The SEL of plasmodesmata is clearly highly regulated at both a tissue and developmental level, and a number of mechanisms have been proposed to be involved. Plasmodesmata may be considered to have two potential functional states: closed or open (Lucas et al. 1993; Schulz 1999; Zambryski and Crawford 2000). Closed plasmodesmata are characterised by a lack of all intercellular exchange (Zambryski and Crawford 2000), but since this has often been determined using lower molecular weight fluorescent probes (340 Da) it has not been possible to prove that they are "watertight" (Schulz 1999). Closure of plasmodesmata may be temporary or more permanent, involving the breakdown and removal of plasmodesmata from the cell wall (Duckett et al. 1994; Oparka et al. 1995; Palevitz and Hepler 1985). The deposition of callose within the neck region of plasmodesmata has been implicated in both the transient closure and also in the fine regulation of SEL (Lucas et al. 1993; Roberts and Oparka 2003; Ruan et al. 2004).
Another possibility for regulation of plasmodesmata is that the central ER-derived desmotubule functions as an actin-clad scaffold, which is linked to the plasma membrane by myosin molecules that span the space between the desmotubule and the plasma membrane. In this model, myosin may provide a contractile mechanism for closing the pore aperture, in a similar way to which myosin VIII constricts microvilli in mammalian cells (Baluska et al. 2004; Oparka 2004). Myosin VIII has been detected within plasmodesmata, and it has been suggested that the spokes that radiate from the desmotubule to the plasma membrane may be myosin molecules (Overall and Blackman 1996). Myosin VIII has also been implicated as a structural support of the cortical ER elements tightly underlying the plasma membrane both outside and within plasmodesmata (Volkmann et al. 2003).
Calreticulin is a highly conserved calcium sequestering protein that resides in the ER lumen and is the first ER-resident protein to have been localised within plasmodesmata (Baluska et al. 1999, 2001). It may be involved in regulating plasmodesmatal transport in association with centrin, a calcium-binding contractile protein, localised to the neck region of plasmodesmata (Blackman et al. 1999). An increase in the concentration of cytoplasmic calcium causes a decrease in the phosphorylation of this protein, causing the centrin nanofilaments to contract (Martindale and Salisbury 1990; Black-man et al. 1999). In support of this model, increased levels of calcium have been shown to lead to plasmodesmal closure (Erwee and Goodwin 1983; Tucker 1990; Holdaway-Clarke et al. 2000), and two protein kinases, one calcium-dependent, have been localised to plant cell walls or plasmodesmata (Citovsky and Zambryski 1993; Yahalom et al. 1998).
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