Four isolated populations of the skipper frog, Rana cyanophlictis were first studied in 1965 and then again in 1975. The genetical changes were measured by the incidence of 19 non-metrical skeletal variants. It was found that these populations have changed very little in 10 years, although the inter-population diversity, as judged by the estimates of divergence, is less now than previously. This could be due to the similar environmental conditions prevailing in Delhi and its neighbourhood from where these frog populations were collected.

The alcohol dehydrogenase-1 gene in maize presents advantages for mutational analysis. Foremost among these is the ability to chemically select ADH-negative and ADH-low gametophytes owing to their resistance to allyl alcohol vapour. Immature tassels were irradiated with either 220 kV X-rays or 400 MeV/amu accelerated neon-ions; spontaneous mutants were also selected and recovered. RBE for neon-20 was about 5. A total of 70 presumptive mutants were placed into one of four classes on the basis of allozyme profiles following electrophoresis and ADH staining: (A) dysfunction, (B) underproducer, (C) overproducer, and (D) up-Adh2 gene. Mutants have been recovered and confirmed in the first three classes. These include two male-transmissible deletion-type lesions induced by X-rays, five underproducer transpositions and one overproducer transposition induced by neon-20. Certain of the neoninduced alleles are unstable in their expression. All 70 mutants are chromosomal aberrations; no intragenic lesions were recovered although our experimental design would have preferentially recovered them if they had occurred.

The Discussion considers the mutagenic action of ionizing radiation, and especially the well-documented differences between maize and Drosophila data. In particular, the effect of these chromosome derangements on the ‘programmable’ component(s) of the Adhl cistron is discussed.

Combining data from mitotic crossing over in, and haploidization of, heterozygous diploid strains, 33 markers have been mapped successfully in Verticillium spp. One marker (Hyl), which determines the absence of darkly pigmented resting structures in many stable hyaline strains, showed an irregular segregation. In view of previous evidence from acriflavine treatment and heterokaryon analyses in the fungus, this further substantiated indications of a cytoplasmic pattern of inheritance for this marker. The phenotypic expression of dark pigment genes showing nuclear inheritance, such as Sot., depends upon the cytoplasmically determined (Hyl+) presence of resting structures.

Mice homozygous for the asebia mutation (ab/ab) are char1acterized by defective sebaceous glands, a short sparse hair coat from 7 days and progressive alopecia. In addition, we have found that the initial hair follicle rudiments in the skin of these mice are able to differentiate into relatively normal anagen follicles which are often excessive in length and have minor abnormalities of the inner and outer root sheath components. The inner root sheath fails to form the typical transverse corrugations at the level of the sebaceous glands and its cells apparently remain, partially undegraded, plugging the hair canal and adhering to emerging hair shafts. Defects noted in the outer root sheath may be responsible for the failure of inner root sheath degradation. With increasing age, irregularities in hair cycle duration, loss of the originally parallel arrangement of hair follicles and further abnormalities of the individual follicular components are increasingly evident. Follicles in asebic mice have a tendency to form buds and branches which occasionally begin typical follicular differentiation. The consistent failure of the asebic follicles to pass normally through the catagen stage to the telogen stage results in long twisted follicles with abnormal and often loosely anchored hair clubs. The dermal papillae are often abnormal or absent from telogen follicles, while typical germ cells are not formed. Thus the lack of multiple hair follicles, the disorganization of follicles and the progressive alopecia observed in the asebic mice are accounted for. It is suggested that the altered dermal environment and outer root sheath abnormalities may be responsible for many of the follicular defects.

