1. Serial cytological observations were made on one abnormal seedling from the thornless segregants of the F2 progeny from crossing two tetraploid (2n = 28) Rubus species. The number of root-tip chromosomes was found to vary between 9 and 46 per cell, with the mode always at 35. The wide variation in chromosome number decreased with time, until there was almost stability at 2n = 35. A vegetative (stipule) cell was 2n = 39. The numbers lower than 35 were not due to terminal fusion.

2. Evidence from the number of satellites per cell suggests that not always were the same chromosomes being eliminated, although there is a general increase in satellite number with increased numbers of chromosomes per cell.

3. There was a correlation between the chromosome numbers and corresponding cell sizes within the aneuploid series. This may be associated with the incremental change of DNA following the addition or subtraction of individual chromosomes, which are highly similar in Rubus.

4. The cause of the instability was not definitely established. Its initiation is probably attributable to the egg mother cell, as Rubus pollen reacts sensitively to chromosome unbalance. No abnormalities were observed in the mitoses, and virus infection was not responsible for the instability.

5. Chromosome number instability of this plant is discussed in relation to other examples from the same and different genera: it is suggested that the changes in chromosome number known in various Rubi may have arisen somatically.

Linkage relationships of three gene markers of chromosome 17, namely Brachyury (T), tufted (tf), and Histocompatibility-2 (H-2), to the break-point of T(16; 17)43H male sterile translocation were established. The following order was found: T−tf−T43H−H-2. In all cases the translocation break was found in cis to H-2k, haplotype, no recombinant being found among 218 backcross individuals examined. More than 60 viable and fertile animals trisomic for the proximal part of chromosome 17 (including T-t genetic complex) have been recovered among progeny of T43H/+ female translocation heterozygotes as a result of adjacent −2 disjunction at first meiotic division. Mutation tf has been assigned to band 17B in chromosome 17 by comparing the location of T190Ca and T43H genetic and cytological breakpoints. Recombination between centromere 17 and T43H break was reduced almost to zero in the presence of Rb(16.17)7Bnr translocation. The unexpected restoration of male fertility was observed in T43H/Rb7Bnr hybrids (T43H/+ males being completely sterile) which made it possible to prepare the first homozygotes for T43H male–sterile translocation. Direct estimation of chiasma frequencies in centromere 17−T43H region indicated an 11 cM distance between the centromere 17 and the proximal end of t12 haplotype. The significance of centromere −t (or H-2) distance on the predictable restrictions of the possible haploid manifestation of T-t or H-2 gene products on sperm membrane is discussed.

The dimeric enzyme glucose phosphate isomerase (GPI-1) is regulated in oocytes by a cis-acting temporal gene (Gpi-1t) that maps close to the structural gene (Gpi-1s). Quantitative cellulose acetate electrophoresis of GPI-1 allozymes from unfertilized eggs produced by various Gpi-1sa / Gpi-1sb heterozygous females revealed a new Gpi-1t allele that we have designated Gpi-1tc. This allele is present in 101/H mice and a partially congenie stock that carries the Gpi-lsa gene derived from the AKR strain. We have confirmed that Gpi-1tc is closely linked to Gpi-1s and that it is cis-acting. It produces higher levels of GPI-1 in unfertilized eggs than the other two Gpi-lt alleles that are known (Gpi-1ta and Gpi-1tb) but has no effect on GPI-1 in somatic tissues or spermatozoa. This new Gpi-1t allele represents a third developmental programme for GPI-1 expression in oocytes.

Perculiarities of preimplantation and early postimplantation development were studied in embryos with partial deletions and duplications of chromosomes 7, 9, 14 and 17, in the progeny of mice heterozygous for the unequal reciprocal translocations T(7; 14)2Iem, T(16; 17)43H and T(9; 17)138Ca. Deficiencies for any part of autosomes 9 or 14 combined with duplications of the corresponding segments of autosomes 7 or 17 do not affect preimplantation development, though they are lethal soon after implantation. Deficiency for the distal part of chromosome 7 (Df7F4) induces embryonic death by the early blastocyst stage. Deficiencies for the distal part of chromosome 17 (Df17El–E5), as well as for its proximal region (Df17AB) carrying all genes of the T-t complex, have no detrimental effects on cleavage, blastulation and implantation, but are lethal after implantation, mostly during early neurulation. Deficiency for the middle part of chromosome 17 (Df17CD) is expressed just after a few cleavage divisions, and these embryos all die by the morula stage. It is suggested that the genes of the CD region of chromosome 17 and of the F4 region of chromosome 7 are of major significance for genetic control of early development in the laboratory mouse.

Electrophoretic studies on starch gel demonstrated the existence in the European eel of four haemoglobins, not two as believed from agar gel studies. The two minor fractions have been shown to be neither polymers nor methaemoglobin derivatives of the two principal fractions.

