked to original sources

pTAC3 and pTAC14 are required for binding of plastid-encoded RNA polymerase to DNA

Plastid-encoded RNA polymerase (PEP) is a bacterial-type multisubunit RNA polymerase responsible for the majority of transcription in chloroplasts. PEP consists of four core subunits, which are orthologs of their cyanobacterial counterparts. In Arabidopsis thaliana, PEP associates with 12 PEP-associated proteins (PAPs), which serve as peripheral subunits of the RNA polymerase. The exact contributions of PAPs to PEP function are still poorly understood. We use ptChIP-seq to show that PAP1/pTAC3, a peripheral subunit of PEP, binds to the same genomic loci as RpoB, a core subunit of PEP. The pap1/ptac3 mutant shows a complete loss of RpoB binding to DNA throughout the genome, indicating that PAP1/pTAC3 is necessary for RpoB binding to DNA. A similar loss of RpoB binding to DNA is observed in the pap7/ptac14 mutant, which is defective in another peripheral PEP subunit. We propose that the peripheral subunits of PEP are required for the recruitment of core PEP subunits to DNA. KEY MESSAGEThe peripheral subunits of plastid-encoded RNA polymerase play a crucial role in recruiting the core PEP subunits to DNA in Arabidopsis chloroplasts.

plant biology↗

Disrupting microglial TGF-β signaling triggers region-specific pathology in the spinal cord

Transforming growth factor-{beta} (TGF-{beta}) signaling is critical for microglial maturation during development and the maintenance of microglial homeostasis in adulthood. It remains unclear whether regional susceptibilities to the loss of TGF-{beta} signaling in microglia also exist, and the contributing factors have yet to be identified. We find that deletion of Tgfbr2 on microglia leads to microglial activation and demyelination in mouse spinal cords, primarily in the dorsal column (DC). Tgfbr2-deficient microglia exhibit distinct transcriptomic changes, and those sorted from the DC display a more proinflammatory profile compared to those from the ventral column (VC) and grey matter (GM). Single nucleus RNA sequencing (snRNA-seq) of the spinal cord uncovers a microglial subtype that emerges exclusively following Tgfbr2 deletion (termed TGF{beta} signaling-suppressed microglia, TSM), exhibiting high expression of Mmp12, Gpnmb, Lgals3, Mgll, and Alcam, predominantly located in the DC. Phenotypically, disruption of microglial TGF-{beta} signaling results in behavioral deficits that are more severe in female and older mice, whereas young male mice are less affected. Mechanistically, we reveal a significantly higher level of TGF-{beta}1/TGFBR2 in the spinal cords of normal older mice compared to the young mice, with the DC region richer in genes of the TGF-{beta} signaling pathway than the VC and GM regions. This indicates that older mice and the DC region require more TGF{beta}1 to maintain tissue homeostasis and, reciprocally, are more responsive and sensitive to the disruption of TGF-{beta} signaling in microglia. Herein, we report a demyelinating disease with region-specificity and its susceptibility to the loss of microglial TGF-{beta} signaling with gender and age differences. Our findings contribute valuable information to our understanding of the importance of microglia in regulating myelin health, especially during the aging process.

neuroscience↗