The abstract is read at the publisher; the summary is JClub's.
Loss of Brother of CDON (BOC) and Cell adhesion molecule-related, Down-regulated by Oncogenes (CDON) in SHH-expressing cells blunts protrusion-localized Cdc42 activity, shortening cytonemes.
- Why it matters: Pathway-specific cytoneme formation and the molecular control of actin organization for elongation and stability remain unclear, limiting understanding of contact-mediated signaling transport.
- What they did: The study examined SHH cytoneme biogenesis and found BOC and CDON functionally repurposed to recruit actin regulators FARP1 and Cdc42, using loss-of-function analyses and live imaging in developing murine spinal cords.
- The result: In SHH-expressing cells, CDON loss reduces neuroepithelial cytoneme frequency and alters neuronal cell fate specification, supporting a model that SHH-binding proteins promote long cytoneme formation for ligand transport.
The findingWhy it mattersWhat they didThe result
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