We are pleased to share our new publication in Journal of Cell Biology, entitled: “A force-sensitive mutation reveals a non-canonical role for dynein in anaphase progression.”

In this collaborative study, a series of Drosophila dynein heavy chain missense mutations were generated—including some linked to human neurological disease—to dissect how dynein’s mechanical properties shape its functions. Findings identify a novel microtubule-binding domain mutation that specifically blocks the metaphase–anaphase transition, independent of dynein’s canonical role in silencing the spindle assembly checkpoint. Optical trapping experiments and our lab’s all-atom molecular dynamics simulations further reveal that this mutation impairs dynein’s performance under load, offering insights into a previously unrecognized, force-sensitive role of dynein in anaphase progression.

Citation
Salvador-Garcia, D., Jin, L., Hensley, A., Golcuk, M., Gallaud, E., Chaaban, S., Port, F., Vagnoni, A., Planelles-Herrero, V.J., McClintock, M.A., Derivery, E., Carter, A.P., Giet, R., Gur, M., Yildiz, A., Bullock, S.L. (2024). A force-sensitive mutation reveals a non-canonical role for dynein in anaphase progression, Journal of Cell Biology, 223 (10): e202310022 (5-year IF: 8, IF: 7.3)

View the publication
https://rupress.org/jcb/article/223/10/e202310022/276835/A-force-sensitive-mutation-reveals-a-non-canonical