️ Episode 225: VRK-1 and BAF-1 release meiotic chromosomes
In this episode of PaperCast Base by Base, we explore VRK-1 phosphorylates BAF-1 to remove chromatin from the nuclear periphery during early meiotic prophase in C. elegans, and failure of this step impairs pairing and synapsis and generates heritable genome lesions
Study Highlights:The authors used an auxin-inducible VRK-1 depletion system and genetic perturbations to show that VRK-1 phosphorylates BAF-1 (Ser4) to release chromatin–nuclear periphery contacts during leptotene–zygotene. VRK-1 loss or a BAF-1 Ser4 phospho-mutant increases chromatin tethering at the nuclear envelope, delays homolog pairing, slows and disrupts synaptonemal complex assembly, and elevates apoptosis. VRK-1 depletion produces oocytes with increased DAPI bodies, intrachromosomal bridges and fragmentation that depend on SPO-11 and MSH-5, while baf-1 RNAi rescues overtethering phenotypes. Transient VRK-1 loss during the chromosome movement window yields offspring with an increased burden of deletions and duplications detected by long-read sequencing, implicating VRK-1–BAF-1 in preserving genome integrity
Conclusion:Timed VRK-1–mediated phosphorylation of BAF-1 is required to detach chromatin from the nuclear periphery during meiotic chromosome movements to ensure correct pairing, synapsis, and genome stability
Music:Enjoy the music based on this article at the end of the episode.
Reference:Paouneskou D., Baudrimont A., Elkrewi M., Kölbl C., Tiemann-Boege I., Vicoso B., Jantsch V. BAF-1–VRK-1 mediated release of meiotic chromosomes from the nuclear periphery is important for genome integrity. Nature Communications. 2025;16:10446. https://doi.org/10.1038/s41467-025-65420-9
License:This episode is based on an open-access article published under the Creative Commons Attribution 4.0 International License (CC BY 4.0) – https://creativecommons.org/licenses/by/4.0/
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On PaperCast Base by Base you’ll discover the latest in genomics, functional genomics, structural genomics, and proteomics.

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