Segregations at five loci on the left arm of chromosome VII and other data from published sources were used to test a new mathematical model of meiotic segregation in trisomics of the yeast Saccharomyces cerevisiae. Results support this model which predicts that non-centromere-linked genes in trivalent complexes segregate at random. The data indicate that bivalent–univalent complexes are infrequent in trisomics and that recombination between all three homologues is frequent in regions close to the centromere. A test of homologue interference produced no evidence that a crossover between two homologues has any influence on the probability that the same two homologues will be involved in an adjacent crossover.

Two systems of hybrid dysgenesis, the P–M system and the I–R system, are characterized by two different specific types of non-reciprocal hybrid sterility referred to, respectively, as GD and SF sterility. In order to determine the relationship between these two systems, strains representative of the four single-system interactive types were crossed in almost all possible combinations and tested for both types of sterility. The results suggest that the two systems are at least partially independent of one another. There are several examples of single strains that contribute the maternal component for interaction in the P–M system and contribute the paternal component in the I–R system. Using parents with the potential for the two types of interaction and. appropriate temperature manipulation, both GD and SF sterility can be manifested in the same hybrid females. In other crosses, a single type of sterility is observed, or none at all, according to the dual designation of the parental strains. The evidence from a number of additional crosses suggests that most strains of this species have the potential for both types of interaction to varying degrees when mated in appropriate combinations. Some theoretical and practical implications of these results are discussed.

Hybrid dysgenesis has been described as a syndrome of aberrant traits including sterility, male recombination, and mutation, which occurs in some inter-strain hybrids of Drosophila, but only from one of the two reciprocal crosses. In a series of experiments in which hybrids of various pedigrees were tested for sterility, it was found that a case of hybrid dysgenesis could be most easily interpreted as the interaction of two components. One component was found to be a polygenic Mendelian factor linked to each of the major chromosomes of π2, the paternally contributing strain (‘P strain’). These chromosomes were capable of causing sterility when inherited from either parent, provided the appropriate maternal component was also inherited. The ability to transmit this maternal component was designated ‘cytotype’ to indicate that it is a property of the entire cell. It was possible to classify nearly all hybrid females as either P or M cytotype on the basis of their ability to produce sterile daughters. All daughters of the M-cytotype mothers were susceptible to the sterilizing effects of the π2 chromosome, whereas all, or nearly all daughters of P-cytotype mothers were immune. When more than one of the π2 chromosomes were received by daughters of M-cytotype females, chromosomal interactions could be detected statistically, but the model of independent action remained a useful approximation. Cytotype was shown to be determined by chromosomal factors, but with limited cytoplasmic transmission. This unusual mode of inheritance can be compared with other cases of hybrid dysgenesis where the behaviour resembles that of self-replicating cytoplasmic particles which are dependent on certain chromosomes. The lack of sterility from intra-strain crosses can be explained by the fact that chromosomes capable of causing sterility also induce the P cytotype, and thus prevent sterility in the next generation.

There is a strong genetic component to fertility differentials among individuals of ponderosa pine. Prolific cone-producers as a group were markedly different from low cone-producers at the three protein loci which were monitored. The two groups did not differ significantly in age, but trees with high cone production had slower growth rates and smaller diameters than trees with low cone production. To our knowledge, these results provide the first demonstration of fertility differentials associated with specific genes in a woody plant.

