Signaling Systems Linking Cell Proliferation and Cell Expansion

After eliminating the above hypotheses for the mechanisms of compensation and the mechanisms that integrate cell proliferation and cell enlargement, the last possibility is that cell proliferation regulates post-mitotic cell expansion through some unknown linking mechanisms. Such a signal is thought to be produced in mitotic cells and to regulate cell expansion in post-mitotic cells. In this model, four modes of signaling action are possible, as shown in Fig. 2. The hypothetical signal might have a positive (Fig. 2A,C) or negative (Fig. 2B,D) effect on post-mitotic cell expansion and might work either cell-autonomously (Fig. 2A,B) or non-cell-autonomously (Fig. 2C,D).

In all of these models, the strength of the hypothetical signal(s) should correlate with the size of mature cells. If the signal(s) is negative, it should be

Fig. 2 Models of leaf size control suggested by compensated cell enlargement. To interpret compensation, signals that link cell proliferation and post-mitotic cell expansion are assumed. The hypothetical signals are produced in mitotic cells and function in post-mitotic cells. They exert positive (A and C) or negative (B and D) effects on postmitotic cells and are subjected to negative or positive regulation, respectively, according to the cell proliferation activity. The signals are retained in the cell in the course of leaf development and act cell-autonomously (A and B) or are released from mitotic cells and act non-cell-autonomously on post-mitotic cells (C and D). In A and B, mitotic and post-mitotic cells are shown in the lower and upper rows, respectively. In C and D, leaf primordia are shown in which mitotic and post-mitotic cells are located in the lower and upper regions of leaf primordia, respectively. In compensation-exhibiting mutants, the strength of positive and negative signals is expected to be stronger and weaker, respectively, leading to enhanced cell expansion in post-mitotic cells

Fig. 2 Models of leaf size control suggested by compensated cell enlargement. To interpret compensation, signals that link cell proliferation and post-mitotic cell expansion are assumed. The hypothetical signals are produced in mitotic cells and function in post-mitotic cells. They exert positive (A and C) or negative (B and D) effects on postmitotic cells and are subjected to negative or positive regulation, respectively, according to the cell proliferation activity. The signals are retained in the cell in the course of leaf development and act cell-autonomously (A and B) or are released from mitotic cells and act non-cell-autonomously on post-mitotic cells (C and D). In A and B, mitotic and post-mitotic cells are shown in the lower and upper rows, respectively. In C and D, leaf primordia are shown in which mitotic and post-mitotic cells are located in the lower and upper regions of leaf primordia, respectively. In compensation-exhibiting mutants, the strength of positive and negative signals is expected to be stronger and weaker, respectively, leading to enhanced cell expansion in post-mitotic cells weaker in compensation-exhibiting mutants than in the wild-type, and if it is positive, the signal(s) should be stronger in compensation-exhibiting mutants. This hypothetical signal(s) should have one important feature: its action should be saturated in wild-type leaf primordia if it is negative, or it should be ineffective if it is positive. This conclusion is deduced from the basic nature of compensation: although a reduction in cell numbers due to the loss of function of cell-proliferation activator genes, such as ANT or AN3, induces accelerated cell expansion, the overproduction of cells caused by the overexpression of the same genes does not affect the cell size (Mizukami and Fischer 2000; Horiguchi et al. 2005). This hypothetical feature of the signal is also predicted by the fact that certain mutants with moderately decreased numbers of leaf cells do not exhibit compensation (Horiguchi et al. 2006a,b). Whether the signal(s) act cell-autonomously or non-cell-autonomously is unknown, but should be revealed through the construction and analysis of chimeric leaf primordia of compensation-exhibiting and wild-type plants. Identification ofthe above signals should open up a new and exciting field of research on the organ-wide regulation of cell proliferation and cell enlargement.

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