Cellulose biosynthesis inhibitors

The cellulose biosynthesis inhibitors (CBIs) are a small group of chemically unrelated compounds including the herbicides dichlobenil, isoxaben and flupoxam (Figure 11.1). They are all effective CBIs, and because this site of action is not shared with mammals, they may be ideal choices for the purposes of registration and selective herbicidal activity. A lack of observed resistance in the field may enable them to become useful agents in the control of resistant weeds. Furthermore, they have become valuable probes in our understanding of cellulose biosynthesis and cell wall formation in plants.

Cellulose is an integral part of the plant cell wall and hence cellulose synthesis is vital in order for the cell wall to be synthesised. The cell wall determines to some extent both the morphology and the function of a cell, but even more importantly it controls the degree to which a cell can expand. It is suggested that if cellulose biosynthesis is inhibited then weakened cell walls will result, causing expansion of the cell and disruption of cellular processes. This in turn leads to abnormal or restricted growth and subsequent plant death. As most CBIs are used pre-emergence then seedling growth is inhibited. Post-emergence use of CBIs leads to stunted growth and swollen roots in treated plants.

It appears that CBIs do not have a common site of action in the synthesis of cellulose, which is a process carried out by multi-enzyme complexes situated at the cell's plasma

*Cl dichlobenil

*Cl dichlobenil

.OCH3 O

isoxaben isoxaben

CH2CH3

CHCH3

CH2CH3

H3C.

N N xNH2 H

Figure 11.1 Chemical structures of the four major cellulose biosynthesis inhibitor herbicides.

CONH2

CONH2

Cl CF2CF3

flupoxam

N N xNH2 H

triaziflam (pre- and post-emergence in turfgrass)

Figure 11.1 Chemical structures of the four major cellulose biosynthesis inhibitor herbicides.

membrane. Research to date has identified at least two separate points at which CBIs inhibit. Dichlobenil analogues have been shown to bind to an 18-kDa polypeptide associated with the multi-enzyme complex. It is postulated that this may be a regulator subunit associated with cellulose synthase, as it appears to be too small to be the enzyme itself. Reported effects of dichlobenil treatment include synthesis of callose in place of cellulose. Callose is a P-1, 3 glucan, often formed in plants as a wounding response. It is not usually present in the cell walls of undamaged cells. It is postulated that dichlobenil inhibits the incorporation of UDP-glucose into cellulose and this is therefore shunted into callose (and xyloglucan) synthesis. Isoxaben has been demonstrated to inhibit the incorporation of 14C-labelled glucose into the cell wall. Other studies have revealed that the synthesis of both cellulose and callose is reduced by this herbicide. This suggests an inhibition of cellulose synthesis at an earlier stage than dichlobenil, preventing incorporation of glucose into both cellulose and callose. It has been postulated that the step where isoxaben acts may be at the point where UDP glucose is formed from sucrose. Flupoxam appears to inhibit at a similar point, although less information on this herbicide's mode of action is available. Quinclorac, an auxin-type herbicide for broad-leaf weed control, also appears to inhibit cellulose biosynthesis in susceptible grasses, although the mechanism by which

Figure 11.2 5-fert-butyl-carbamoyloxy-3-(3-trifluoromethyl) phenyl-4-thiazolidonone (Compound 1).

Figure 11.2 5-fert-butyl-carbamoyloxy-3-(3-trifluoromethyl) phenyl-4-thiazolidonone (Compound 1).

it accomplishes this has yet to be deduced. This implies that quinclorac has a second site of action in monocots, unrelated to its primary mechanism in dicots (Koo et al., 1997). A new herbicide, 5-tert-butyl-carbamoyloxy-3-(3-trifluoromethyl)-phenyl-4-thiazolidinone (Figure 11.2), also appears to inhibit cellulose biosynthesis at the same place as isoxaben (Sharples et al.,1998).

