Modulation of Spindle Assembly Checkpoint efficiency by cell fate in a chordate embryo

Abstract

The spindle assembly checkpoint (SAC) is a surveillance system which preserves genome integrity by delaying anaphase onset until all chromosomes are correctly attached to spindle microtubules. Recruitment of SAC proteins to unattached kinetochores generates an inhibitory signal that prolongs mitotic duration. Chordate embryos are atypical in that spindle defects do not delay mitotic progression during early development, implying that either the SAC is inactive or the cell-cycle target machinery unresponsive. Here we show that in embryos of the chordate Phallusia mammillata the SAC delays mitotic progression from the 8th cleavage divisions. Unattached kinetochores are not recognized by the SAC machinery until the 7th cell cycle when the SAC is acquired. Following acquisition, SAC strength, manifest as the degree of mitotic lengthening induced by spindle perturbations, is specific to different cell types and is modulated by cell size showing similarity to SAC control in early Caenorhabditis elegans embryos. We conclude that SAC acquisition is a process likely specific to chordate embryos, while modulation of SAC efficiency in SAC proficient stages depends on cell fate and cell size similarly to non-chordate embryos.