Agriculture Reference
In-Depth Information
with a cellulose biosynthesis inhibitor led to the formation of thickened cell plates
with increased callose and increased plasmodesmal density (Vaughn
et al.
, 1996).
Secondary plasmodesmata are formed post-cytokinetically in existing cell walls
(Jones, 1976; Lucas
et al.
, 1993; Ehlers & Kollmann, 2001). Secondary plasmod-
esmata can form along any wall of the cell, allowing cells to increase their potential
for molecular trafficking, and also to create connections between cells that are not
cytokinetically related (van der Schoot
et al.
, 1995; Ding & Lucas, 1996; Volk
et al.
, 1996; Itaya
et al.
, 1998; Oparka
et al.
, 1999; van der Schoot & Rinne, 1999).
Secondary plasmodesmata cannot be unambiguously distinguished from primary
plasmodesmata on the basis of structural criteria. Therefore, most models of sec-
ondary plasmodesmata formation are based on studies of plasmodesmata formed in
walls between cells that were initially separated (Ehlers & Kollman, 2001). Exam-
ples of such studies include the following: protoplast fusion in cell tissue culture
(Monzer, 1990; Ehlers & Kollmann, 1996); graft unions (Kollmann & Glockmann,
1985, 1991); host-parasite connections (Dorr, 1987; Dawson
et al.
, 1994); organs
fused post-genitally (carpel-fusion walls) (van der Schoot
et al.
, 1995); and the
genetically distinct cells of plant chimaeras (Steinberg & Kollmann, 1994).
Various models of the mechanism of secondary plasmodesmata formation have
been proposed (Jones, 1976; Juniper, 1977; Lucas & Gilbertson, 1994; Ding &
Lucas, 1996). The most favoured model is described by Jones (1976), in which it is
proposed that secondary plasmodesmata form by the endoplasmic reticulum becom-
ing adnated to the plasma membrane, together with locally restricted enzymatic wall
degradation. The wall thinning continues to a point where the plasma membrane and
endoplasmic reticulum of either cell can penetrate the existing cell wall from one
or both sides and subsequently fuse. This is followed by new wall deposition and
the branching of endoplasmic reticulum (described by Ehlers & Kollman, 2001). To
date, it is not known how the cell predicts the sites at which secondary plasmodes-
mata will form. Similarly, nothing is known concerning the process of synchronous
wall thinning, or how the formation of each 'half plasmodesma' is coordinated be-
tween the adjacent cells (Kollmann & Glockmann, 1999). The formation of primary
and secondary plasmodesmata has been reviewed in depth by Ehlers and Kollmann
(2001).
Both primary and secondary plasmodesmata are initially simple in structure, but
during tissue development may become complex, branched structures with a central
cavity. Plasmodesmata in the newly formed cell wall may undergo post-cytokinetic
structural modifications (Ehlers & Kollmann, 1996). During wall maturation, the
secondary wall is deposited on the inner face of the primary wall (Fry, 2001), and
further endoplasmic reticulum tubules, continuous with the desmotubule, may be-
come trapped. This process can give rise to the formation of elongated simple plas-
modesmata, or branched primary plasmodesmata (Kollmann & Glockmann, 1999).
Branching of secondary plasmodesmata is also encompassed in the Jones model
(Jones, 1976). As with primary plasmodesmata, endoplasmic reticulum tubules, con-
tinuous with the desmotubule, may become gradually embedded by Golgi-derived
wall material as the cell wall is built up in the thinned areas where the secondary
