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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Microtubule cytoskeleton in hyphal growth. Response to nocodazole in a sensitive and a tolerant strain of the homobasidiomycete Schizophyllum commune.

In the wild-type strains of the homobasidiomycete Schizophyllum commune microtubules were totally depolymerized by low concentrations of nocodazole, while high concentrations of benomyl only modified the structure of microtubule cytoskeleton. In the nocodazole-tolerant mutant strain NT30 the microtubule cytoskeleton remained partly functional at a nocodazole concentration which demolished the microtubules in the wild-type strains. The continuation of apical growth for several hours in the wild-type strain without cytoplasmic microtubules indicated that microtubules are not the major elements in hyphal extension growth. However, the irregular branching of the treated apical cells both in the nocodazole-sensitive and -tolerant strain suggested that an intact microtubule cytoskeleton is needed for maintaining the direct extension of the leading hyphae at the colony edge. In the nocodazole-sensitive strain growth in the absence of polymerized microtubules frequently led to the death of the apical cells even when the drug was removed. In the tolerant strain the nuclear divisions continued in spite of nocodazole, but the uninucleate hyphal compartments became multinucleate. This probably resulted from poor segregation of nuclei and septation of hyphae at telophase, which indicated that these processes might be dependent on proper polymerization of cytoplasmic microtubules in higher fungi. The different electrophoretic mobility of the beta-tubulin from the NT30 strain and its parental strains suggested that the tolerance of the NT30 to nocodazole could be due to a mutation in a beta-tubulin encoding gene.[1]


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