Analyse der Sorbose-Resistenz von Neurospora crassa an Heterokaryen sorboseresistenter Mutanten; ein Beitrag zur Genetik des aktiven Transports, I.

Summary

Suitable auxotrophic markers were introduced into sorbose-resistant mutants and the sorbose-sensitive wildtype strain. Pairwise combinations of one resistant and one sensitive strain each as well as of two sensitive strains were then grown on minimal-agar to obtain forced heterocaryons. The growth behaviour of these on minimal-agar with and without added sorbose was compared.

Of seven resistant mutants, representing six separate genes, among which were genes A and B, six mutants were recessive to the wildtype. The seventh, representing gene C, was recessive only with regard to colony-size, but intermediate with regard to germination counts. Heterocaryons forced between pairs of 2 closely linked mutants (intragenic case of the type A⁻ ₁+A⁻ ₂) were resistant, as were the separate mutants. However two heterocaryons forced between pairs of unlinked mutants (intergenic case of the type A⁻+B⁻) were sorbose sensitive. Heterocaryons forced between A or B-mutants and the C-mutant mentioned, unlinked to either A or B (intergenic cases of the type A⁻+C⁻ and B⁻+C⁻) were more sensitive than the separate mutants but more resistant than the wildtype.

It follows that sorbose-resistant mutants in heterocaryons of the intergenic types can complement each others defects (no growth complementation), but can not do so in heterocaryons of the intragenic type. Their complementation is considered to be the result of the activity of the intact wildtype genes homologous to the defective ones that are contained together in the multinucleate cells of the heterocaryons. This complementation may be taken as evidence for the recessiveness resp. intermediate expression of the different resistant mutants.

Since none of the mutants checked so far were dominant compared to the wildtype, none of them can be a regulator-mutant. The possibility of explaining them as suppressor mutants is restricted by their recessiveness to mechanisms of suppression giving a recessive phenotype. An alternative explanation suggests that the respective wildtype genes may contain structural information for the synthesis of permeases involved in sorbose transport. The mutants would then be resistant due to defective permeases. Their recessiveness is in full accord with this suggestion.