The selective advantage of sexual reproduction is widely regarded as a major unsolved problem in biology. Recently, it has been proposed that the fundamental selective advantage of sex is its promotion of recombinational repair and hence survival of DNA in the germ line of organisms. A bacteriophage T4 system was set up to test this theory. After a phage T4 injects its DNA into an Escherichia coli cell it quickly establishes a barrier, through its immunity function, to infection by a second phage T4, arriving at a later time. This barrier causes phage T4 to reproduce asexually. The immunity barrier has a selective advantage in preserving the host cell as a sole resource for the first phage. If the first phage's DNA is damaged by UV irradiation, however, it has a reduced probability of being able to survive in the host cell when it is there alone. It was found that UV irradiation, in addition to reducing the first phage's viability, also prevents the first phage from raising an effective immunity barrier. This UV-induced reduction in immunity now allows sexual interaction with later-arriving secondary phage or sexual reproduction. It was found that these secondary phage enhanced survival of genes of the UV-damaged first phage. This supports the theory that under DNA-damaging conditions, which should be prevalent in nature, sex would have a selective advantage.

Cold-resistant revertants of the cold-sensitive, ribosomal suppressor suaC109 have been isolated, with a view to obtaining mutations in new ribosomal protein genes. Many revertants had reduced suppressor activity and were classified as antisuppressor mutants. Both intragenic and extragenic reversions were found. In seven strains the extragenic reversion to cold resistance segregated with the antisuppressor phenotype, and these were designated asu mutations. Three of the five asu genes, C, B and D were mapped to linkage groups, I, II and V respectively. The antisuppressors are not gene-specific, although they mainly antagonize the activity of ribosomal suppressors. The antisuppressors altered all aspects of the phenotype of suppressor suaC109 including sensitivity to aminoglycoside antibiotics, and are therefore thought to be mutations in ribosomal protein genes.

The inheritance of alleles at ten enzyme loci of Stagnicola elodes (Lymnaeidae) was analysed by laboratory crosses. Alleles for alanine aminopeptidase (2 alleles), leucine aminopeptidase (2 alleles), aspartate aminotransferase (2 alleles), β-hydroxybutyrate dehydrogenase-1 (4 alleles), 6-phosphogluconate dehydrogenase (2 alleles), esterase-2 (2 alleles), esterase-3 (2 alleles), esterase-7 (2 alleles), esterase-13 (2 alleles) and esterase-18 (2 alleles) segregate in the F2 generation according to Mendelian expectations. Contingency X2 tests for linkage done on F2 progeny from crosses between strains homozygous for alternate alleles at two loci showed that β-hydroxybutyrate dehydrogenase-1, esterase-13 and esterase-18 are presumably linked.

In this paper we describe the use of a free duplication, sDp2 (I;f), for the recovery, maintenance, and analysis of mutations defining essential genes in the left third of Linkage Group I of Caenorhabditis elegans. The lethals were induced in a strain of genotype (sDp2) + /dpy-5 + unc-13/ dpy-5 unc-15 +, using either 12 mM ethylmethane sulphonate or 1500 r of gamma radiation. Lethal mutations linked to the dpy-5 unc-13 chromosome were recognized by the absence of Dpy-5 Unc-13 individuals amongst the self progeny and were maintained by isolating Unc-13 hermaphrodites. These strains – which have two mutant alleles of the essential gene and a wild-type allele on the duplication – are balanced, since crossing-over does not occur between sDp2 and the normal homologues. Using this sytem we have recovered 58 EMS-induced mutations. These have been characterized with regard to map position and complementation. Twenty-nine of the EMS-induced mutations lie to the left of dpy-5 and define 20 complementation groups; 3 were inseparable from dpy-5 and define 3 complementation groups; 21 were to the right and define 17 complementation groups. Among a set of 29 gamma radiation-induced lethal mutations, 17 appear to be single gene mutations or are very small deletions. We estimate that we have identified from one-sixth to one-half of the essential genes in the sDp2 region.

Two separate, but interacting, genetic systems underlie the variation in seasonal cycles among members of the Chrysoperla carnea species-complex. The two systems are expressed as all-or-none reproductive responses to photoperiod and prey (i.e. short-day/long-day requirement for reproduction versus long-day reproduction and prey requirement for reproduction versus reproduction without prey). In each case the alternative to reproduction is reproductive diapause. The photoperiodic responses are determined by alleles at two unlinked autosomal loci. The expression of dominance by the alleles at these loci varies among geographical populations. The genes that determine the photoperiodic responses also act as suppressors of the genes that govern responsiveness to prey. An autosomal, polygenic system, with a threshold for the expression of diapause, determines responsiveness to prey. The two genetic systems are important to seasonal diversification and speciation within the C. carnea species-complex.

P-element mutagenesis was used to contaminate M-strain second chromosomes with P elements. The effect of P-element transposition on abdominal and sternopleural bristle scores and on female productivity was deduced by comparing the distributions of these quantitative traits among the contaminated second-chromosome lines with a control population of M-strain second-chromosome lines free of P elements. Estimates of P-element-induced mutational variance, Vm, for these characters are very high, and mutational ‘heritabilities’ (Vm/Ve, the ratio of mutational variance to environmental variance) are of the same order as heritabilities of these traits from natural populations. P-element-induced mutational variance of abdominal bristle score is roughly two orders of magnitude greater than spontaneous and X-ray-induced Vm/Ve for this trait.

Animal models which emulate defects similar to those in man are required for medical research. Many investigations on the cellular, developmental and molecular aspects of cataractogenesis use the cataract Fraser (CatFr) mouse. This report shows that the CatFT and Lop lens abnormalities are linked, and are probably allelic genes on chromosome 10. It also shows that the CatFT gene is maintained on an inbred genetic background which differs from 79 other strains; it is proposed that this strain be named CAT.

NMRI/Han mice ovulate significant numbers of diploid oocytes after gonadotrophin stimulation, most of them arrested at metaphase I. In contrast, females from other mouse strains ovulate only oocytes having completed meiosis I. We investigated the heritability of the trait Dipl I by analysing F1 hybrid females from crosses between the sensitive NMRI/Han stock and two mouse strains (C3H/HeHan and BALB/c) considered as non-sensitive, and females from backcrosses to NMRI/Han males (only crosses with C3H/HeHan). The results show (1) that the trait Dipl I is inheritable; (2) that an X-chromosomal (location proximally from the X–Y pairing region) or autosomal recessive mode of inheritance is excluded; and (3) that the expression of the trait, measured as frequency of diploidy, is modulated by a maternally transmitted factor.

Under a two-locus model with additive genes which combine multiplicatively to determine a quantitative trait, heterosis is generally observed in the F1 It is positive only if both frequencies of the best allele at each locus are not higher in the same parental population. In the F2, heterosis depends on the rate of recombination between the two loci. If linkage is tight, F1 superiority is nearly halved in the F2. But if the two genes are independent, heterosis is maintained in the F2 at the same level as in the F1.