One of the early changes upon tuber induction is the switch from apoplastic to symplastic unloading. Whether and how this change in unloading mode contributes to sink strength has remained unclear. In addition, developing tubers also change from energy to storage-based sucrose metabolism. Here, we investigated the coordination between changes in unloading mode and sucrose metabolism and their relative role in tuber sink strength by looking into callose and sucrose metabolism gene expression combined with a model of apoplastic and symplastic unloading. Gene expression analysis suggests that callose deposition in tubers is decreased by lower callose synthase expression. Furthermore, changes in callose and sucrose metabolism are strongly correlated, indicating a well-coordinated developmental switch. Modelling indicates that symplastic unloading is not the most efficient unloading mode per se. Instead, it is the concurrent metabolic switch that provides the physiological conditions necessary to potentiate symplastic transport and thereby enhance tuber sink strength .

The cellulose-biosynthesis inhibitor (CBI) herbicides all selectively inhibit the synthesis of cellulose despite significant chemical differences. With the exception of quinclorac, they are most effective in inhibiting cellulose synthesis in dicot plants. Dichlobenil and isoxaben are the oldest and best studied of these herbicides, whereas flupoxam is a more recent introduction and acts in many ways similarly to isoxaben. Quinclorac is unusual in that it seems to act as a cellulose inhibitor in grasses but as an auxinic herbicide in dicots. These herbicides inhibit cell plate formation at one of two relatively late stages without affecting microtubule function. The effects of dichlobenil are different from other CBI herbicides; dichlobenil inhibits cellulose synthesis but promotes callose synthesis in its place. Suspension cells of both Lycopersicon esculentum and Nicotiana tabacum can become habituated to normally inhibitory concentrations of dichlobenil or isoxaben by replacing the normal cellulose network in their walls with pectin and extensin. Natural resistance to CBI herbicides is rare and has only been found in red algae species. Arabidopsis lines produced by mutagenesis all share changes in active site rather than alterations in uptake, translocation, or metabolism of these herbicides. The lack of cross-resistance to different CBI herbicides of these mutants indicates that no fewer than three different sites in the cellulose biosynthesis pathway are affected by the different herbicides in this class.

Except for a small number of cases in which biocontrol agents were introduced from the site of origin of a weed (classical biocontrol), there have been few cases where a pathogen was virulent enough to perform cost effectively in the field as a mycoherbicide. Mycoherbicides are typically weed species specific, so compatibility with herbicides used to control other weeds is often studied. There can be a synergy between mycoherbicides and herbicides at the field level due to overlapping weed spectra (such synergies are not discussed in depth herein). Two approaches have been used to ascertain whether there is synergy in controlling the target weed: (1) random screening with herbicides; (2) using herbicides as antimetabolites to inhibit specific pathways, enhancing virulence. Glyphosate is the most common herbicide to synergize mycoherbicides, possibly due to its dual function as an inhibitor of biosynthesis of phenylpropanoid phytoalexins by suppressing enolphosphate-shikimate phosphate synthase, or by suppressing callose production (by inhibiting callose synthase) as well as inhibiting other calcium-dependent pathways due to the calcium-chelating properties of glyphosate.

The interaction between the race 1 of the cowpea rust fungus (Uromyces vignae Barclay) and the resistant cowpea (Vigna unguiculata (L.) Walp.) cv. Queen Anne is characterized by the deposition of callose around intracellular fungal structures. Ultrastructural examination of the early stages of infection by basidiospores of the fungus revealed two types of deposits induced by intracellular hyphae: a non-callose collar at the penetration site and a callose encasement around the invasion hypha. The callose encasement was developed from the site where the fungus encountered the inside of the plant cell wall and was separated from the fungus by the extrahyphal membrane and an extension of plant plasma membrane. The incidence of encasements was reduced in plants treated with inhibitors of transcription (actinomycin D), protein synthesis (cycloheximide), protein glycosylation (tunicamycin) and microfilament polymerization (cytochalasin E). Inhibitors of Golgi-associated vesicle transfer (monensin, brefeldin A) and anti-microtubule agents (colchicine, oryzalin) had no effect. When the fungus was killed by heat treatment in either the resistant or the susceptible cultivar, callose was deposited at various locations along the fungus, mostly in the extrahyphal matrix. The data suggest that unlike the extrahaustorial membrane surrounding D-haustoria of this fungus, the extrahyphal membrane is capable of generating callose. Since this process does not normally occur in the susceptible or the resistant cv. even when callose is deposited in the latter by regions of the plasma membrane not associated with the fungus, we conclude that the deposition of callose by the extrahyphal membrane is inhibited by the living fungus.