PPB is a ring-shaped cortical microtubular structure first discovered by Pickett-Heaps and Northcote (1966) though electron microscopy, which is laid down before mitosis, girdling the cell where the cell plate will fuse with the parental cell walls. They found PPB in both root tips and developing stomata in symmetrical and asymmetrical divisions. Subsequent work has shown that such kind of microtubule array occurs in a wide range of cell types in many species, even in moss (Gunning, 1982; Doonan et al., 1987). Although the PPB disappears as the mitotic spindle is established, the memory of its placement is retained, and at cytokinesis the new cell plate is guided to fuse with the parent cell walls along the line delineated previously by PPB. Thus, the PPB can be regarded as an indication of the commitment of a cell to divide in a particular location and orientation. Nevertheless, several types of cell division are known in absence of the PPB: one is the division of the unorganized cells, like callus and endosperm cells Gunning, 1992); another is the division of protoplasts (Wick, 1991); division of filamentous cells of moss also lacks the PPB, but arises at the time of leafy shoot formation (Doonan et al., 1987). The correlation between the lack of morphogenetic order and the lack of PPB suggest that PPB may involve in the morphogenesis through the determination of the position of cell plates. Nevertheless, a recent observation reveals that PPB may not be essential for morphogenesis: a mutant in Arabidopsis which lacks PPB can still initiate morphogenesis although the morphologies of the organs have been altered greatly (Traas et al., 1995). Another possible function of the PPB is to guide the cell plate fusion with parental walls. This assumption comes from an observation that cells with incomplete cell walls lack PPB (Sack and Paolillo, 1985). Funaria stomate is a single cell with two nuclei, in which cytokinesis can initiate but never complete. Attempts to find a PPB in these cells were failed (Sack and Paolillo, 1985).
There are two major events in plant cytokinesis: phragmoplast formation and vesicle trafficking. Formation of a phragmoplast, which is parallel aligned microtubules and microfilaments at right angles to the forming cell plate, is to generate a guiding and supporting matrix for the deposition of new cell plate. In addition, plant cell plate formation also comprises a complex series of vesicle trafficking events, which entail the production, ordered aggregation and fusion of membranous vesicles derived from Golgi bodies (Gunning, 1982 and Staehelin et al, 1991). The row materials for constructing the new cell wall are synthesed in Golgi complex, and packaged into small vesicles, and then transport to the interzone of the phragmoplast, with the help of microtubules and microfilaments (Fig. 4). Formation of the cell plate, with the fusion of these vesicles, starts from the middle of the phragmoplast and expanded radially until finally fused with parental walls. As a result, the membranes of these vesicles make up the new plasma membrane at the new cell surface and the content of the vesicles gives rise the amorphous matrix of the new wall. Only the cellulose and callose of the cell wall components are synthesised on the cytoplasm membrane (Staehelin et al, 1991).
The translocation of macromolecules in membrane-bounded vesicles is a fundamental process of all eukaryotic cells. This vesicle trafficking requires guidance systems as well as recognition and sorting mechanisms to ensure that vesicles and their molecular cargoes arriving at the right destinations at the right time. A remarkable convergence of two approaches, the genetic dissection of the yeast secretory pathway and the biochemical characterization of the vesicle membrane protein in mammalian nerve termini, suggests that a common mechanism may underlie in a wide variety of vesicle-mediated transport steps. (Kaiser and Schekman, 1990; Bennett & Scheller, 1993 and Söllner et al, 1993). It is of interest to know whether there is a similar machinery in plants to ensure precise vesicle trafficking and fusion with target membrane at the time of cell plate formation.
There is no doubt that a lot genes are involved in cytokinesis. To find such genes, we need mutants which can then be used to carry out molecular studies. The first plant cytokinesis-defective mutant was found few years ago in pea (Liu et al, 1996). In this page, you will see some pictures of this mutant.
The pictures above show how the cytokinesis-defective embryo and seeds look like. The one at the top-left is a wild-type pea embryo, and the one
at the top-right is a homozygous cyd mutant embryo. The picture at the bottom shows an opened pea pod
from a heterozygous plant. The segragation of this gene produces 25% embryo-lethal seeds and 75% wildtypes.
These two red arrowheads indicate the seeds containing mutant
embryos, in comtrast to the rests containing wild-type embryos.
Click each picture to view
