The met 1 mutation in Chlamydomonas reinhardtii causes arrest at mitotic metaphase with persisting p34 cdc2 -like H1 histone kinase activity that can promote mitosis when injected into higher-plant cells

Summary The met 1 mutation in Chlamydomonas reinhardtii causes metaphase arrest. Arrested cells have disassembled cortical microtubules, a fully assembled spindle, condensed and aligned metaphase chromosomes and abundant mitotic phosphoproteins recognised by MPM-2 antibody in the nuclear region. Protein purified by affinity for the mitotic protein p13 suc1 contains p34 cdc2 -like H1 histone kinase activity at times when control cells have inactivated this enzyme. The active enzyme, when microinjected into Tradescantia stamen hair cells, accelerated progress through prophase to normal completion of mitosis, indicating that the mutation did not disable the mitotic Cdc2 protein kinase enzyme complex. The mutation prevented the normal lowering of this kinase activity that accompanies anaphase. A defect at time of mitosis rather than earlier in the cycle was indicated by temperature shifting of synchronous cells, which identified the earliest faulty progress as occurring near the beginning of mitosis and the time at which the essential function is completed near the end of mitosis. The met 1 gene mapped approximately 33 cM from ery-2 and extended the known limits of the linkage group XIV.