This paper tests the hypothesis that haplodiploidy or X linkage leads to less genetic variability. Although haplodiploid organisms exhibit a low level of genetic variability the wide variation existing between different diploid organisms implies that factors other than the genetical system could also be responsible. In order to test the hypothesis critically it is necessary to compare the level of genetic variability between X-linked and autosomal genes within a closely related group of organisms. For kangaroos, the ascertainment bias for X-linked loci has been removed by assuming the correctness of Ohno's law of conservation of the mammalian X, i.e. that genes found to be X-linked in man can be assumed to be X-linked in kangaroos. For Man and Drosophila, it has been assumed that the percentage of the karyotype which is X chromosome can be used as the expectation for the percentage of X-linked polymorphisms. No difference between the two classes of loci is evident in kangaroos and man for percentage polymorphism. The data however have confidence limits which would allow autosomal loci to have three times greater percentage polymorphism. In Drosophila the published data of Prakash show that autosomal loci are polymorphic about twice as frequently as are their X-linked counterparts. Thus there may be a modest reduction in percentage polymorphism as a result of X-linkage (i.e. haplodiploidy). No reduction in the number of alleles per locus or average heterozygosity at those loci which are polymorphic is evident in kangaroos, man, or Drosophila. More data on more X-linked enzymes are necessary to establish firmly that there is a real reduction in percentage polymorphism and to estimate its extent. The kangaroo data are incompatible with the hypothesis that a large fraction of the variability is maintained by simple overdominance since overdominance is very unlikely in the quasi-haploid genetical system which results from the paternal X inactivation mode of dosage compensation used by kangaroos. This is the first report on level of enzymic variability in marsupials. 17% of autosomal loci and 18% of X-linked loci are polymorphic, average heterozygosity is 4% for autosomal and 4% for X-linked loci and number of alleles per locus is 1·25 for autosomal and 1·21 for X-linked loci. These figures are somewhat lower than for eutherian mammals.

Strains of Escherichia coli harbouring a conjugative plasmid that carries a transposon for tetracycline resistance (Tn1771) were found to be adaptable to very high tetracycline concentrations. The molecular analysis of plasmids isolated from strains with enhanced levels of tetracycline resistance revealed an intramolecular amplification of the resistance determinant of the tetracycline transposon.

A model for the molecular structure of the transposon is presented, which suggests that there are three repetitive DNA segments on Tn1771. This accounts for the properties both of transposition and of gene amplification.

Methionine-sensitive mutants of Schizosaccharomyces pombe were found to map at 16 loci, min1–min16, seven of which are allelic to known ade loci involved in adenine biosynthesis. The mutant min1–106 was shown to be located within the ade6 locus by intragenic recombination analysis. Methionine sensitivity of these mutants is reversible by adenine supplementation and their pigmentation is similar to that of the corresponding ade mutants. We conclude, therefore, that these min mutants are incompletely blocked in adenine biosynthesis. These observations further indicate that adenine biosynthesis in S. pombe is inhibited by methionine or a metabolite derived from it. For some other min mutants showing reversibility of methionine sensitivity by leucine or proline, no allelism to known leu or pro loci was detected.

A viable t-haplotype, t38, has been shown to distort linkage relations in the T−tf region of mouse chromosome 17. Separate experiments were done with two different interstitial markers, Low and qk, which map respectively about 5 and 4 centimorgans (cM) from the locus of T in female T + tf/ + (Low or qk)+ heterozygotes. In females that carried t38, however (i.e. t38+ + / + Low tf or t38+ + / + qk tf), there was virtually no recombination between t38 and either interstitial marker, although the t38−tf distance was normal. These observations suggest that t38 suppresses recombination in the lefthand part of that region and strongly enhances it further to the right.

The recessive lethal T/t-complex haplotype tw75 was isolated from Jena, East Germany, prior to 1973. It was at first thought to be a standard member of the tw5 complementation group because matings of T/tw75 × T/tw5 produced tailless offspring only (Dunn, Bennett & Cookingham, 1973). Cross tests with all other complementation groups and embryological studies have recently been completed, with results demonstrating that tw75 does not complement the members of either the tw5 or the tw1 complementation groups. Histological studies show that compound embryos tw75/tw5 and tw75/tw1 die with symptoms indistinguishable from tw5/tw5 and tw1/tw1 homozygtes respectively. Thus tw75 represents the first confirmed isolation of a t-haplotype that overlaps two complementation groups.