Contrary to what their name asebia implies, mice homozygous for the ab gene do possess actively secreting sebaceous glands which develop normally from the follicular outer root sheath, at 18 days post-conception. However, by the 20th day post-conception, these mice exhibit the abnormal sebaceous cytodifferentiation which remains typical of the asebic glands throughout life. Nests of outer root sheath cells below the sebaceous glands also undergo atypical sebaceous differentiation. The smooth membrane system and mitochondria, which appear to be responsible for the orderly accumulation of lipid droplets and sebum production in normal mice, become increasingly abnormal in asebic mice. Fewer lipid droplets form, the smooth endoplasmic reticulum becomes distorted and dilated, and the normal transformation of mitochondria does not occur. Atypical differentiation occurs randomly and ‘differentiated’ cells often degenerate within the asebic sebaceous glands. Of the larger specialized sebaceous-type glands studied, only the Meibomian glands are similarly affected by the asebia mutation, while the anal and preputial glands appear to undergo a more normal cytological differentiation. The abnormalities seen in the asebic sebaceous glands seem to be due to defective regulation of the synthetic or degenerative processes necessary for completion of normal sebum production. Both the defects of sebaceous glands and the unusual characteristics of the epidermis and hair follicles in asebic mice may be initiated by the abnormal underlying dermis or the apparently abnormal endocrine system.

Analysis of tetraparental Hfr × F− matings of Escherichia coli strains showed that mating complexes were predominantly pairs or small aggregates of cells. Many physically associated complexes of donor and recipient cells gave rise to no recombinant cells. The observed linkage of genetic markers in recombinants is sensitive to multiple mating events, and should therefore be measured under well-defined conditions giving pairwise matings only.

Adult females from 19 strains of mice were injected with either coumarin or 7-ethoxycoumarin and the urinary excretion of the umbelliferone produced by the metabolism of these substances was measured. With the exception of C57L the strains fell into three classes as follows: high metabolizers (DBA/1 and DBA/2), medium metabolizers (CBA, 129/Rr, NZB and NZW) and low metabolizers (the other 12 strains). The difference in metabolizing ability between the medium group and the low group of strains was also evident when the 4-methyl derivatives of the same two substances were used. However with the 4-methyl derivatives there was no difference in metabolizing ability between the medium group and the high group. The results are interpreted as evidence that the gene Coh on chromosome 7 comprises two closely linked genes which determine cytochrome P-450 isozymes with different substrate specificities.

A combined cytological and genetic analysis has been carried out to determine whether the spontaneous male recombination associated with a line of Drosophila melanogaster derived from Southern Greece (31.1 MRF) involves chromosome breakage and random reunion. In all crosses showing male recombination, extensive abnormalities involving anaphase bridges and fragments were found at first and second meiotic divisions. This confirms that the low level of recombination associated with male recombination lines is not produced by normal, controlled crossing-over of the type found in females, but by chance reunions, following more erratic breakage events at first and second anaphase. In addition the occurrence of some limited premeiotic recombination cannot be excluded. The 31.1 MRF system shows higher recombination levels at elevated temperatures (29 °C) and chromosome abnormality frequency is also greatly increased. The 31.1 MRF induces both male recombination and chromosomal abnormalities at meiosis when it is inherited from females deriving their cytoplasm from stock other than CyL4/Pm. It is concluded that this factor acts independently of sex and that the reciprocal cross effect is caused by a cytoplasmic factor which the 31.1/CyL4 strain inherited from the CyL4/Pm stock.

Curing of an F-prime plasmid by imipramine was most efficient on bacteria growing semianaerobically at 37 °C. The plasmid curing effect of imipramine was increased in the presence of methylene blue, whilst fluorescein, chlorpromazine-sulphoxide and tetraoxyanthrachinon antagonized the plasmid curing action of the drug. In addition to its plasmid curing effect, imipramine treatment selected for Lon mutants at high frequency. Lon mutants show increased resistance to the drug but cured strains, if Lon+, are not resistant.

Incidence of colourblindness among 3325 males belonging to 21 endogamous Dhangar castes (shepherds) of Maharashtra, India, has been reported. Of the 21 castes studied 5 lacked the gene for colourblindness, while in other groups it varied from 1% to 55%, with a series average of 2·65%. The low incidence of observed colourblindness has been discussed in the light of the nomadic way of the life of some of the Dhangar castes. The results have been compared with other nomadic populations of Maharashtra. The results, in general, are compatible with the Post and Pickford's hypothesis of differential selection for colourblindness.