The evidence for complementation maps being linear is examined by analysis of all known complementation maps in micro-organisms, and by constructing maps from mutants randomly sampled from amongst those at the leu-2 locus in Neurospora with known complementing properties. Eleven loci out of thirty-five examined in six micro-organisms have non-linear complementation maps. Two linear maps, his-3 and ad-3b (having 25 and 35 complementation groups respectively) have a sufficiently large number of groups for it to be likely that if they do not remain linear on testing further mutants, they will at least have a lower frequency of mutants exceptional to linearity than known non-linear loci. On the basis of maps made from mutants sampled from the leu-2 data, it seemed unlikely that non-linearity would be observed with less than 24 complementing mutants or 13 complementing groups in the sample, and therefore many loci with linear maps are likely to be found to have non-linear maps when larger samples of mutants are tested. This conclusion is important in attempting to correlate the structure of complementation maps with recombination maps and with functional data concerning enzyme activities.The relationship between the number of complementing mutants, number of groups and number of units at the leu-2 locus is described and a statistical method of determining the total number of groups at a locus is discussed.Known complex complementation maps have been replotted according to consistent rules, and are illustrated in a shorthand form. The form of the complex maps is discussed in relation to current hypotheses concerning the interpretation of complementation maps. In particular an interpretation of the ‘circular’ leu-2 map is given in terms of the theory of complementation proposed by Crick & Orgel (1964).

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S U M M A R YThe relationship between various parameters of growth of Neurospora crassa on solid media in tubes is described. These are (a) the relationship between culture weight and linear growth rate on various media; (b) the relationship between 'lag' in growth and inoculum size on various media. This latter relationship appears to obey a log law, enabling an inoculum doublingtime to be calculated. Adaptation of the arginine auxotroph arg-I (46004) to diminution of arginine in the medium first occurred by decrease in mycelial weight and then by decrease in linear growth rate. The inoculum doublingtime did not appear to vary systematically with arginine concentration.

SUMMARYThree methods of detecting respiratory variation in Neurospora crassa have been investigated. They involved the addition of dyes (pontamine sky blue and eosin yellowish) tellurite or tetrazolium to a complete medium containing ethionine. The latter prevented conidiation and enabled the colours of the colonies to be seen clearly. These methods were used to distinguish nuclear and cytoplasmic cytochrome mutants (cyt-I, cyt-2, mi-I, mi-3, SG-3 and SG) from wild-type colonies on the basis of colour. Tetrazolium violet (2.5-diphenyl-3-(1-napthyl)-tetrazolium chloride) incorporated into modified Nagai medium with ethionine is recommended for distinguishing cytoplasmic mutants of Neurospora from wild-type. Certain other nuclear mutants were also distinguishable from wild-type in some of these tests. These were ac-I, ac-2, acr-3, ad-4, leu-5, nit-I, OXD-I. Thirty-two wild-type strains in reciprocal crosses were tested on these media to find whether these tests would distinguish any nuclear or cytoplasmic variation. No new cytoplasmic variants were found. Three new nuclear genes, B m (mauve on dye media), Tet-R (ability to reduce tetrazolium) and su-(suppressor of mi-3) are described and have been mapped. All three loci were linked to the mating type locus on chromosome I. Tet-R was found in only certain wild-type strains of mating type a (e.g. 74-0~8-1a), and Tet-W (unable to reduce tetrazolium) was found in all wild-type strains of mating type A (e.g. 74-0~23-1A) and certain wild-types of mating type a ; f , a suppressor of mi-I, also suppressed SG-3 and SG, but not mi-3; su-suppressed mi-3, but none of the other cytoplasmic mutants.

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