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 [1, 2]. 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 [3, 4]. 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 [5, 6] in unicellular Arabidopsis trichomes. During wild- type development, trichomes undergo an average of four endoreduplication cycles, leading to a DNA content of approximately 32C [7, 8]. 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 [9]. Additional overexpression of CYCLIN B1;2 in a siamese mutant background caused a strongly enhanced phenotype