Ectopic B-type cyclin expression induces mitotic cycles in endoreduplicating Arabidopsis trichomes.

Cell differentiation is frequently accompanied by a switch from a mitotic division cycle to an endoreduplication cycle. In endoreduplicating cells, DNA synthesis continues in the absence of cell divisions, and it is speculated that endoreduplication represents a shortened mitotic division cycle. In animals, it has been shown that cells switching from mitotic to endoreduplication cycles continue to express factors controlling the G1-S transition, whereas the transcription of mitotic factors controlling the G2-M transition is negatively regulated. It is unknown how the mitotic factors are repressed and what the functional significance of their suppression is. To test the function of two mitotic cyclins in an endoreduplication cycle, we expressed CYCLIN B1;1 and CYCLIN B1;2 in unicellular Arabidopsis trichomes. During wild-type development, trichomes undergo an average of four endoreduplication cycles, leading to a DNA content of approximately 32C. We find that ectopic expression of CYCLIN B1;2, not CYCLIN B1;1, induces mitotic divisions resulting in multicellular trichomes. The CYCLIN B1;2-triggered cell divisions appeared normal with respect to both nuclear division and cytokinesis. We show that CYCLIN B1;2 is misexpressed in the siamese mutant, which also produces multicellular trichomes. Additional overexpression of CYCLIN B1;2 in a siamese mutant background caused a strongly enhanced phenotype.