The esterase zymograms of eel sera exhibit up to eight fractions. The individual differences observed suggest genetic polymorphism and the same applies to the esterase pattern of various tissues.

This approach is of value for the collection of phenotypic frequency data with a view to solving the Atlantic eel problem.

Wild-type Friend murine leukaemia (clone 707) cells and two thymidinekinase-deficient subclones, 707BUE and 707BUF, were compared for sensitivity to killing and mutagenesis by the chemical mutagens, ethyl methane sulphonate (EMS), N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), mitomycin C (MMC), and methyl methane sulphonate (MMS). The two thymidine-kinase-deficient subclones were significantly more sensitive to killing by each of the four chemical mutagens than were wild-type cells. The increased sensitivity to killing by the four mutagens was also reflected in increased mutagenesis (per unit dose of mutagen) to 6-thioguanine resistance. In the light of these results, the significance of thymidine kinase in DNA repair and mutagenesis is discussed.

The basis of inheritance of the extra cytoproct (XP) character in Paramecium tetraurelia, stock d4-154, is shown to be nuclear and probably a single dominant gene, Ec, with reduced penetrance in heterozygotes. When the mutant gene is replaced by its wild-type allele, loss of the XP phenotype in some lines of descent occurs before 15 cell generations, but in more than half of the lines this occurs after 15–120 or more cell generations. The possibility is considered that these extremely long and variable ‘lags’ may be due to extranuclear (cortical) inheritance of cortical changes initially produced by gene action.

Male mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

The T/t–H-2 region on mouse chromosome 17 is known from complex natural variants (‘t-haplotypes’) to contain numerous genes, including some affecting the immune system and the development of the embryo. Rapid progress in the isolation of recombinant DNA clones for this 50 megabasepair region is generating the material for its complete molecular anatomy. A crucial step in revealing the biological functions controlled by the region is to obtain mutants in which genes are inactivated individually. We have used a pair of inbred mouse strains and a series of classical breeding schemes that permit the detection of recessive lethal and detrimental mutations in the T/t–H-2 region.

In this initial phase of our study, 280 gametes mutagenized in the male germ line by ethylnitrosourea (ENU) have yielded eleven independent pre-natal recessive lethal mutations. Four have been mapped against T mutations and have been shown to complement one another in all pairwise combinations.

Oocyte pachytene analysis of embryos heterozygous for the fd translocation confirmed the facts of this translocation as described by Ohno and Cattanach. Besides that it revealed that a small piece of the X-chromosome has been transferred to the autosome where in about 25% of cases it shows less stainable expansion.

Chromosome 5R of Secale cereale var. Imperial has been substituted for chromosomes 5A, 5B and 5D of hexaploid wheat. There is evidence of compensation, in terms of vigour, in all substitution lines. Chromosome 5R rectifies the male sterility of nullisomics 5A and 5D; however, it is unable to circumvent the meiotic irregularity and male sterility of 5B-deficient stocks. Another instance of wheat-rye chromosome pairing, in the absence of chromosome 5B, is reported. The data reported here demonstrate that the long arm of 5R is the more essential arm and indicate that chromosome 5R is homoeologously related to the group 5 chromosomes of wheat.

Populations of Drosophila melanogaster were subjected to selection for differing oviposition preference under allopatric and sympatric conditions. Flies were presented with the choice of a potato-based medium and a medium containing sugar and killed yeast on which to lay their eggs. Some gene flow was possible under sympatric conditions. In the allopatric lines selection was successful in rapidly generating an increased preference for sugar, and in the sympatric lines divergent oviposition preferences were generated in two cases out of four. A significant degree of reproductive isolation between one pair of allopatric lines was generated after eighteen months of selection.

Eggs from reciprocal hybrids between the C57BL/6By and BALB/cBy strains were tested for their susceptibility to attack by hyaluronidase and pronase. There were significant reciprocal differences between the F1 females in the responses of their unfertilized eggs to both enzymes. The F1 hybrids from BALB mothers showed the increased susceptibility characteristic of C57BL whilst the F1 hybrids with C57BL mothers were more resistant to both enzymes, like BALB mice. Eggs from the four kinds of reciprocal F2 hybrid females also showed patroclinous patterns of susceptibility. A patroclinous difference was found between reciprocal crosses of the CXBD and CXBE recombinant inbred strains but not in crosses between recombinant inbred strains with similar phenotypes. Cross fostering did not alter the phenotypes of the C57BL and BALB females or those of their reciprocal F1 hybrids. The findings are interpreted in terms of differential genomic imprinting of paternally inherited information. The possible general usefulness of patroclinous differences between reciprocal F1 females in revealing differences in imprinting is noted.

Complementing diauxotrophic mutants of P. glycinea were mated in combination in which one or both mutants contained a resistance plasmid. The transfer of chromosmal markers was scored by the appearance of prototrophy at one or more of the auxotrophic loci. The resistance plasmid RP1 was equally or slightly more efficient than R6886 in the transmission of chromosomal genes.