Beschreibung:
<jats:p> <jats:italic>Aspergillus nidulans</jats:italic> is one of the model ascomycete fungi. Transposition events have never been described in this organism. We have determined that this organism has at least 13 copies of a Fot1‐related element. These copies are transcribed, non‐methylated and polymorphic in various wild isolates. In spite of this, we have failed to isolate transposon insertions when the resident <jats:italic>niaD</jats:italic> gene is used as a transposon trap. This contrasts with the situation described previously in <jats:italic>Fusarium oxysporum</jats:italic>. We show that two elements of <jats:italic>F. oxysporum</jats:italic>, <jats:italic>Fot1</jats:italic> and <jats:italic>impala</jats:italic>, transpose efficiently in <jats:italic>A. nidulans</jats:italic>. We have developed the <jats:italic>impala</jats:italic> system by tagging it with the <jats:italic>yA</jats:italic> gene. This permits the visual detection of the transposon by the colour of the conidiospores. We demonstrate that no endogenous transposase of <jats:italic>A. nidulans</jats:italic> is able to act in <jats:italic>trans</jats:italic> on a defective <jats:italic>impala</jats:italic> element, whereas its own transposase driven by two different promoters is able to mobilize this element. The frequency of excision of these modified elements is between 10<jats:sup>−4</jats:sup> and 10<jats:sup>−5</jats:sup>. Loss of the transposable element occurs in about 10% of all excision events. In the remaining 90%, the transposon seems to be integrated at random positions in the genome. The availability of mitochondrially inherited mutations has allowed us to demonstrate that hybrid dysgenesis is apparently absent in <jats:italic>A. nidulans.</jats:italic> The development of this system opens the way to investigating the mechanism underlying the paucity of transposition events leading to visible phenotypes. It should allow us to develop efficient gene‐tagging tools, useful in this and other fungi.</jats:p>