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Plant Cell Advance Online Publication
Published on August 7, 2009; 10.1105/tpc.109.068072

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Received April 21, 2009
Returned for revision July 9, 2009
Accepted July 22, 2009

SUMO E3 Ligase HIGH PLOIDY2 Regulates Endocycle Onset and Meristem Maintenance in Arabidopsis

Takashi Ishida 1, Sumire Fujiwara 1, Kenji Miura 2, Nicola Stacey 3, Mika Yoshimura 1, Katja Schneider 1, Sumiko Adachi 4, Kazunori Minamisawa 4, Masaaki Umeda 4, and Keiko Sugimoto 5*

1 RIKEN Plant Science Center, Tsurumi, Yokohama, Kanagawa, 230-0045, Japan
2 Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba 305-8572, Japan
3 Department of Cell and Developmental Biology, John Innes Centre, Norwich, NR4 7UH, United Kingdom
4 Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama-cho, Ikoma, Nara, 630-0101, Japan
5 RIKEN Plant Science Center, Tsurumi, Yokohama, Kanagawa, 230-0045, Japan; Department of Cell and Developmental Biology, John Innes Centre, Norwich, NR4 7UH, United Kingdom

* To whom correspondence should be addressed. E-mail: sugimoto{at}psc.riken.jp.

Endoreduplication involves a doubling of chromosomal DNA without corresponding cell division. In plants, many cell types transit from the mitotic cycle to the endoreduplication cycle or endocycle, and this transition is often coupled with the initiation of cell expansion and differentiation. Although a number of cell cycle regulators implicated in endocycle onset have been identified, it is still largely unknown how this transition is developmentally regulated at the whole organ level. Here, we report that a nuclear-localized SUMO E3 ligase, HIGH PLOIDY2 (HPY2), functions as a repressor of endocycle onset in Arabidopsis thaliana meristems. Loss of HPY2 results in a premature transition from the mitotic cycle to the endocycle, leading to severe dwarfism with defective meristems. HPY2 possesses an SP-RING domain characteristic of MMS21-type SUMO E3 ligases, and we show that the conserved residues within this domain are required for the in vivo and in vitro function of HPY2. HPY2 is predominantly expressed in proliferating cells of root meristems and it functions downstream of meristem patterning transcription factors PLETHORA1 (PLT1) and PLT2. These results establish that HPY2-mediated sumoylation modulates the cell cycle progression and meristem development in the PLT-dependent signaling pathway.




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