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Cytological Observations of the Infection Process by Phomopsis helianthi (Munt.‐Cvet) in Leaves of Sunflower
Author(s) -
Heller A.,
Gierth K.
Publication year - 2001
Publication title -
journal of phytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.53
H-Index - 60
eISSN - 1439-0434
pISSN - 0931-1785
DOI - 10.1046/j.1439-0434.2001.00635.x
Subject(s) - vascular bundle , biology , phloem , vascular tissue , cell wall , chloroplast , hypha , parenchyma , cytoplasm , apoplast , ultrastructure , plasmodesma , botany , electron microscope , biophysics , microbiology and biotechnology , biochemistry , optics , gene , physics
The infection process of Phomopsis helianthi and the specific degradation of infected tissue were studied in detail using light and transmission electron microscopy. In comparison with other vascular pathogens, the infection and degradation process was in some aspects different. The favourite tissue for the pathogen to grow in was the phloem. Parenchymatic cells in and around vascular bundles were extremely sensitive to infection long before hyphae arrived, probably due to a toxin. In the parenchymatic cells the first changes were visible at the chloroplasts where electron‐dense material accumulated in the thylakoid space. The chloroplast stroma changed contrast and later the whole cytoplasm also appeared electron dense. In the vascular bundles, first the phloem was destroyed and then hyphae invaded the adjacent mesophyll, the cambium, and finally the vessel elements. In particular, the compact mesophyll of the midvein was severely affected. Vessel elements were lined with electron‐dense material and some were filled with flocculent material. Severe wall destruction indicated the action of a complete set of cell wall‐degrading enzymes before hyphae entered the tissue; it always started at the innermost wall layer. Wall degradation in vascular tissue and adjacent parenchyma with intercellular spaces was different. Before the degradation of the protoplasts started, the cell walls were completely metabolized and only the secondary walls of the vessels resisted for longer. There were no host–cell reactions visible that could be interpreted as a defence reaction.