The ability to repress P-element-induced gonadal dysgenesis was studied in 14 wild-type strains of D. melanogaster derived from populations in the central and eastern United States. Females from each of these strains had a high ability to repress gonadal dysgenesis in their daughters. Reciprocal hybrids produced by crossing each of the wild-type strains with an M strain demonstrated that repression ability was determined by a complex mixture of chromosomal and cytoplasmic factors. Cytoplasmic transmission of repression ability was observed in all 14 strains and chromosomal transmission was observed in 12 of them. Genomic Southern blots indicated that four of the strains possessed a particular type of P element, called KP, which has been proposed to account for the chromosomal transmission of repression ability. However, in this study several of the strains that lacked KP elements exhibited as much chromosomal transmission of repression ability as the strains that had KP elements, suggesting that other kinds of P elements may be involved.

1. A three-year study was conducted to test the efficacy of inter- and intra-specific blood transfusions in domestic poultry for inducing heritable changes in the recipients. The latter were pure-bred White Leghorns. Pure-bred Broad Breasted Bronze turkeys and New Hampshire chickens served as blood donors to two distinct lines of recipients. All injections started when the recipient chicks were 2–5 days old. Altogether, more than 3000 chicks from blood injected lines were involved in the study, conducted between 1959 and 1961 and distributed between the parental and three subsequent generations. Each injected chick received a total of some 155 ml. of whole blood in the course of a five-month injection period. An adequate number of control (non-injected) birds was used throughout. Observations were made on plumage colour, body-weight, egg-weight, egg-shell colour, fertility and hatchability. Furthermore, blood plasma and muscle tissue of appropriate birds were subjected to immunological, chromatographic and electrophoretic analyses.

2. On the basis of all these criteria, no evidence of heritable shifts in the direction of the donor organism was discerned among birds belonging to either of the two treated lines.

The relationship between the transfer systems of several plasmids was investigated, using as criteria complementation of a series of transfer-deficient Flac mutants, the efficiency of plating of F-specific phages, and identification of surface exclusion systems. The transfer systems of ColV2 and ColVBtrp were similar to that of F except for surface exclusion: ColVBtrp specified a surface exclusion system different from that of F, and ColV2 did not specify any detectable system. The transfer system of R1–19 was also similar to that of Flac, but the products of traA, traI and traJ were plasmid-specific. R1–19 determined the same surface exclusion system as ColVBtrp, and this was under the control of the transfer inhibitor. The transfer systems of ColIbdrd and Flac were unrelated. ColEl was transferred by Flac traI− mutants, but not by mutants in other cistrons.

Sorting out of cytoplasm determinants can be achieved in Podospora anserina by the use of protoplasts. In this way four cytoplasmic mutations have been isolated. These mutations affect a precise stage of development of the fungus. In crosses with wild-type strains, the mutants show maternal inheritance when no cytoplasmic contact precedes fertilization. However, when cytoplasmic mixing occurs before fertilization, the cytoplasmic wild-type factor shows dominant and/or suppressive properties over the mutant factor.

Three Harwich P sublines with different P-element activity potential were used to investigate the influence of P-derived chromosomes on snω mutability and vg suppression and to relate the induction of these dysgenic traits to the number and structure of P elements. Destabilization of the snω allele, a measure of P transposase activity, was differentially influenced by the major autosomes. Chromosome 2 of the standard Harwich subline, Hw, induced only 60% of the level of mutability relative to chromosome 3, whereas chromosome 3 of the weakest Harwich subline, Hf, induced only 50% of the mutability relative to chromosome 2. In somatic suppression of the vg21–3 allele, chromosome 3 of the Hf subline produced a lower level of complete suppression as compared to chromosome 3 of the Hw or the Hs subline (the high hybrid-dysgenesis-inducing subline). The level of these dysgenic traits and GD sterility, was not correlated with the number of P elements per individual (67–68) or per chromosome arm which was very similar among the sublines. The number of complete P elements per genome, based on Southern blot analysis of the X and major autosomes, ranged from 15 to 19. Destabilization of the snω allele and vg suppression by chromosome 3 was correlated with a greater number of complete P elements. Two novel unexpected observations emerged from these studies: both snω mutability and vg suppression data demonstrated high P-element activity in hybrids derived from non-dysgenic crosses irrespective of Harwich subline, indicating a lack of P-cytotype regulation. Mutability in non-dysgenic males ranged from 40 to 60% of the level found in dysgenic males. The high snω mutability and low GD sterility in non-dysgenic hybrids suggests that these traits may arise by a different mechanism.

The semi-dominant X-linked gene tabby (Ta) in the mouse, and one of its recessive autosomal mimics, downless (dl) each produces a mutant syndrome that includes absence of hairs on the tail due to failure of tail hair follicle initiation. However, whereas downless tails failed to produce hair follicles in culture on the chick chorioallantoic membrane, which is in keeping with the adult phenotype of both downless and tabby mice, tabby tails produced follicles at about 40% of the control level. Furthermore, in contrast to previous findings for downless, the culture of mixed genotype epidermis-dermis combinations provided no evidence of a primary epidermal effect in tabby.

