Dutch Elm Disease | Cycle | Elm | Host respons to DED HOST RESPONSE TO DED Index document Barrier zones (wall 4)

    Gels and tyloses (wall 1)

    Vascular occlusion and a subsequent limitation of the upward movement of O. ulmi s.l. may result from embolism (i.e., entry of air into the vessels), accumulation of fungal hyphae, and the formation of gels (gums) and tyloses in the xylem vessels and the tracheids {[230],[681],[692],[696]}. Gels (gums) are vascular plugs with a fibrillose structure formed by material secreted from adjacent xylem parenchyma through membranes of half-bordered pit pairs. Although the precise chemical composition is not yet known, pectin, hemicellulose, and phenolics appear to be basic components of gels {[237],[681],[692]}. Tyloses are outgrowths of the parenchyma contact cells surrounding the xylem vessels that protrude through the pit cavities into the vessel's lumen (Photo 8 and 9, {[684],[ 798]}).

    The nucleus of the parenchyma cell migrates into the tylose. After tylose formation, the reacting parenchyma cell remains in continuous contact with its protrusion {[692]}. Tyloses (and gels) are sporadically found in fibers {[237]}. Besides in response to pathogen infection, tyloses can be formed after injury or in aging elm vessels that become non-functional {[685],[686],[687],[688],[689],[690],[691],[692]}.

    The partial or complete embolism usually detected during these processes is thought to give rise to a massive increase in xylem water potential {[254]}. Subsequently, the contact cells adjoining the vessels absorb water until the elasticity of their cell walls prevents any further swelling. Contact cells form a protective layer containing pectic polysaccharides after completion of the secondary cell wall {[254],[ 237]}. This layer is situated either unilaterally against the paratracheal cell wall or along the whole cell wall with a thickened deposit on the vessel side {[693]}. Although pit membranes of contact cells lack a secondary cell wall, they are covered by the protective layer. Once the pressure built up by the excessive water uptake has exceeded a certain limit, the protective layer is no longer able to contain the osmotic pressure of the contact parenchyma cells. As a consequence, these cells bulge through the pit cavities into the xylem vessels to form tyloses {[254]}.


    Photo 8:  Tyloses in a xylem vessel of an elm infected with O. ulmi s.l.

     
    Photo 9:
      Scanning electron microscopic photograph of tyloses in a elm xylem vessel.

    Embolism inducing a change in water potential may be the main cause triggering the formation of vessel occlusions {[254],[696],[703]}. In the latter case, the xylem becomes non-functional before any other form of plugging becomes evident {[696]}. Tylosis formation may preserve the tissue pressure by turning the embolized-vessel gas space into incompressible parenchyma {[703]}. Recently, Shen et al. {[712],[713]} observed seasonal and diurnal variations of xylem embolism in U. pumila. There appears to be an inverse relationship between water potential and xylem embolism; the lower the water potential, the higher the xylem embolism.

    Rioux et al.{[83]} analyzed the well-developed cell wall composition of tyloses in DED-infected U. americana. The primary wall of the tylose was shown to contain cellulose and a small amount of pectin. The flexibility of this wall permits expansion of the tylose. Increased esterification of the primary wall after tylosis maturation might improve resistance to attack by fungal pectinases. Secondary wall formation was rarely detected in tyloses of the American elm. However, a suberized layer was formed against the primary wall layer (or internal to the secondary layer, when present) in tyloses that had completed their expansion {[83]}. Suberin is a protective coating, consisting of long chain fatty acids, hydroxylated fatty acids, long-chain alcohols, and phenolics (primarily ferulic acid). The phenolics are thought to bind the lipid fraction of the suberin (up to half of the total suberin) to the cell wall {[695]}. Suberized tyloses are randomly formed in U. americana {[699]}. Occasionally, the internal suberized layer appears to be covered with an additional layer containing (1(4)-D-glucans {[83]}.

    The formation of such defense-related compounds as suberin, lignin, and a number of phytoalexins is catalyzed by phenyl ammonia lyase (PAL), the key enzyme of the phenylpropanoid pathway. There is conflicting evidence concerning a possible correlation between DED resistance and a rapid, transient increase in PAL activity {[194],[495]}. Besides PAL, elms have been reported to synthesize several enzymes potentially involved in signal transduction pathways {[194],[243]}.

    Secretion of pectin occurs during the formation of gels (gums) and tyloses in American elm. In continuation with the protective layer, the primary cell wall of expanding tyloses secretes pectin microfibrils into the vessel elements. The material appears to be pushed towards areas that cannot be clogged completely by the tylosis primary wall, such as chambers of bordered and half-bordered pits, void spaces left between the tylose and the vessel wall, the vicinity of the rim of vessel perforation plates, and in vessel areas where the curving angle of the secondary wall is very pronounced. In places where the tylosis primary wall exhibits close contact with the xylem vessel wall, the pectic layer is very thin and hardly discernible {[699]}. Besides a complete blockage of the vessel elements, the secreted pectin may promote cohesion of the tylosis wall to other structures {[237]}.

    Recent experiments by Rioux et al. {[237]} showed the vascular blockage by gels and tyloses in U. americana around 4 to 6 days post-inoculation at 2 to 3 mm from the inoculation wound. Elgersma {[594]} observed vascular occlusions as early as two days after DED infection. At 3 to 5 days post-inoculation the number of vessels showing tyloses appears to be significantly higher in resistant elms compared to susceptible trees {[697]}. The rate of tylosis formation exhibited by a particular elm appears to be independent of the fungal pathogen used to infect the tree. The DED-susceptible U. hollandica "Belgica" and the resistant U. hollandica clone 390 exhibit no difference in the rapidity of tylosis formation after infection with either the aggressive O. novo-ulmi, the non-aggressive O. ulmi, or Fusarium oxysporum f.sp. lycopersici {[698]}. The latter fungus is not pathogenic to elms.

    In general, tylosis formation does not seem to be involved in early host-response to DED infection. However, occlusion of vessels by tyloses and gels may support the accumulation of phytoalexins {[694]}.

HOST RESPONSE TO DED HOST RESPONSE TO DED Barrier zones (wall 4) Barrier zones (wall 4)