Previous analyses of tso1 mutants revealed a loss of control of directional cellular expansion and coordination of growth of adjacent cells, and defects in karyokinesis

Abstract

Plant morphogenesis requires tight coordination among a range of processes. Because plant cells do not migrate, morphogenesis is ultimately dependent on appropriate directional cell expansion and division. Expansion and division must be integrated with positional information such that new structures form at proper locations and in the appropriate orientation. In addition, growth must often be coordinated among large numbers of cells that are not directly in contact with each other to produce bilaterally symmetrical organs such as leaves, sepals, petals, and ovules. While histology of plant growth and development has been well characterized, less is known about how these processes are regulated at the molecular level. Some of the same components that regulate mitosis in other organisms have similar functions in plants (for review see Doonan and Fobert, 1997). However, cytokinesis occurs via a different mechanism in plants than it does in animals. In a dividing animal cell, constriction of a ring of actin filaments results in the formation of a cleavage furrow and eventual division into two daughter cells. In plants, however, division occurs by deposition of a new cross wall or cell plate separating the two daughter cells (for review see Staehelin and Hepler, 1996). These differences imply the existence of novel proteins involved in cytokinesis in plants. A number of the proteins involved in plant cytokinesis and directional cell expansion have been identified through mutant screens for plants with altered morphology (Assaad et al., 1996; Liu et al., 1995; Lukowitz et al., 1996). Most such mutants are embryo or seedling lethal because cell division is necessary from the very earliest stages of plant development. The tso1 mutants, however, exhibit normal vegetative development, but defects in cell division and expansion occur during flower and ovule development (Hauser et al., 1998; Liu et al., 1997). Cells of tso1-1 flowers showed abnormally high nuclear DNA levels, aberrant spindle apparatuses and incomplete formation of the cell plate (Liu et al., 1997). Gross flower morphology in the weaker tso1-3 allele was nearly indistinguishable from wild type. In tso1-3 ovules, however, the embryo sac failed to form and defects in integument development resulted from aberrations in directional expansion of cells and/or coordination of growth among adjacent cells (Hauser et al., 1998). Defects in the assembly, structure, or function of cytoskeletal elements, or processes they direct, might account for all of these phenotypes (Hauser et al., 1998; Liu et al., 1997). Herein we describe the cloning of TSO1. Based on the nature of changes observed in tso1 mutants, we propose explanations for the differences in phenotypes among the tso1 alleles. We also describe the relation of the TSO1 protein to other proteins in plants and animals, and discuss possible roles for this protein in cell growth and division. 2219 Development 127, 2219-2226 (2000) Printed in Great Britain © The Company of Biologists Limited 2000 DEV0287

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