An additive-multiplicative model is found to describe diallel cross data rather well. Estimates of the model's parameters are highly correlated from generation to generation.

The mouse mutant curly tail is thought to be inherited as an autosomal recessive (ct/ct) with incomplete penetrance so that approximately 60% of ct/ct individuals exhibit the curly tail (CT) phenotype. By outcrossing ct/ct with mouse stock carrying specific heterozygous combinations of Robertsonian (Rb) chromosomes, trisomy 16 (Ts16) and Ts19 mouse fetuses (and their chromosomally balanced littermates) were derived which were heterozygous for the ct gene. All of the Ts16 (ct/Rb;Rb) fetuses, studied between days 14–19 gestation had tail malformations, 86% of which were tail flexion defects (TFD) apparently very similar to the curly tail phenotype. Neither Ts19 nor any of the chromosomally balanced (ct/Rb) littermates from both experimental crosses showed any type of tail or other spinal malformation. At the 27–29 somite stage of development, Ts16 (ct/Rb;Rb) fetuses did not show any significant delay in the closure of the posterior neuropore (PNP) compared with their littermate controls, suggesting that the tail malformation observed in Ts16 (ct/Rb;Rb) occur as a result of mechanisms which differ significantly from those thought to be responsible to causing the curly tail malformation.

The spontaneous reversion to white of three purple mutants of Coprinus lagopus has been demonstrated to be due to suppression. Forty-one of the fifty suppressed purples isolated were crossed to wild-type and all crosses gave fewer than 25% purple progeny, i.e. all the suppressors appeared to be linked to the gene suppressed. Values for the percentage of purples segregated from these crosses varied continuously from 0% to nearly 20%. The functional relationships of the fifty suppressors were investigated by the technique of complementation in dicaryons. The pattern of results formally indicate two suppressor loci with extensive inter-allelic complementation at one of them. The functional allelism indicated by the complementation results is not compatible, in conventional terms, with the apparent positional spread of the suppressors. Several possible explanations are discussed but more data are required before a choice can be made between them. It seems most probable that the same genetic entity is involved in each independent event of suppression and that the characteristic segregations of purples from crosses of suppressed purples with wild-type will have to be explained in terms other than of normal recombination.

Several temperature-sensitive mutants of Escherichia coli were isolated which lyse at the restrictive temperature. Some of these possess a biochemically defined lesion in cell-wall mucopeptide synthesis. Three genes, termed murC, E and F, have been localized between the azi and leu markers. From transductional data a fine structure map was constructed of the mur mutations, establishing the order of the genes. The genetic relationship between these cell wall genes and neighbouring genes involved in cell division is discussed.

Expression of three wing-cell death mutants in Drosophila melanogaster was used to survey cryptic polygenic modifiers of cell death in wild type strains. Females carrying the X-linked mutants Beadex-3, notchoid and scalloped were crossed to males from each of 20 isofemale strains. Phenotypic variation in the amount of cell death was measured in F1 mutant males that were heterozygous for polygenic loci segregating in the wild strains. As expected, each mutant uncovered a broad range of polygenic variation among strains. Yet, when cluster analyses were used to evaluate the degree of correlation among the expressions of Bx3, sd and nd, the isofemale strains could be partitioned into a small number of groups that were similar in the effects they had upon the severity of cell death. Chromosome mapping of one cell death suppressor strain demonstrated that different polygenic loci could produce the same phenotype in different mutant backgrounds.

Mutations, sulA and sulB, that suppress the UV sensitivity conferred by the lon mutation have been isolated and precisely positioned on the linkage map of Escherichia coli. The E. coli B strains Bs-3 and Bs-8 have been shown to possess sulA mutations. Also the E. coli K12 strain J6271 that possesses a suppressor of the lon mutation, previously designated as suf, has been shown to be a sulA mutation. A series of methylmethane sulphonate resistant derivatives of an E. coli K12 lon strain has been isolated and genetically characterized. In addition to sulA mutations, a second suppressor sulB was identified and located between leu and azi genes on the chromosome. Neither sulA or sulB mutations result in increased sensitivity to the antibiotics ampicillin, rifampicin, or actinomyein D, nor do they have any significant effect upon the overproduction of mucopolysaccharide caused by the lon mutation. Under some growth conditions the sulB mutation causes cells to be temperature sensitive for the cell division process at 42 °C.

Coleoptile anthocyanin pigmentation in the hexaploid variety of wheat, Hope, is due to at least eight anthocyanins including four acylated forms. All are derivatives of either cyanidin or peonidin. Two homoeologous chromosomes, 7A and 7B, are involved in anthocyanin production. Both chromosomes carry genes that promote the synthesis of the same anthocyanins from flavonoid precursors. The roles of chromosomes 7A and 7B in anthocyanin biosynthesis and the consequences of interallelic interaction and dominance of possibly homoeologous loci are discussed.

A long-established laboratory stock was found to contain many individuals that were heterozygous for a lethal gene, called tailless-Edinburgh (te). Heterozygotes are indistinguishable from normals except by breeding tests with special tester stocks supplying brachyury (T) gametes, when tailless (Tte) progeny distinguish carrier parents from normal parents that produce only short-tailed (T +) progeny. When males are mated to tester females providing brachyury eggs, the ratio of Tte: T + progeny reflects the ratio of te: + spermatozoa. The proportion of te spermatozoa measured in this way led to the expectation that 62% of individuals in the original stock would be carriers, whereas 80% was found. Independent evidence is presented for + te males that the incidence of te in their effective spermatozoa was higher when normal eggs were fertilized in matings within the original stock than when brachyury eggs were fertilized in outcross matings to the tester stock. These observations suggest that the proportion of te spermatozoa partaking in fertilization was modified by the genotypes of the females or of their eggs.

Mouse embryo banking has become an important asset to geneticists. Individual laboratories can now maintain a far greater diversity of stocks than by conventional breeding alone. Also, many mutations that in the past would have been discarded due to lack of space, can now be preserved for future use. Recent advances in cryopreservation techniques have simplified procedures and, in certain cases, resulted in increased rates of survival.