CESICOP
Elucidating the control of cell size in plants
| Coordinatore | UNIVERSITAET POTSDAM
Organization address
address: AM NEUEN PALAIS 10 contact info |
| Nazionalità Coordinatore | Germany [DE] |
| Totale costo | 169˙969 € |
| EC contributo | 169˙969 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-2009-IIF |
| Funding Scheme | MC-IIF |
| Anno di inizio | 2010 |
| Periodo (anno-mese-giorno) | 2010-10-01 - 2012-09-30 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
UNIVERSITAET POTSDAM
Organization address
address: AM NEUEN PALAIS 10 contact info |
DE (POTSDAM) | coordinator | 169˙969.00 |
Mappa
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Obiettivo del progetto (Objective)
'Cell size is a crucial determinant of overall organ size. The size of a cell can be influenced by various hormones; it depends on the identity of the cell; and it is positively correlated with the cell’s ploidy level. However, the molecular mechanisms that determine when cell expansion stops to ensure an appropriate cell size are poorly understood. In plants, the presence of a cell wall means that the extent of cell expansion, and thus the amount of cell wall synthesized, is also of paramount economic importance, given our dependence on plant cell-wall material for classical uses (paper, textiles, etc.) and for bioenergy production. The Lenhard group have recently isolated mutations in an Arabidopsis kinesin, a microtubule-based motor protein, that lead to larger cells despite normal ploidy levels. The kinesin associates with Golgi-stacks and appears necessary to ensure their even distribution within the cell. Given the importance of the Golgi-apparatus for secretion of cell-wall material, the current working hypothesis is that more uneven cell-wall biosynthesis in the mutants resulting from the uneven distribution of the Golgi-stacks triggers cell-wall integrity-sensing pathways, which in turn lead to the synthesis of more cell wall and excess cell expansion. This proposal will address the basic function of the identified kinesin by analyzing plants lacking also a highly similar, probably functionally redundant kinesin; study the mechanism of action of the kinesin in question by analyzing an identified interacting protein; assess the cellular basis for the observed cell enlargement by testing several of the assumptions and predictions of the working hypothesis outlined above; and investigate the relation between the excess cell enlargement in the kinesin mutant and that seen in the phenomenon of ‘compensation’. Together, these studies will provide important new insight into the regulation of cell-wall synthesis and cell expansion in plants.'