It has been proved that the suppression of seven different auxotrophic mutant alleles is brought about by a single super-suppressor allele designated S. Super-suppressor S is allele-specific rather than locus-specific and is dominant to its wild-type allele.

Suppressible mutant alleles show no linkage relationships either among themselves or with the suppressor S.

Super-suppressor S has been shown to be closely linked (about 5 stranes) to one of the centromeres other than those of linkage groups I to XII. This establishes a new thirteenth linkage group.

The possible mechanism of action of the super-suppressor is discussed.

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).

1. A form of syndactylism (jt) involving two or three digits on one or more feet has been found in the descendants of Swiss-albino mice treated with HN2. The fusions are in a proximo-distal direction and usually involve only the skin and soft tissues; digits 1 and 5 are unaffected.

2. This type of syndactylism is apparently due to a single recessive gene, jt, whose penetrance is influenced by ‘genetic background’. Apparently the identical mutation has occurred independently in stock maintained at Bar Harbor and Stanford. Linkage tests indicate that jt is not linked with c or lu.

3. Embryological studies of the developing footplate reveal a loss in both preaxial and postaxial footplate tissue, primarily the latter, prior to and during the condensation of mesenchyme into the precartilage of the digital elements in the jt/jt limb.

4. The importance of the shape and amount of footplate tissue to the resultant morphology of the foot is apparent. It is evident that genes such as jt are responsible for changes in footplate development, but the immediate underlying factors which cause these alterations remain an unsolved problem.

Examination, in the salivary gland nuclei of D. melanogaster males, of four cases of translocation between the X and fourth chromosome, involving breaks of the X in widely different positions, disclosed no influence of the rearrangement on the width, morphology or chromatin-staining of either of the separated parts of the X, or on the fourth chromosome. Both parts of the single X were distinctly narrower than were the double major autosomes, as is true for the X of normal males but not for the double X of females. At the junction between a portion of a translocated single X and the double fourth chromosomes the transition in width, morphology and staining was abrupt and striking. As in structurally normal males, however, the parts of a single X, here removed from one another by the translocation, did appear to be somewhat swollen, as compared with half of a double chromosome, but to be correspondingly paler in stain, so as to indicate an unaltered amount of chromatin (see also Offermann, 1936; Rudkin, 1964; Pavan & Frota-Pessoa, 1964).

The above evidence of the regional autonomy in characteristics of the different parts of the X studied by us, and also of the fourth chromosome, is in contrast to the lack of such autonomy found in translocation studies on mammals, where the X chromosome and that joined with it are subject to an influence diffusing along them and thus acting ‘wholesale’, rather than ‘piecemeal’. Likewise, a re-examination of the earlier genetic evidence on dosage compensation in Drosophila leads back again to a decidedly ‘piecemeal’ interpretation of its operation and evolution, according to which most genes in the X, and sometimes even different phases of the action of the same gene, have their own system of separately evolved, scattered compensators, which are also located in the X.

The fact that two so differently working compensation mechanisms as those in Drosophila and mammals have evolved independently to serve the same function emphasizes the importance of that function. That is, it points up the survival value of having the effectiveness of normal genes regulated to a very exact level. For the compensation enables the single representative of the X in the male cell to become equivalent to the two representatives of the X in the female cell. Moreover, this equivalence is of a considerably finer grade than that already afforded by the phenomenon termed ‘dominance’, which has evolved to meet the same basic need (that of phenotypic stabilization), and which has, incidentally, made even the uncompensated effects of one and two doses of either sex-linked or autosomal normal genes not readily distinguishable in most cases.

Taken by itself, the ‘piecemeal’ mechanism of Drosophila provides far stronger evidence for this conclusion than does the ‘wholesale’ mechanism in mammals. For the former must have required the establishment of far more numerous mutational steps and, taken individually, each of these steps was of correspondingly lesser survival value. Since they nevertheless affected fitness enough to become established, it also follows that usually a normal gene—or at any rate one of the kinds whose mutants have usually been studied—confers a significantly higher fitness when not heterozygous for such a mutation in it, despite the seeming recessiveness of most mutations. Thus, the expression ‘normal gene’ continues to have a very high validity.

Artificially selected diploids of Coprinus lagopus when mated in compatible combinations, either together or with haploids, produce dikaryotic mycelia which are typical of normal haploid-haploid dikaryons. In a diploid-haploid dikaryon, the diploid nucleus is not as stable as when alone in a monokaryon but it can persist through repeated sub-culturing into a fruiting body and eventually through meiosis into the basidiospores. In a diploid–diploid dikaryon either one or the other nucleus becomes haploid so that fruiting bodies with two diploid nuclei are never formed. This fact constitutes a restriction on diploidy in nature and a useful method of reducing diploids to the haploid state.

Matings that might be considered to be incompatible at the B mating gene show a significant difference which is related to the number of B alleles common to the mating colonies. Matings with one B allele in common, e.g. B3B6+B2B3 produce fully compatible and normal dikaryons. Matings with two B alleles in common, e.g. B3B6+B3B6 have, at first while the diploid nuclei still persist, the appearance of an incompatible common B haploid heterokaryon. This indicates that the B incompatibility system is based not on a complementary action between different B alleles but on an oppositional action between the same alleles neutralizing the B gene product which is necessary for dikaryon formation.

