AbstractA histological study of several vascular wilt diseases (tomato infected with Fusarium oxysporum f.sp. lycopersici or Verticillium albo-atrum and pea infected with Fusarium oxysporum f.sp. pisi was made by light and electron microscopy in an attempt to elucidate mechanisms of resistance and induction of water stress. There were extensive similarities in invasion by all pathogens of root epidermis and cortex in resistant and susceptible cvs. Hyphae of tomato pathogens often adhered to root cell walls of cvs but remained separated by extracellular electron-opaque material. Hyphae of F. oxysporum f.sp. pisi on roots of both pea cvs were embedded in a mucilaginous sheath. Both forms of adhesion were associated with a localised disruption of adjacent host wall structure. Initial penetration was by intercellular hyphae; subsequent intercellular colonisation often elicited the formation of wall appositions and papillae within epidermal and cortical cells. Penetration of host walls was achieved by constricted hyphae which formed small "bore holes". Extensive wall degradation was uncommon but did occur at high inoculum concentrations. Continued deposition of material around penetrating hyphae often resulted in penetration papillae (syn. lignitubers) from which hyphae were never seen to emerge. The only differential expression of varietal resistance detected in pea and tomato roots occurred at the endodermis. Accumulation of electron-opaque material in tomato endodermal cells and deposition of suberin and autofluorescent material in pea appeared to limit colonisation of the stele. However, pathogens entered xylem vessels via unlignified immature xylem elements at root tips (devoid of mature endodermis) rather than by direct penetration from mature regions of the root. During colonisation of xylem vessels hyphae were normally in close proximity to vessel walls. Lateral growth occurred via inter-tracheary pits in tomato but this was never observed in pea. Extensive erosion of vessel secondary walls occurred in resistant and susceptible tomato cvs. In contrast, secondary walls in infected pea were largely unaltered but there was extensive swelling and degradation of the primary wall of pit fields in susceptible plants. Xylem parenchyma cells underwent various changes in infected susceptible plants which included necrosis, formation of protective layers, hyperplasia and deposition of electron-opaque material with- in cell walls. The possible effects of these alterations on water absorption are discussed. Tylosis was a common response to infection in resistant tomato cvs and was accompanied by the accumulation of electron-opaque material in vacuoles of xylem parenchyma cells. Tylosis was not observed in pea but a corresponding reaction was the occlusion of vessels by gels; gel formation was also induced by wounding. The origins and involvement of tyloses, gels and vessel lining material in resistance and induction of water stress are considered. Non-host resistance of tomato was also examined.
|Date of Award||1980|
Ultrastructure of vascular wilt diseases.
Bishop, C. D. (Author). 1980
Student thesis: Doctoral Thesis › PhD