TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates

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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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2025-12-21
DOI
https://doi.org/10.64898/2025.12.19.695442
Primary Topic
interferon and immune responses
Type
article
Field-Weighted Citation Impact
0.00

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article

TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates

bioRxiv (Cold Spring Harbor Laboratory)
interferon and immune responses
article

TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates

article en

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.

bioRxiv (Cold Spring Harbor Laboratory)
Southwestern Medical Center (US), The University of Texas Southwestern Medical Center (US)
University of Texas Southwestern Medical Center
Openalex Percentile: Top 53%
interferon and immune responses
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TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates · bioRxiv (Cold Spring Harbor Laboratory) (2025) | TGRS Research Map | TGRS