Structural aspects of ectomycorrhiza of Pinus pinaster (Ait.) Sol. formed by an IAA-overproducer mutant of Hebeloma cylindrosporum Romagnési

Authors

  • L. GEA,

    Corresponding author
    1. Laboratoire de Pathologic Végétale INA P-G, 16, Rue Claude Bernard, 75231 Paris Cedex 05 France
    2. Université Pierre et Marie Curie, Physiologie du Développement du Plantes {Tour 53), 4, Place Jussieu, 75252 Paris Cedex 05 France
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  • L. NORMAND,

    1. Université Claude Bernard Lyon 1, Unité d'Ecologie Microbienne du Sol associée au CNRS (Ba̧t. 405), 43, Boulevard du 11 Novembre 1918, 69622 Villeurbanne Cedex France
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  • B. VIAN,

    1. Laboratoire de Pathologic Végétale INA P-G, 16, Rue Claude Bernard, 75231 Paris Cedex 05 France
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  • G. GAY

    1. Université Claude Bernard Lyon 1, Unité d'Ecologie Microbienne du Sol associée au CNRS (Ba̧t. 405), 43, Boulevard du 11 Novembre 1918, 69622 Villeurbanne Cedex France
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*To whom correspondence should be sent, at address (1).

summary

Mycorrhizas formed on Prinus pinaster by an IAA-overproducer mutant strain (h1 FIR 4 h1 F1 331) of Hebeloma cylindrosporum are described. The wild strain (hl) was used as reference. The wild type mycorrhiza had a thin mantle and a uniseriate Hartig net, which reached the second layer of cortical cells, as generally described. Conversely, the mutant type mycorrhiza had special features; a large mantle and a highly developed Hartig net (up en seven layers of hyphae in width) which reached the endodermis. Even when the Hartig net was formed of several layers of hyphae, the cortical cells remained alive, indicating that the fungus may aid survival of the host cells. Intracellular hyphae surrounded by invaginated host plasmalemma and by interfacial material, were frequently seen in cortical cells, In this case, both fungal and host cells were alive. Even if the mutant strain is more invasive, the IAA overproduction dries not seem to modify its symbiotic status. It is possible that IAA plays a role in cell wall loosening, allowing the fungus to overcome barriers which normally prevent the invasion of living cortical cells.

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