A mutational analysis of conidial development in Aspergillus nidulans.

NDIVIDUAL morphological mutants have been studied in many higher organ' isms such as Drosophila (HADORN 1955) and the mouse (GRUNEBERG 1952), but a rigorous mutational analysis of the type employed on many biochemical pathways is readily carried out only in microorganisms. The most remarkable study of this type is the work on bacteriophage T4 (EPSTEIN et al. 1963) in which the whole of the development of the virus is open to analysis. In more complex organisms the spectrum of morphological mutants obtainable is very broad (e.g., in Neurospora: GARNJOBST and TATUM 1967) and analysis can only be carried to any depth if attention is confined to a process such as sporulation (reviewed in HALVORSON, VARY and STEINBERG 1966). or to mutants affecting an individual enzyme (e.g., BRODY and TATUM 1966). Aspergillus nidulans, unlike most eukaryotes, lends itself to a similar approach since it can be treated as a microorganism and has a well-studied genetic system (PONTECORVO et al. 1953). The conidial apparatus is a particularly suitable subject, as the structure is a well-defined one, and the spores possess a distinctive green pigment so that mutants lacking this can readily be picked up and examined for modification or absence of conidia. Most important, however, is the fact that the conidia are dispensable structures, inessential for normal growth, and indeed, inessential for storage and propagation since the sexual cycle in this homothallic organism provides an alternative source of spores. The structure of the conidial apparatus of Aspergillus nidulans is shown in Figures 1 and 2. Like the hyphae, the conidiophores and vesicles are multinucleate, but the sterigmata and conidia are uninucleate (PONTECORVO et al. 1953; CLUTTERBUCK 1969). Initiation of conidiation in ascomycetes is complex (MORTON 1961 ; TURIAN 1966), and preliminary studies in A. nidulans suggest that there is a balance between conidiation and production of cleistothecia or aerial mycelia. Considering this complexity, it was decided to accept for study only those mutants that had a normal density of conidiophore initials; that is, to confine the study to the processes following conidiophore initiation. A second limitation imposed on this analysis is the rejection of mutants whose linear growth rate on agar is less than that of the wild type. This is done in order to exclude the many mutants in which there is a defect in their normal metabolism that only has a serious effect during conidiation. Since the subject of this