308 Z. Hong · D.P.S. Verma
sion may require the expression of a new set of proteins because this process
is highly amplified during cell plate formation. The entire exocytosis machin-
ery appears to be engaged in generating a population of homotypic vesicles
during the early cell plate formation while both homotypic and heterotypic
vesicles are produced as the cell plate matures.
3.1
Cell Plate Vesicles
Cell plate vesicles originating from the Golgi apparatus fuse in a unique
manner at the center of the phragmoplast, giving rise to the new plasma
membranes of the two daughter cells (Fig. 3). They carry cargo for the forma-
tion of the cell plate matrix (Gunning and Wick 1985; Hepler and Bonsignore
1990; Staehelin and Moore 1995). Disassembly of the Golgi apparatus by
treatment with brefeldin-A (BFA) blocks the completion of cytokinesis by
shutting off the supply of cell plate vesicles (Yasuhara et al. 1995; Staehelin
and Moore 1995; Satiat-Jeunemaitre et al. 1996). However, initiation of cell
Fig. 3A proposed model for cell plate formation. The Golgi-derived vesicles carrying cal-
lose synthase, phragmoplastin (Phr) and other associated proteins are transported along
the microtubules. Once they reach the equatorial plane of the future cell plate, they are
squeezed by phragmoplastin into tubular structures, which fuse with each other in an
end-to-end fashion, creating a tubular fence (vesiculo-tubular network or VTN). The
conversion of the round-shaped vesicles into tubular structures is a fundamental and
essential step in de novo membrane formation, and avoids ballooning of the fused mem-
brane structures. The fusion brought about by KNOLLE syntaxin (Kn) is followed by
activation of callose synthase. The callose synthesized dilates these tubules and closes the
gaps, forming a flat sheet at the forming cell plate. Phragmoplastin may be removed once
the callose synthase is activated