Agriculture Reference
In-Depth Information
(Radford & White, 1998; Samaj
et al.
, 2000). The activity of ATPase, which is also
found in the neck region together with calcium-binding sites, has been shown to de-
crease with the addition of a calcium-chelating agent (Belitser
et al.
, 1982). Roberts
and Oparka (2003) note that calreticulin, a calcium-sequestering protein shown to
be a component of the cortical endoplasmic reticulum (Baluska
et al.
, 1999, 2001),
could potentially be involved in aperture regulation at the neck by buffering calcium
levels.
5.3.5
'Coarse' regulation by callose
Callose (b -1,3-glucan) is known to be deposited at plasmodesmata during wounding
(Hughes & Gunning, 1980). Mechanical wounding of leaf tissue stimulates a rapid
deposition of callose at plasmodesmata (Currier, 1957; Schulz, 1999). However,
the rate of callose deposition and subsequent degradation varies depending on the
system studied (Overall & Blackman, 2001). Callose deposition at plasmodesmata
is thought to be a ubiquitous plant response to pathogen spread (Roberts & Oparka,
2003), and has been observed in the late phase of the hypersensitive response to TMV
infection (Susi, 2000). However, callose has also been detected in plasmodesmata
outside the visible necrotic lesions of plants infected with PVX, suggesting that it
may function as an early defence strategy against PVX (Allison & Shalla, 1974).
Callose has also been reported to inhibit the long-distance trafficking of viruses
(Leisner & Turgeon, 1993; Choi, 1999). Callose deposition has been found to block
plasmodesmata during infection by the oomycete
Phytophthora sojae
(Enkerli
et al.
,
1997), and fungal xylanase has been found to elicit a hypersensitive response in
tobacco associated with callose deposition (Bailey
et al.
, 1990). Interestingly, a low
concentration of Brefeldin A, a fungal agent produced by
Penicillium brefeldianum
,
which disrupts the endomembrane system in plants (Satiat-Jeunemaitre & Hawes,
1992a,b), triggers callose synthesis in onion epidermal cells (Kartusch
et al.
, 2000).
Callose deposition at plasmodesmata has also been shown in response to aluminium
toxicity (Jones
et al.
, 1998; Sivaguru
et al.
, 2000).
Olesen and Robards (1990) and Lucas
et al.
(1993) have proposed a model that
depicts the enzyme b -1,3-D-glucanase as an integral membrane protein that produces
b -1,3-glucan between the plasma membrane and the cell wall. The precise regula-
tion of b -1,3-glucan deposition is thought to regulate plasmodesmal SEL. Enhanced
callose deposition at plasmodesmata has been reported in mutant plants where the
activity of b -1,3-glucanase has been blocked, causing a reduction in SEL but not
absolute closure of plasmodesmata (Beffa
et al.
, 1996). Recently, three host proteins
(TIPs) that interact with the 12-kDa protein of the triple gene block of PVX, a protein
required for movement by PVX, have been identified (Fridborg
et al.
, 2003). All
three TIPs were found to interact with b -1,3-glucanase, suggesting that regulation
of b -1,3-glucanase activity by viral MPs might be a means by which some viruses
overcome host deposition of callose during infection (Iglesias & Meins, 2000).
In addition to wounding and pathogenesis, callose deposition is also implicated in
plugging of the neck region plasmodesmata, for example, by the formation of neck