The murine mutation, Cat Fraser (CatFr), causes dominantly inherited ocular cataracts. Lenses of adult mice bearing this mutation contain reduced amounts of all seven γ-crystallin proteins and their corresponding transcripts. Levels of other lens proteins and transcripts appear normal and no extra-ocular effects of the mutation have been observed. The selective effect of this mutation on the γ-crystallins is consistent with the possibility that the site at which it occurs is involved in the coordinated regulation of the family of genes which encodes them. We have shown that several restriction fragment length polymorphisms in the γ-crystallin genes segregate independently of the CatFr mutation. Therefore, despite its selective effect on the expression of the γ-crystallin genes, the mutation is not linked to them. This observation rules out the possibility that the mutation is in a cis-acting regulatory site.

A total of 207 wild mice trapped at different localities in southern Germany were tested for the presence of antigenic determinants controlled by class I genes (K and D) of the H-2 complex. The test was based on the complement-dependent killing of lymphocytes in the micro-cytotoxicity assay. Both private (allele-specific) and public (shared) determinants were tested using polyclonal and monoclonal antibodies. The results of the H-2 typing were in agreement with karyological typing which divided the sampled mice into 5 populations. Each population was characterized by a certain antigenic profile (occurrence of individual determinants at certain frequencies); the profiles of the individual populations were sufficiently unique to differentiate these populations but at the same time sufficiently similar to indicate common origin of the populations. The karyological typing of the same mice reveals that all 5 populations share 1 pair of metacentric chromosomes, Rb(4.12)1Tu, but that, in addition, each population has at least one metacentric chromosome differentiating it from other populations. We interpret these findings as evidence that all wild mice in southern Germany stem from a common stock in which the Rb(4.12)1Tu translocation became fixed and which subsequently differentiated into the individual populations. This differentiation is accompanied by the fixation of new Robertsonian translocations (different ones in different populations) and the acquisition of characteristic H-2 antigenic profiles.

A locus, Dlb-1, controlling the binding of the lectin from Dolichos biflorus to the intestinal epithelium and vascular endothelium of mice has been located on chromosome 11, 3.1 ± 1.4 centimorgans proximal to Rex, using recombinant inbred strains and conventional backcrosses with three-point linkage tests.

The two alleles so far discovered at this locus behave unusually. The Dlb-1a allele causes binding to the vascular endothelium but not to the intestinal epithelium while Dlb-1b induces the exact reciprocal binding pattern, and the heterozygote shows both patterns.

Some quantitative implications of the gene conversion models of Holliday and Whitehouse & Hastings are discussed. These models predict two kinds of mispairing when a heterozygous mutant is in hybrid DNA. It is pointed out that the latter model, in contrast to statements in the literature, does not require identical repair rates in both kinds of mispairing.

Furthermore, some peculiarities are discussed which result if, among the corrected fractions of hybrid sites, the frequency of repair to wild-type is the same in both kinds of mispairing (r = s). In the Holliday model a minimum results under this condition for the frequency of asci which show a normal 4:4 segregation, but which have originated by repair from meioses with hybrid DNA.

Plasmodial formation in the myxomycete Physarum polycephalum is controlled by a mating type (mt) locus, with heterothallic amoebae normally being unable to form plasmodia in pure clones. We report the isolation by mutagenesis of selfing mutants from heterothallic strains, and their analysis. Various amoebal strains of different mating types were mutagenized with a range of mutagens, and a number of selfing mutants (designated Het−) were isolated. A specific sensitivity of mt2 amoebae to mutagenesis by NMG was observed. This sensitivity segregated as a single locus closely linked or allelic to the mt2 locus. When the Het− clones were incubated at 30 °C, selfing was greatly inhibited. This property was used to determine the mt specificities of four Het− clones. The process of plasmodial induction in pure clones of CL was also studied using the 30 °C temperature effect.

In this report we examine the meiotic segregation of compound second autosomes sharing varying extents of heterochromatic and euchromatic homology. The second chromosome heterochromatin does not appear to influence the random meiotic segregation of compound second autosomes during spermatogenesis; however, the proximal euchromatin is implicated in male meiotic pairing. We conclude that male autosomal meiotic pairing sites are specific euchromatic chromosomal regions.

Sandy (sdy) is a mouse mutant with diluted pigmentation which recently arose in the DBA/2J strain. Genetic tests indicate it is caused by an autosomal recessive mutation on mouse Chromosome 13 near the cr and Xt genetic loci. This mutation is different genetically and hematologically from previously described mouse pigment mutations with storage pool deficiency (SPD). The sandy mutant has diluted pigmentation in both eyes and fur, is fully viable and has prolonged bleeding times. Platelet serotonin levels are extremely low although ATP dependent acidification activity of platelet organelles appears normal. Also, platelet dense granules are extremely reduced in number when analysed by electron microscopy of unfixed platelets. Platelets have abnormal uptake and flashing of the fluorescent dye mepacrine. Secretion of lysosomal enzymes from kidney and from thrombin-stimulated platelets is depressed 2- and 3-fold, and ceroid pigment is present in kidney. Sandy platelets have a reduced rate of aggregation induced by collagen. The sandy mutant has an unusually severe dense granule defect and thus may be an appropriate model for cases of human Hermansky-Pudlak syndrome with similarly extreme types of SPD. It represents the tenth example of a mouse mutant with simultaneous defects in melanosomes, lysosomes and/or platelet dense granules.