Abstract
AbstractSpindly is a mitotic checkpoint protein originally identified as a specific regulator of Dynein activity at the kinetochore. In metaphase, Spindly recruits the Dynein/Dynactin complex, promoting the establishment of stable kinetochore-microtubule interactions and progression into anaphase. While details of Spindly function in mitosis have been worked out in cultured human cells and in the C. elegans zygote, the function of Spindly within the context of an organism has not yet been addressed. Here we present loss- and gain-of-function studies of Spindly in Drosophila. We investigated the requirements of distinct protein domains for the localisation and function of Spindly. We find that knock-down of Spindly results in a range of mitotic defects in the female germ line and during cleavage divisions in embryogenesis. Overexpression of Spindly in the female germ line is embryonic lethal and results in altered egg morphology. To determine whether Spindly plays a role in post-mitotic cells we altered Spindly protein levels in migrating cells and found that ovarian border cell migration is sensitive to the levels of Spindly protein. Our study uncovers novel functions of the mitotic checkpoint protein Spindly in Drosophila.
Publisher
Cold Spring Harbor Laboratory