A genetic investigation of the ad9 cistron of Aspergillus nidulans

The purpose of this work was to construct a fine genetic map of the ad9 cistron in Aspergillus nidulans and to discover if any correlation exists between the genetic and functional relationships of some of the ad9 alleles. Preliminary results suggested that certain of the ad mutant strains investigated carried inversions spanning part of the ad9 cistron, and further experiments were therefore carried out to elucidate the nature of these inversions. It had previously been shown by Calef (1956) that, among the four alleles ad9, ad13, ad15 and ad17, only ad15 and ad17 complement one another. In the present investigation ad32 and ad33 were identified as alleles of ad9. All possible pairs of the six mutants were tested for complementarity, and one new complementing pair was discovered, namely ad32 and ad17. Analysis by means of mitotic and meiotic recombination gave the sequence of mutant sites as ad33 - adl3 - ad9 - ad32 - ad17 - ad15 (in non-inverted strains). There was no apparent relationship between the genetic and complementation maps. Complementation was inhibited in vivo in the presence of mercuric ions, suggesting that S-S linkages may be involved 11 in the complementation mechanism, possibly in the formation of a hybrid polymer of polypeptide chains, as proposed by Crick and Orgel (unpublished). It was established by analysis of mitotic and meiotic recombination that the ad13 strains used most probably contained an inversion spanning the sites of adl3, ad9 and ad32. Recombination studies suggested that the ad17 strains contained an inversion identical with the adl3 inversion and that ad15 strains carried an inversion for part of the ad9 cistron which apparently differed from the adl3 inversion. The ad13 inversion (and the ad17 inversion) does not apparently give rise to a detectable mutant phenotype. Because of the location of the mutant sites analysed in the present studies, it was not possible to establish whether the suspected ad15 inversion also determines a non-mutant phenotype. The significance of the "wild-type" inversion in relation to gene function is discussed. Localised negative interference was found, in agreement with results of previous workers. Inversions increased negative interference in mitotic and possibly also in meiotic recombination. It was concluded that the effects on recombination of intra-cistronic inversions are compatible with the "effective pairing" hypothesis of Pritchard (1955)