The A-Type Cyclin CYCA2;3 Is a Key Regulator of Ploidy Levels inArabidopsisEndoreduplication

Abstract

Plant cells frequently undergo endoreduplication, a process in which chromosomal DNA is successively duplicated in the absence of mitosis. It has been proposed that endoreduplication is regulated at its entry by mitotic cyclin-dependent kinase activity. However, the regulatory mechanisms for its termination remain unclear, although plants tightly control the ploidy level in each cell type. In the process of searching for regulatory factors of endoreduplication, the promoter of an Arabidopsis thaliana cyclin A gene, CYCA2;3, was revealed to be active in developing trichomes during the termination period of endoreduplication as well as in proliferating tissues. Taking advantage of the situation that plants encode highly redundant cyclin A genes, we were able to perform functional dissection of CYCA2;3 using null mutant alleles. Null mutations of CYCA2;3 semidominantly promoted endocycles and increased the ploidy levels achieved in mature organs, but they did not significantly affect the proportion of cells that underwent endoreduplication. Consistent with this result, expression of the CYCA2;3-green fluorescent protein fusion protein restrained endocycles in a dose-dependent manner. Moreover, a mutation in the destruction box of CYCA2;3 stabilized the fusion protein in the nuclei and enhanced the restraint. We conclude that CYCA2;3 negatively regulates endocycles and acts as a key regulator of ploidy levels in Arabidopsis endoreduplication.

Jasmonate Controls Leaf Growth by Repressing Cell Proliferation and the Onset of Endoreduplication while Maintaining a Potential Stand-By Mode

“…3). Our QRT-PCR analysis confirmed the expression pattern of another negative regulator of endoreduplication, CYCA2;3 (At1g15570; Imai et al, 2006), as being similar to the above genes in Col gl1. With the exception of CYCD3;2 (At1g47210; Yu et al, 2003), all the above genes are significantly up-regulated also in the aos mutant ( Fig.…”

Eternal Youth, the Fate of Developing Arabidopsis Leaves uponRhodococcus fasciansInfection

“…Expression of CDKA;1 and CYCA2;3, as a complex involved in the negative regulation of endocycling (Imai et al, 2006), was also specifically down-regulated as control leaves differentiated (Fig. 5,A and B).…”

“…Cell cycle exit and endoreduplication onset are accomplished through down-regulation of the mitotic CDK activity by inhibitors, such as KIP-related proteins (Wang et al, 1998;De Veylder et al, 2001;Verkest et al, 2005;Weinl et al, 2005;Nakai et al, 2006;Pettkó -Szandtner et al, 2006) and SIAMESE (SIM;Churchman et al, 2006). Other important control mechanisms for CDK activity are regulation of cyclin transcription and stability, and proteolysis by the anaphase-promoting complex-activating protein CELL CYCLE SWITCH52A (CCS52A; den Boer and Murray, 2000;Kondorosi and Kondorosi, 2004;Imai et al, 2006). Recently, in Arabidopsis, E2Fe/DEL1, a member of the E2F transcription factors present exclusively in mitotic cells, has been shown to repress the CCS52A2 activity, preventing cells from engaging in the endoreduplication program (Vlieghe et al, 2005;Lammens et al, 2008).…”

Non-cell-autonomous rescue of anaphase-promoting complex function revealed by mosaic analysis of HOBBIT , an Arabidopsis CDC27 homolog

“…It is unknown at this point which factor triggers the switch from mitotic cycles to endocycles. One candidate is CycA2;3, which has been identified as a regulator of endocycles in Arabidopsis (29). HBT protein is degraded in the elongation zone because transcription is restricted to the G 2 ͞M phase of the cell cycle, which limits endoreduplication and sets a maximum cell size.…”