Compensation as a Clue to Understanding the Mechanisms of Leaf Size Control

In this section, we present an overview of our present understanding of the leaf-size control system based on information obtained from studies of Arabidopsis mutants (Tsukaya 2006). Before discussing these topics, let us first re-examine classic and new ideas of organ-size regulation, since this re-examination has led us to studies of a yet unknown, organ-wide control system of leaf size.

To date, two theories, the cell theory and the organismal theory, have been postulated for the mechanisms by which genes control development in plants (Kaplan and Hagemann 1991; Sitte 1992; Hagemann 1992; Kaplan 1992; Tsukaya 2002, 2003). The cell theory posits that the cell is the unit of morphogenesis in leaves. According to this theory, the final leaf size is determined by the sum of behaviors of individual cells, which are under cell-autonomous control. In contrast, the organismal theory proposes that the unit of morphogenesis is the organ, and pre-determined organ space is filled by an increase in cell mass that is achieved through either cell proliferation or cell expansion. Thus, the organismal theory predicts a genetic mechanism that determines leaf shape and size independent of the behaviors of individual cells (Kaplan and Hageman 1991; Sitte 1992; Tsukaya 2002, 2003). In re-examining the validity of these theories by studying leaf morphology mutants, we found that the cell theory is more likely (Tsukaya 2002, 2003). For example, in the an-gustifolia (an) mutant, a narrow cell shape due to the inhibition of polar cell expansion directly results in the narrow leaf phenotype (Tsuge et al. 1996;

Kim et al. 2002). In addition, a number of mutants show reduced leaf area due to a specific decrease in the number of cells (Horiguchi et al. 2006a,b). These examples show that changes in the behaviors of cells directly influence leaf shape.

However, leaf size and shape are not always a simple sum of the behavior of individual cells (Tsukaya 2002, 2003), as mentioned in the introduction. This is clear in mutants and transgenic lines that exhibit compensation. Since compensation appears to function to replace the leaf area that is lost due to impaired cell proliferation, one would expect that this phenomenon would support the organismal theory. Organismal theory predicts the existence of a system that maintains a constant leaf size during developmental fluctuations. However, such a regulatory mechanism is highly unlikely since a number of mutants that show decreased cell numbers show no increase in cell size. Likewise, an increase in the cell number caused by the overexpression of AN3 or ANT results in a corresponding increase in the leaf area (Mizukami and Fischer 2000; Horiguchi et al. 2005; reviewed in Tsukaya 2002, 2003). In addition, the leaf area in mutants exhibiting compensation is usually smaller than that in wild-type plants.

In contrast, several possibilities could explain the occurrence of compensation based on the cell theory, with slight modification (Tsukaya 2002, 2003). Namely, compensation can be explained by the "neo cell theory", in which the cell is considered the unit of morphogenesis and the pathway(s) of cell proliferation and cell enlargement are integrated in some way at the organ level (Tsukaya 2002, 2003). In this context, compensation can be regarded as a reflection of certain mechanisms that integrate cell proliferation and cell enlargement. We examine below several possible mechanisms of compensation (or the integration mechanisms) based on available genetic and molecular data. Next, we interpret compensation as the result of a short-range signaling mechanism that operates during leaf morphogenesis.

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