ArticleInternational journal of molecular sciences2026
The CCHCR1-UBAP2L Interaction Promotes UBAP2L Release from P-Bodies for Stress Granule Assembly.
Article in International journal of molecular sciences, 2026. 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
Ribonucleoprotein granules such as processing bodies (P-bodies) and stress granules (SGs) are membrane-less organelles that regulate mRNA metabolism through liquid-liquid phase separation. UBAP2L drives SG assembly and can bridge P-bodies with SGs, yet how it is mobilized between these compartments remains unclear. Here, using co-immunoprecipitation, GST pull-down, CRISPR-Cas9-mediated knockout, and immunofluorescence microscopy, we demonstrate that CCHCR1 directly binds UBAP2L and that this interaction is dynamically regulated by stress intensity. Under mild oxidative stress, CCHCR1 retains UBAP2L in P-bodies; as stress intensifies, this interaction weakens, permitting UBAP2L release for SG assembly. CCHCR1 deficiency aberrantly traps UBAP2L in P-bodies via enhanced DDX6 association, resulting in defective SG assembly, delayed maturation, and increased P-body-SG fusion. These findings establish CCHCR1 as a stress-responsive switch that controls UBAP2L partitioning between P-bodies and stress granules, thereby controlling the threshold and kinetics of SG biogenesis.
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