Although the size of an organism is a defining feature, little is known about the mechanisms that set the final size of organs and whole organisms. Here we describe Arabidopsis DA1, encoding a predicted ubiquitin receptor, which sets final seed and organ size by restricting the period of cell proliferation. The mutant protein encoded by the da1-1 allele has a negative activity toward DA1 and a DA1-related (DAR) protein, and overexpression of a da1-1 cDNA dramatically increases seed and organ size of wild-type plants, identifying this small gene family as important regulators of seed and organ size in plants. Supplemental Many experiments suggest that organs possess intrinsic information about their final size and grow until they reach a final predetermined mass (Conlon and Raff 1999;Day and Lawrence 2000), but the mechanisms setting the limits of growth are not well characterized despite their central importance. Recently, a key pathway suppressing cell proliferation during organogenesis has been identified (Dong et al. 2007) that is conserved in insects and mammals. However, many of the factors regulating organ size in animals have no obvious counterparts in plants, suggesting that the control of plant organ size involves novel mechanisms. Although external cues such as light, day length, and temperature influence plant growth and adapt sessile plants to their prevailing environment, the final size of plant seeds and determinate organs is reasonably constant within a given species, whereas interspecific seed and organ size variation is remarkably large, demonstrating that developing seeds and organs also possess intrinsic information about their final size (Tsukaya 2006). The mechanisms that establish the final size of seeds and organs and mediate environmental inputs into growth are poorly understood, despite their fundamental importance and relevance to crop plant improvement.Plant organ growth occurs by an initial proliferative phase in which cell numbers increase while their size remains fairly constant, followed by dramatic cell size increases that cease when the set size of the organ is reached. Increases in cell ploidy occur during later stages of organ growth that can be associated with the final size of cells (Sugimoto-Shirasu and Roberts 2003). In leaves, the transition from cell proliferation to cell expansion follows cell cycle arrest fronts that move from the tip to the base (Donnelly et al. 1999). Modulation of the time and location of cell proliferation arrest (Nath et al. 2003;Dinneny et al. 2004;Disch et al. 2006;White 2006) have been established as key regulatory points during leaf and petal formation that set final organ size and establish its shape. Interaction between organs also influences seed size. Reduced maternal integument size reduces final seed size (Garcia et al. 2005), and reduced endosperm proliferation arrests cell elongation in the integument (Garcia et al. 2003).The growth regulator auxin promotes growth through ARGOS (Hu et al. 2003), which mediates expression of AINTEGUMEN...

The size of seeds affects not only evolutionary fitness but also grain yield of crops. Understanding the mechanisms controlling seed size has become an important research field in plant science. Seed size is determined by the integrated signals of maternal and zygotic tissues, which control the coordinated growth of the embryo, endosperm, and seed coat. Recent advances have identified several signaling pathways that control seed size through maternal tissues, including or involving the ubiquitin-proteasome pathway, G-protein signaling, mitogen-activated protein kinase (MAPK) signaling, phytohormone perception and homeostasis, and some transcriptional regulators. Meanwhile, growth of the zygotic tissues is regulated in part by the HAIKU (IKU) pathway and phytohormones. This review provides a general overview of current findings in seed size control and discusses the emerging molecular mechanisms and regulatory networks found to be involved.

Plant mechanical strength is an important agronomic trait. To understand the molecular mechanism that controls the plant mechanical strength of crops, we characterized the classic rice mutant brittle culm1 ( bc1 ) and isolated BC1 using a mapbased cloning approach. BC1 , which encodes a COBRA-like protein, is expressed mainly in developing sclerenchyma cells and in vascular bundles of rice. In these types of cells, mutations in BC1 cause not only a reduction in cell wall thickness and cellulose content but also an increase in lignin level, suggesting that BC1 , a gene that controls the mechanical strength of monocots, plays an important role in the biosynthesis of the cell walls of mechanical tissues.