Cell plate formation in plants is a complex process orchestrated by the targeted delivery of Golgi-derived and endosomal vesicles containing cell plate components to the phragmoplast midzone. It has long been hypothesized that vesicles are directionally transported along phragmoplast microtubules by motor proteins. However, the mechanisms governing the accumulation and immobilization of vesicles at the phragmoplast midzone remain elusive, and the motor protein responsible has yet to be identified. Here we show that the plant-specific class II kinesin-12 (kinesin12-II) functions as a motor protein that drives vesicle transport towards the phragmoplast midzone in the moss Physcomitrium patens. In the kinesin12-II mutant, the directional movement of cell plate materials towards the midzone and their retention were abolished, resulting in delayed cell plate formation and phragmoplast disassembly. A macroscopic phenotype arising from kinesin12-II disruption was the impediment to gametophore development. We showed that this defect was attributable to the production of aneuploid and polyploid cells in the early gametophore, where chromosome missegregation and cytokinesis failure occurred. These findings suggest that plant kinesin-12 has evolved to acquire a unique and critical function that facilitates cell plate formation in the presence of phragmoplasts.
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