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NudE regulates dynein at kinetochores but is dispensable for other dynein functions in the early embryo. | LitMetric

NudE regulates dynein at kinetochores but is dispensable for other dynein functions in the early embryo.

J Cell Sci

Instituto de Biologia Molecular e Celular, Universidade do Porto, 4200-135 Porto, Portugal

Published: January 2018

AI Article Synopsis

Article Abstract

In mitosis, the molecular motor dynein is recruited to kinetochores by the Rod-Zw10-Zwilch complex (RZZ) and Spindly to control spindle assembly checkpoint (SAC) signaling and microtubule attachment. How the ubiquitous dynein co-factors Lis1 and NudE contribute to these functions remains poorly understood. Here, we show that the NudE homolog NUD-2 is dispensable for dynein- and LIS-1-dependent mitotic spindle assembly in the zygote. This facilitates functional characterization of kinetochore-localized NUD-2, which is recruited by the CENP-F-like proteins HCP-1 and HCP-2 independently of RZZ-Spindly and dynein-LIS-1. Kinetochore dynein levels are reduced in embryos, and, as occurs upon RZZ inhibition, loss of NUD-2 delays the formation of load-bearing kinetochore-microtubule attachments and causes chromatin bridges in anaphase. Survival of embryos requires a functional SAC, and kinetochores without NUD-2 recruit an excess of SAC proteins. Consistent with this, SAC signaling in early embryos extends mitotic duration and prevents high rates of chromosome mis-segregation. Our results reveal that both NUD-2 and RZZ-Spindly are essential for dynein function at kinetochores, and that the gain in SAC strength during early embryonic development is relevant under conditions that mildly perturb mitosis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818066PMC
http://dx.doi.org/10.1242/jcs.212159DOI Listing

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