This is a representative of a novel class of N- phenyl - lactam - carbamate herbicides patented by Syngenta in 1994. It shows potential for the pre-emergence control of a range of grass weeds (including Setaria viridis, Echinochloa crus-galli and Sorghum halepense) and small seeded broad-leaf weeds (including Amaranthus retroflexus and Chenopodium album) in soybean, at an application rate of approximately 125-250 g ha-1. Root growth was completely inhibited at 2 ||M and visual symptoms typically included stunted and swollen roots, with no lateral branches. It was shown by Sharples et al. (1998) to be a potent inhibitor (IC5 0 of 50 |M) of the incorporation of 3H-labelled glucose into the acid-insoluble polysaccharide cell wall fraction of Zea mays roots - which is assumed to be cellulose. Similar inhibition was observed by isoxaben and dichlobenil, and cross-resistance was demonstrated to an isoxaben-resistant Arabidopsis mutant (Ixr1-1) which implies a shared molecular binding site with isoxaben. These authors conclude that the final identification of this site will require a combination of molecular approaches and traditional biochemistry.

The formation of cell plates in the presence and absence of CBIs has received detailed scrutiny in both light and electron microscope studies. Cell plates are the cell walls formed to separate daughter nuclei after cell division. In the presence of dichlobenil, cell plates develop more undulated and thicker regions than in untreated tissues, resulting in cell walls that are incomplete or attached to only one existing cell wall. Treated cell walls also are enriched in callose compared with controls. This may imply that the inhibition of cellulose biosynthesis has increased the amount of UDP- glucose available for callose or xyloglucan synthesis. Conversely, treatment with either isoxaben or flupoxam results in the production of a thin cell plate, with no callose nor xyloglucan enrichment.

Another useful experimental system for the study of CBIs (Vaughn, 2002) is the developing cotton fibre, whose secondary wall is composed almost exclusively of cellulose. Fibre development is severely inhibited by the CBIs. The cell wall of control fibres consists of two layers, an outer wall area enriched in pectin and an inner layer enriched in cellulose-xyloglucan. After treatment with diclobenil, the inner layer became enriched in callose and cellulose was absent. On the other hand, treatment with isoxaben and flupoxam generated relatively more outer wall, highly enriched in de-esterified pectin.

3n summary, dichlobenil appears to divert cellulose biosynthesis into callose, while isoxaben and flupoxam inhibit the production of both cellulose and callose in both cell plates and cotton fibres. The further identification of the enzymes involved in the presence of CBIs is awaited with interest.

The most recently discovered cellulose biosynthesis inhibitors, flupoxam and triazi-flam, are active at much lower rates (100-250 gha" than their predecessors, such as dichlobenil (3,000 gha-1). This may open up the possibility of more imitative chemistry in future to lower the dosage used in this herbicide class. According to Grossman and colleagues (2001), triaziflam may also affect photosynthetic electron transport and micro-tubule formation. This multiple activity may be a positive feature and may delay the onset of herbicide-resistant weeds.

The relationship between cellulose microfibrils and cortical microtubules has long been debated. Paradez and colleagues (2006) have fluorescently labelled cellulose synthases that assemble into functional cellulose synthase complexes in Arabidopsis hypocotyl cells. They have demonstrated that the cellulose synthase complexes move in the plasma membrane along tracks that appear to be defined by co-labelled microtubules. It appears that the force for the movement of the cellulose synthase complex is derived from cellulose microfibril production itself. According to Emons et al. (2007), this breakthrough discovery provides the experimental tools that may allow us to answer the following questions:

• How do the cellulose synthase complexes enter the plasma membrane, via exocytosis?

• Where are they inserted into the plasma membrane?

• How are they activated, for how long and how are they regulated?

• Which gene products influence microfibril production?

• How does the network of molecules involved in cellulose production function?

Note that in these studies oryzalin was added to depolymerise the cortical microtubules, showing the value of this herbicide as a tool in unravelling this complex process.

Was this article helpful?

0 0
Brand Spanking New Detoxify

Brand Spanking New Detoxify

How To Safely Detoxify Your Body And Revitalize. Here's A Step-By-Step Plan To GetA Proper Mindset, Get Positive,And Most Of All... Find Your Special, Customized Detox Plan.

Get My Free Ebook


Post a comment