Fine-tuning mRNA tails: How maternal PAN2 safeguards early embryo development
Peer-Reviewed Publication
Updates every hour. Last Updated: 27-Oct-2026 00:16 ET (27-Oct-2026 04:16 GMT/UTC)
A new study in Science Bulletin reveals that maternal PAN2 protein is essential for early embryonic development by regulating mRNA poly(A) tail length. Using an oocyte-specific conditional knockout mouse model, researchers found that PAN2 deficiency causes embryos to arrest at the two-cell stage due to abnormal poly(A) tail elongation, maternal mRNA accumulation, and impaired zygotic genome activation. PAN2 recognizes substrates via the PAN3-PABPC1 complex, preferring tails lacking guanosine but enriched in uridine.
A research team led by Prof. Yi Sun at Zhejiang University, reported a unexpected finding that the combination of KrasG12D activation and genetic inactivation of UBE2M in the lung triggers the cGAS-STING-NF-κB signal to form a inflammatory tumor microenvironment (TME). Mechnistically, KrasG12D promotes the mitochondrial biogenesis, whereas UBE2M depletion inhibits Parkin neddylation and mitophagy, together causing the cytoplasmic release of damaged mitochondrial DNA. The STING antagonist H-151 rescues TME, indicating a causal role of the cGAS-STING signal. The study therefore demonstrates a unexpected role of UBE2M in prevention TME induced by Kras mutant.
A comprehensive in silico scan of human respiratory viruses identified 3CLpro cleavage motifs within influenza NP and PA. Experimental validation confirmed that 3CLpro-mediated cleavage triggers rapid protein degradation and cytoplasmic mislocalization. Consequently, both ectopic 3CLpro expression and SARS-CoV-2 replication effectively inhibit replication across diverse influenza virus strains, revealing a broad-spectrum antiviral mechanism.