Complementation at the Ad-4 Locus in Neurospora Crassa

Woodward, Dow O.; Partridge, Chris; Giles, Norman H.

doi:10.1073/pnas.44.12.1237

Cited by 52 publications

(21 citation statements)

References 7 publications

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“…In E. coli there appears to be no additional pathway to ornithine. 4 The study has been extended to include not only arginine-repressible strains but also strains in which arginine does not have this effect.…”

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An Enzymatic Difference Among Pyr-3 Mutants of Neurospora Crassa

Davis¹

1960

Proc. Natl. Acad. Sci. U.S.A.

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The pyrimidine-3 mutants of Neurospora crassa have received considerable attention in the past. Mitchell and Mitchell' described experiments, using pyr-3a (37301), 3b (37815; temperature sensitive), and 3d (45502), which indicated that the pyr-3a and 3b mutations represent a genetic unit distinct from 3d. The evidence for this view was that pyrimidine-independent heterocaryons could be formed by the combination of pyr-3a or 3b with 3d; that 3d, unlike 3a or 3b, was unaffected by a suppressor, s; and that crosses between 3a or 3b and 3d gave rise to a few (less than 0.01 per cent) wild type progeny. The segregation of a closely linked colonial marker (co), however, suggested that the wild type progeny arose through a mechanism different from simple reciprocal chromosome exchange during meiosis.Suyama et al.2 have confirmed and extended these data with a large series of independently isolated pyr-3 mutants. Their work indicates that the pyr-3 locus consists, on the basis of heterocaryon complementation, of two functional units, and that a large portion of the wild type progeny arising from intercrosses of mutants can be ascribed to a mechanism ("gene conversion") which does not involve the recombination of closely linked genetic markers. All of the pyr-3 mutants, including both functional units revealed by heterocaryon complementation, appear to be arranged in a continuous, linear order, and reasonable additivity of distances prevails in the genetic map. The maximum percentage of prototrophs from crosses of mutants was approximately 0.02 per cent, which indicated a very short length of the pyr-3 complex. (The pyr-3d mutant is reported to be identical with a mutant, KS36, in one of the functional units described by Suyama et al.;2 pyr-3a and 3b presumably represent the other unit.)Because the patterns of heterocaryon complementation or suppressor relationship observed among pyr-3 mutants has been observed in other mutant series concerned with one36 or with more than one enzyme, it cannot be decided with the evidence available whether or not all pyr-3 mutations affect a single metabolic function.This investigation was designed to relate enzymatic features of the pyr-3 mutants to the implied physiological differences between them and to the genetic structure of the pyr-3 locus. Preliminary data have indicated that pyr-3a, 3b, and 3d, like the wild type strain, all contain the series of enzymes required for the transformation of ureido-succinic acid (US; = carbamyl aspartic acid) to uridylic acid via the orotic acid pathway, and that deficiencies in the activity of certain of these enzymes are responsible for the pyrimidine requirement of other pyr mutants.7 US does not satisfy the nutritional requirement of any of the pyr-3 mutants. The preliminary enzymatic studies, however, were considered compelling evidence that the metabolic block in pyr-3 mutants concerned the synthesis of US or earlier steps of pyrimidine metabolism.8 Attention was therefore directed to the synthesis of 677

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confidence: 99%

An Enzymatic Difference Among Pyr-3 Mutants of Neurospora Crassa

Davis¹

1960

Proc. Natl. Acad. Sci. U.S.A.

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“…The majority of the alleles are group A members, which show no complementation with any other alleles. Woodward, Partridge and Giles (1958) found that the greater the distance between two ranges of action, as represented on the cornplementation map, the more vigorous was the heterocaryotic growth.…”

Section: Results (I) Heterocaryon Corn Piementationmentioning

confidence: 99%

Complementation and recombination between Methionine-2 alleles in Neurospora crassa

Murray

1960

Heredity

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AMONGST the many new methionine mutant strains of Jt[eurospora crassa which have been isolated (Murray, 1960) the sulphur requirement of forty-two is satisfied by homocysteine or methionine, but not by cystathionine. Heterocaryon tests show that the mutant genes in these strains are physiologically allelic with H98 and 48004 (me-2) and that some pairs of them exhibit the phenomenon of interallelic complementation. Methionine-2 is located in• the right arm of linkage group IV, in a region well supplied with genetic markers, and as interallelic crosses proved to be relatively fertile, it appeared that this gene would be suitable for the investigation of the relationship between genetic and complementation maps. The data from ordered tetrads (Murray, 1960) indicated that me-2 is 87 units distal to typ-4 and 37 units proximal to pan-I. Therefore, trp-4 and pan-I were chosen as suitable markers for the analysis of recombination between me-2 alleles. The discovery of recombination between the two physiologically allelic mutants "Star" and "asteroid" in Drosophila (Lewis, 1945), and more recently between alleles at loci in Aspergillus (Pritchard, 1955), JVeurospora (Giles, 1951, 1956; Mitchell, 1955a, I.955b) and yeasts (Roman, 1956; Leupold, 1957), suggests that the gene may be interpreted as comprising a number of linearly arranged mutable sites which are separable by crossing-over. Pritchard (1955) was able to arrange a number of adenine alleles of Aspergillus in linear order by an analysis controlled by markers on each side of the locus. In general, recombination between the adenine alleles was accompanied by recombination of the associated markers. Prototroph formation was therefore explicable as the result of a single cross-over between the defective sites of the locus. Such a cross-over would produce one normal and one doubly mutant chromatid strand, and Pritchard was able to recover the doubly mutant recombinant. Other adenine prototrophs, of parental phenotype with respect to the marker genes, could not be interpreted as the products of single intragenic cross-overs, but were, perhaps, comparable in origin with the prototrophs from crosses of allelic pyridoxine mutants of .J'Teurospora (Mitchell, 1955a, i955b). By studies of ordered tetrads Mitchell showed that * Work done while holder of a postgraduate grant from the

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“…Almost all amylase mutant genes belong to one locus with the exception of one gene (ae5) according to the results from the present genetic studies. In this point further details of the characterization of these amylase genes have been investigated with the heterocaryon-test for complementation (Giles et al 1957;Woodward et al 1958 <Lacy and Bonner 1961), resulting in restoration of growth on starch.…”

Section: Discussionmentioning

confidence: 99%