Abstract
The regulation of organ size in higher organisms is a fundamental issue in developmental biology. In flowering plants, a phenomenon called “compensation” has been observed where a cell proliferation defect in developing leaf primordia triggers excessive cell expansion. As a result, final leaf size is not significantly reduced compared to that expected from the reduction in leaf cell numbers. Recent genetic studies have revealed several key features of the compensation phenomenon. Compensation is induced either cell autonomously or non-cell autonomously depending on the trigger that impairs cell proliferation; a certain type of compensation is induced only when cell proliferation is impaired beyond a threshold level. Excessive cell expansion is achieved by either an increased cell expansion rate or a prolonged period of cell expansion via genetic pathways that are also required for normal cell expansion. These results indicate that cell proliferation and cell expansion are coordinated through multiple pathways during leaf size determination. Further classification of compensation pathways and their characterization at the molecular level will provide a deeper understanding of organ size regulation.
Highlights
Organ size regulation is an essential process for the optimal growth and appropriate function of multicellular organisms
The molecular mechanisms underlying cell proliferation and postmitotic cell expansion have been investigated extensively, mainly through the characterization of the cell cycle and endocycle in which multiple rounds of DNA replication occur without cell division (Inzé and De Veylder, 2006; Breuer et al, 2010)
In addition to these cell cycle regulators, a number of genes have been identified over the last decade that regulate the size of lateral organs through the modulation of cell proliferation and/or cell expansion (Gonzalez et al, 2009; Krizek, 2009; Micol, 2009)
Summary
Organ size regulation is an essential process for the optimal growth and appropriate function of multicellular organisms. In the modern molecular genetics era, compensation has been observed in transgenic plants in which the cell cycle was inhibited through manipulation of core cell cycle regulators such as CDKA;1 (Hemerly et al, 1995) and KIP-related protein2 (KRP2; De Veylder et al, 2001), and in mutants defective in positive regulators of cell proliferation, such as AINTEGUMENTA (ANT; Mizukami and Fischer, 2000) and ANGUSTIFOLIA3/GRF-INTERACTING FACTOR1 (AN3/GIF1; Kim and Kende, 2004; Horiguchi et al, 2005).
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