Spatiotemporal dynamics of RAD51C between the Golgi and nucleus regulates homologous recombination and genomic stability.
Abstract
Intra-organelle communication is essential for cellular homeostasis, but the coordination between nuclear processes and cytoplasmic compartments remains poorly understood. Here, we uncover a novel spatiotemporal regulatory pathway linking the Golgi complex to the nucleus upon DNA damage. We show key DNA repair proteins, including RAD51C, dynamically shuttle between these organelles in response to distinct types of DNA damage. Mechanistic analysis reveals that RAD51C is anchored at the Golgi by Giantin. Disrupting this interaction leads to premature RAD51C nuclear localization, impaired homologous recombination signaling, genomic instability, and increased cell proliferation. Our findings establish Golgi-nuclear communication as a critical regulator of DNA repair, offering new insights into genomic integrity maintenance with profound implications for cancer and aging-related genomic instability.
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Research summary
The paper explores the role of RAD51C in DNA repair and its connection to genomic stability, which is relevant to the mechanisms underlying aging and age-related diseases. However, while it provides solid insights into the regulatory pathways involved in DNA repair, the findings are more of a solid research contribution rather than a major breakthrough, limiting its overall impact on the field of longevity research.
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