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The YTHDC1 glutamate-rich domain docks to the ADAR1 Zα Domain, linking the N6-methyladenosine modification of pre-mRNAs to dsRNA editing

Created on 14 Jul 2026

Authors

Gromak, D., Shaytan, A. K., Herbert, A., Poptsova, M.

Abstract

The p150 isoform of the double-stranded RNA editing enzyme ADAR1 binds Z-DNA and Z-RNA through the conserved winged helix-turn-helix Z domain. Here, we describe an inverse computational design strategy to map protein interactors of Z. We used RFdiffusion and ProteinMPNN to generate around 10,000 synthetic binders optimized for the Z recognition surface, then used their sequences as structural templates for BLASTp searches against the human proteome. Multi-stage screening of around 1,200 candidate regions from 298 proteins via ColabFold pDockQ identified 79 candidates for high-resolution AlphaFold3 modeling, which revealed the m6A reader YTHDC1 as the top-ranked interactor. AlphaFold3 predicts that a glutamate-rich poly-E disordered region of YTHDC1 (residues 199-254) docks into the basic recognition pocket of Z through a charge-complementary mechanism that mimics the phosphate backbone of Z-RNA. Microsecond molecular dynamics simulations confirmed stability of the binary ADAR1p150-YTHDC1 complex, with the Z-poly-E interface maintaining RMSD below 3 Angstrem throughout. Ternary complex simulations showed that dsRNA acts as a co-anchoring scaffold stabilizing simultaneous engagement of both proteins in a catalytically dormant conformation. YTHDC1 localizes to transcription-associated YT bodies where nascent RNAs undergo m6A modification and negative supercoiling promotes Z-DNA formation, suggesting that YTHDC1 recruits ADAR1p150 to promote editing of intron-containing substrates prior to splicing.

Preprint server: bioRxiv
The authors list and abstract were imported from bioRxiv on 14 Jul 2026.

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