ArticlebioRxiv : the preprint server for biology2025
TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dysregulation of the E3 ubiquitin ligase TRIM37 is associated with tumor formation and Mulibrey nanism, a recessive developmental syndrome. TRIM37 regulates steady-state levels of centrosome proteins and limits their ectopic assembly, but how it recognizes and ubiquitinates its substrates is poorly understood. We found that TRIM37 directly ubiquitinates the centrosome-forming protein Cep192 at 7 lysines clustered near its C-terminus. TRIM37 binds Cep192 at a C-terminal intrinsically disordered region followed by an ASH domain (IDR+ASH8). Mutation of the 7 lysines or the IDR+ASH8 domain increased Cep192 levels and stability in cells, indicating loss of TRIM37-based regulation. Fusing IDR+ASH8 to an unrelated protein (GFP-EB1) was sufficient to enable its degradation via TRIM37. Biochemical assays revealed that IDR+ASH8 is primarily monomeric and binds TRIM37 via two separate coiled-coil motifs with mid-nanomolar affinity. We propose that the IDR+ASH8 motif is a bipartite degron for TRIM37, enabling it to target centrosome proteins and adjust their levels.
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