1. In the transduction pro-401 (×) + some of the transductants are surrounded by several hundred small wild-type satellite colonies; these transductants spontaneously release phage which transduces pro-401 to wild-type at high frequency (HFT phage).

2. When the HFT phage is used to infect pro-401 at very low multiplicities of infection, most of the transductants are defective lysogens and segregate proline-requiring phage-sensitive derivatives; these transductants are apparently heterogenotes. At higher multiplicities of infection, or with lysogenic recipients, a higher proportion of satellited transductants is found.

3. The HFT phage preparations transduce only the proline region of the donor genome.

4. The existence is inferred of a defective P22 particle specifically incorporating the proline region of the Salmonella chromosome; these defective particles can establish themselves as prophage and confer immunity upon the infected cell, but are unable to replicate unless a normal prophage is also present. Satellited transductants are lysogenic both for a normal and defective (proline region carrying) phage, and so on lysis release transducing phage.

5. This system is compared with the λdg-gal and P1-dl-lac systems in E. coli.

The 150 independently isolated thy− mutants of E. coli K12 Hfr 3.OSO were studied genetically and phenotypically. Variants were found among the mutants in respect to the lag period of thymineless death, and temperature sensitivity. The latter correlates with mutations located at a specific site on the genetical map.

The thy locus is located between the cys and ser/gly genes, and is a linear structure where 134 thy mutants are distributed over more than 17 sites. The site distribution of the mutants is not regular: about a half of them (62) are localized within one site and all these are temperature-sensitive.

Two further genes involving utilization of thymine—tlr and td—were found. Mutations of tlr lead to a reduced thymine requirement (0·5 μg./ml. instead of 20 μg./ml.). A mutation of td results in thymidine sensitivity.

This latter character is expressed when the td-s allele is transferred into E. coli K12, prototrophic for thymine, by conjugation. Thymidine inhibition can be reversed by the addition of any riboside to the growth medium. Both genes map at the proximal end of the Hfr 3.OSO chromosome and are linked with the thr gene. The most probable gene order is: tlr-td-thr.

The following results have been obtained from 14C-thymine incorporation experiments with wild-type cells, as well as with thy−tlr+ and thy−tlr− cells: (1) Wild-type cells incorporate exogenous thymine extremely poorly, but incorporate thymidine better. (2) The thy−tlr+ mutants are able to incorporate thymine only when high concentration are used, but can utilize a low concentration of thymidine. (3) The thy− mutants are able to incorporate exogenous thymine as well as thymidine at low concentration. (4) The tlr mutation is a thymine-specific one.

1. Improved methods for the culture and preservation of Physarum polycephalum amoebae have been developed.

2. Strains of amoebae have been isolated which are stably resistant to 4, 8 or 16 μg./ml. actidione.

3. Sensitivity vs. resistance to 4 μg./ml. actidione is probably controlled by a single pair of alleles at a locus unlinked to the mating-type locus.

4. Plasmodia homozygous or heterozygous for the allele determining resistance at this locus are no more resistant to actidione than plasmodia homozygous for the allele determining sensitivity.

Curly-whiskers (cw) is a recessive gene which was found in 1958 by Mr C. J. W. Smith of the Chester Beatty Research Institute, London. It arose in a subline of the CBA/Cbi inbred strain. The first mutant animals were one male and one female in a litter of five. The two mutants were mated together and a sib-mated subline was continued from them in which 500 mice were bred, all of which were curly-whiskered. This established the mutant to be fully penetrant. Curly-whiskers resembles the hair-waving genes in causing waving of the vibrissae, but it has no obvious waving effect on the hairs of the coat. The coat texture is, however, slightly abnormal and Mr Smith noted also that on the CBA background there was an appreciable darkening of the coat colour. Homozygotes (cw/cw) are easily classifiable soon after birth by the curled vibrissae. Heterozygotes (+/cw) often have slightly curled vibrissae, and the gene is therefore not fully recessive; but the distinction between +/cw and +/+ could not be relied on, and in the linkage tests cw was treated as a recessive gene.

The conclusion by Suit, Matney, Doudney & Billen (1964) that Hfr donor cells of Escherichia coli K12, starved of required amino acids can mate, has been re-examined. It appears that their conclusion is not valid and that apparent fertility of amino-acid starved cells is due to cross-feeding by the F− cells. The relationship of this result to the alternative mechanisms for chromosome transfer in E. coli is discussed.

The inducibility of three enzymes (β-galactosidase, tryptophanase and D-serine deaminase) has been measured at various times during the cell cycles of three strains of Escherichia coli (K12 58–161 F−, B/r F– and 15T−). In each strain sharp increases in inducibility of these enzymes occurred at characteristic periods in each cell cycle. Such increases depend on DNA replication and therefore probably reflect synchronized gene replication. It is inferred that chromosome replication in these F− strains is sequential from a fixed origin.

Infection with F′Lack+ results in an extra period of increase in inducibiity of β-galactosidase in each cell cycle. It is concluded that the F′ episome replicates once in each cell cycle at a time soon after cell separation.