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Tian Chen

Publications and source records attributed to Tian Chen.

2 recordsLinked to original sources

Unraveling the coastal marine plastisphere archaeome.

Plastic pollution has created an expanding anthropogenic microbial niche, the plastisphere, raising questions about microbial ecology and associated impacts. Archaea, the third domain of life with fundamental ecological and evolutionary significance, remain poorly understood in this habitat. Here, using paired plastic debris and bulk-water samples from coastal marine ecosystems, key archaeal habitats increasingly threatened by plastic pollution, we characterize the plastisphere archaeome through archaeal amplicon sequencing and metagenomics. We show that the archaeome is significantly reshaped in the plastisphere, exhibiting higher taxonomic diversity, greater community heterogeneity, and selective enrichment of Euryarchaeota and Crenarchaeota. Archaeal genes involved in methane, nitrogen, and sulfur cycling are enriched in the plastisphere. Taxonomic and functional divergence between the plastisphere and bulk water increases with anthropogenic chemical stress. These findings suggest that plastic pollution could alter marine archaeal diversity, biogeography, and biogeochemical potential, extending understanding of plastisphere impacts to the archaeal domain.

Archaea

ZNF593 regulates the cGAS-mediated innate immune response by attenuating cGAS-DNA binding.

The enzyme cyclic GMP-AMP synthase (cGAS) is essential for detecting aberrantly located double-stranded DNA (dsDNA) from genomic, mitochondrial, and microbial origins. Through the synthesis of 2'3'-cGAMP, cGAS triggers the activation of the stimulator of interferon genes pathway, which initiates in vivo innate immune responses. Here, we identify zinc finger proteins ZNF593, which translocate from the nucleus to the cytoplasm after viral infection, as a negative regulator of antiviral type I IFN (IFN-I) production. ZNF593 directly binds to cGAS and suppresses its activation by inhibiting the cGAS-dsDNA interaction. ZNF593 deficiency increases IRF3 nuclear translocation and promotes DNA virus-triggered IFN production. Furthermore, ZNF593 deficiency promotes antiviral innate responses in vivo, improving survival rates in mice against HSV-1 infection. We further find that ZNF593 plays a protective role in systemic lupus erythematosus (SLE) pathology. Notably, replenishing ZNF593 effectively reduced IFN production in peripheral blood mononuclear cells (PBMCs) of SLE patients or in the TMPD-induced murine SLE model. Our findings suggest that ZNF593 negatively regulates IFN-β signaling by targeting cGAS activation, providing new insights into the regulatory mechanisms for antiviral defenses and autoimmune diseases.

Nucleotidyltransferases