By definition, secondary plasmodesmata are formed de novo across existing cell walls (Ehlers and Kollmann 2001). They cannot be distinguished from primary plasmodesmata on the basis solely of their structure, since they also may display simple or branched architectures (Ding et al. 1992b), and therefore can only be identified unambiguously by their location. At the time of their formation some secondary plasmodesmata, like primary plasmodes-mata, have a simple structure that may subsequently be modified. However, other secondary plasmodesmata are branched when formed, and ultimately the majority of secondary plasmodesmata are modified to have a branched morphology (Lucas et al. 1993).
Although secondary plasmodesmata are formed during normal plant development (Jones 1976; Robards and Lucas 1990; Lucas et al. 1993; Ding et al. 1999; Kollmann and Glockmann 1999), detailed studies in a number of systems, including protoplast fusion, graft unions, plant chimeras and parasite-host interactions, have provided evidence for the de novo formation of plasmodesmata across cell types from different developmental origins. In all cases, the ER plays a central role in the formation of these secondary plasmodesmata (for reviews, see Jones 1976; Robards and Lucas 1990; Lucas et al. 1993; Kollmann and Glockmann 1999; Ehlers and Kollmann 2001).
As the outer cell walls of protoplast-derived cultured cells regenerate, half, branched plasmodesmata form by a passive entrapment mechanism resem bling primary plasmodesmata formation (Monzer 1990, 1991; Ehlers and Kollmann 1996). Cytoplasmic ER cisternae become closely associated with the plasma membrane and, along with the enclosing cytoplasmic strands, are trapped by Golgi-derived vesicles carrying cell wall material and fusing with the plasma membrane (Monzer 1990, 1991). The resulting half plasmodesmata, known as "outer-wall plasmodesmata" (Ehlers and Kollmann 1996), are scattered over the cell surface and when cultured cells come into intimate contact, opposite half plasmodesmata may fuse to form continuous, usually branched, plasmodesmata that connect the two cells (Monzer 1990, 1991; Ehlers and Kollmann 1996).
Heterografts of plants with species-specific subcellular markers have been used to identify the mechanism of formation of interspecific secondary plasmodesmata (Jeffree and Yeoman 1983; Kollmann and Glockmann 1985, 1991, 1999; Kollmann et al. 1985). This process involves the local thinning and loosening of the fusion walls between the cells of the graft partners followed by fusion of the plasma membranes which are associated with ER cisternae (Fig. 3d). Once again, during reconstruction of the modified wall parts, cytoplasm and ER cisternae become entrapped on either side of the graft interface (Fig. 3e). Although the resulting interspecific continuous secondary plasmodesmata may be simple strands, they are usually of a complex branched morphology with dilated central cavities in the median fusion plane. An exchange of information signals appears to be involved in this mechanism (Jeffree and Yeoman 1983; Kollmann and Glockmann 1991,1999), and it has been shown that lack of cooperation between cell partners results in the formation of mismatching half plasmodesmata at graft interfaces of incompatible heterografts, between different cell types and between cells at different stages of differentiation (Kollmann et al. 1985).
Although not investigated in detail, it appears that the mechanism of formation of secondary plasmodesmata within chimeras and at host/parasite interfaces is essentially similar to that occurring at graft interfaces (for reviews, see Jones 1976; Robards and Lucas 1990; Lucas et al. 1993; Kollmann and Glockmann 1999; Ehlers and Kollmann 2001). Indeed, it is likely that a common mechanism is involved in the establishment and modification of primary plasmodesmata, as well as the de novo formation and modification of secondary plasmodesmata (Kollmann and Glockmann 1991, 1999; Kragler et al. 1998; Ehlers and Kollmann 1996, 2001).
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