| First Author | Kiyota N | Year | 2025 |
| Journal | Sci Adv | Volume | 11 |
| Issue | 30 | Pages | eadq7105 |
| PubMed ID | 40712007 | Mgi Jnum | J:370159 |
| Mgi Id | MGI:8225972 | Doi | 10.1126/sciadv.adq7105 |
| Citation | Kiyota N, et al. (2025) Role of HAUS7 as a DOCK3 binding partner in facilitating axon regeneration. Sci Adv 11(30):eadq7105 |
| abstractText | The molecular mechanisms involved in reconstructing the eye-to-brain connection and functional recovery following optic nerve damage remain unclear. This study revealed that HAUS augmin-like complex subunit 7 (HAUS7) is a molecule that binds to dedicator of cytokinesis 3 (DOCK3), a regulator of neurotrophic factor signaling and axon regeneration. We observed a distribution pattern of HAUS7 expression, suggesting that neuronal HAUS7 is transported from the cell body to the growth cone under the control of DOCK3. In addition, phosphorylation of DOCK3 at Y562 by tropomyosin receptor kinase B signaling leads to the dissociation of HAUS7, which is considered an important step for microtubule assembly. Deletion of Haus7 in mice significantly reduced microtubule formation and axon regeneration following optic nerve crush (ONC). Transcriptome analysis suggested that HAUS7 levels decrease in glaucoma and after the ONC, while retinal ganglion cells actively regenerating their axons express high levels of HAUS7. In summary, HAUS7 is a binding partner of DOCK3 necessary for axon elongation. |
