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Edinburgh, Scotland, United Kingdom - TAIR

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Leaf size is regulated by a cell-autonomous<br />

system linking cell proliferation and postmitotic<br />

cell enlargement<br />

During leaf development, a defect in cell proliferation often triggers enhanced<br />

post-mitotic cell enlargement. This phenomenon is termed compensation. For<br />

example, a Kip-related protein2 overexpressor (KRP2 o/x) and an angustifolia3<br />

(an3) mutant show atypical compensation. In leaf primordia, differentiating cells<br />

and proliferating cells are found in the apical and basal regions, respectively.<br />

Until now, how, where and when cells in leaf primordia recognize the defect of<br />

cell proliferation remained to be elucidated. In particular, whether compensation<br />

is induced non-cell-autonomously or not is totally unknown. To solve these<br />

questions, we designed an experimental system, which can make mosaic leaves<br />

expressing KRP2 or AN3 by CRE/Lox.<br />

First, we assessed the functionality of our system. When KRP2 overexpression<br />

was shut off within the whole very young leaf primordium, compensation was<br />

restored, suggesting that the system was functional. We next examined whether<br />

KRP2 directly regulates enhanced cell enlargement. When KRP2<br />

overexpression was induced in the postmitotic cells, cell enlargement was not<br />

enhanced, supporting the idea that enhanced cell enlargement was not a direct<br />

function of KRP2 but caused by a defect in cell proliferation. As for cell autonomy,<br />

we analyzed cell size in mosaics. We found that KRP2 mosaics contained two<br />

distinct cell-size classes that were equivalent to wild-type and KRP2 o/x in size,<br />

respectively. This fact indicated that compensation in KRP2 o/x is induced cellautonomously.<br />

Indeed, in the boundary of mosaics, size of genotypically<br />

wild-type and KRP2 o/x cells are not affected by the other genotype. Our results<br />

suggested that the activity of cell proliferation is memorized in each cell at least<br />

in the case of KRP2 o/x. We will discuss the system behind the compensation<br />

based on these results and data from AN3 mosaics now being characterized.<br />

73<br />

C22<br />

Wednesday 17:30 - 17:45<br />

Development<br />

Kensuke Kawade1<br />

Gorou Horiguchi2<br />

Hirokazu Tsukaya1,3<br />

1Graduate School of<br />

Science<br />

The University of Tokyo<br />

Tokyo<br />

Japan<br />

2 College of Science<br />

Rikkyo University<br />

Tokyo<br />

Japan<br />

3 National Institute for<br />

Basic Biology<br />

Okazaki<br />

Aichi<br />

Japan

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