Recessive lethal germline and specific locus somatic mutations were induced efficiently in the zebrafish by exposure of mature sperm to UV light. Mutagenesis of sperm yielded mosaic individuals: clones bearing novel mutations represented approximately 12–25% of the haploid germ cells and 25–50 % of the somatic tissue. Simple methods are described for the reliable identification and propagation of newly arising developmental mutations in zebrafish.

Initial experiments demonstrated that the plasmid R6K cannot be transferred to or maintained readily in the E. coli DNA polymerase I deficient strain JG138 polA1. Results with E. coli MM386 polA12 (R6K), which has a temperature sensitive polymerase I enzyme, showed cell division becomes abnormal when the polymerase I enzyme of the host bacteria is inactivated at the restrictive temperature. Under conditions of polymerase I deficiency, R6K replication, as measured by monitoring R-factor-mediated β-lactamase activity, also becomes abnormal with the loss of multiple R6K copies per cell and the apparent maintenance of a single R-factor copy per cell.

To examine the effects of X-chromosome imprinting during early mouse embryogenesis, we attempted to produce XM0, Xp0, XMXMY, XMXPY and XMXMXP (where XM and Xp stand for the maternally and the paternally derived X chromosome, respectively) making use of mouse strains bearing the translocation Rb(X.2)2Ad and the inversion In(X)1H. Unlike XMXPY embryos, XMXMY and XMXMXP conceptuses suffered from severe growth retardation or abnormal development characterized by deficient extra-embryonic structures at 6.5–7.5 days post coitum (dpc). A cytogenetic study suggested that two XM chromosomes remaining active in certain non-epiblast cells were responsible for the serious developmental abnormality found in these embryos disomic for XM. Although matings involving females heterozygous for Rb(X.2)2Ad hinted at the paucity of XP0 embryos relative to those having the complementary karyotype of XMXMXP, further study of embryos from matings between females heterozygous for In(X)1H and Rb2Ad males did not substantiate this observation. Thus, the extensive peri-implantation loss of XP0 embryos shown by Hunt (1991) may be confined to XO mothers. Taken together, this study failed to reveal a parentally imprinted X-linked gene essential for early mouse embryogenesis other than the one most probably corresponding to the X-chromosome inactivation centre.

A pedigree analysis of several cell-colony generations following a mutagenic treatment with nitrous acid has shown that in S. pombe a genetic instability is produced that replicates several times and produces a mutation in independent lines.

It has been shown that the mutants isolated in the progeny of a mosaic colony all contain a genetic alteration that cannot be resolved by genetic analysis and therefore the mutations have occurred at the same genetic site. This finding is confirmed by interallelic complementation and phenotypic analyses.

Skin and fleece traits have been characterized in four lines of Merino sheep selected for high- and low-fibre diameter (D±) and staple length (L±) from a medium-woolled flock. Over a period of 20 years, each line responded in the desired direction, producing fleeces composed of thick or thin fibres and long or short wool staples. However, variations in the amounts of wool grown that might be expected from these procedures were compensated by changes in unselected characters. Thus a predicted difference in fleece weights between high and low staple length lines was reduced by an increase in fibre crimp frequency in L− sheep. Similarly, changes induced in fibre diameter in the D lines resulted in small effects on fleece weight in comparison to the large (and inverse) effects on follicle numbers. Towards the end of the selection regime, mean follicle density in D− sheep was twice that of D+ sheep. This intriguing response within the follicle population was examined further: an analysis of the relationship between follicle density and fibre diameter amongst the four lines revealed a highly significant, negative linear correlation. The implication of this statistical association is that the numbers of follicles initiated in skin during foetal life had a direct bearing on the sizes of wool fibres eventually produced. It was concluded that both features must be under the control of a single developmental mechanism. Since the expression of each of the characters is separated in time, the mechanism must be activated during the earlier event, i.e. at or before the phase of follicle initiation.

In devising maps of the positions of gene loci along chromosomes, by measurements of crossing-over, it is usual to assume that the chiasmata which give rise to the crossing-over are randomly located, unless there is evidence to the contrary. If chiasmata are in fact preferentially located at certain points or regions this not only affects mapping, but also is of interest for population genetics since it may favour the development during evolution of blocks of genes relatively undisturbed by crossing-over. Preferential localization of chiasmata is well known in a number of disparate organisms (Darlington 1965; John & Lewis, 1965), but has so far been little studied in mammals. Evidence is presented suggesting tha chiasmata are in fact non-randomly located in certain chromosomes of the mouse.

Genetic analysis of 12 mutants of Escherichia coli K12 defective in D-alanine dehydrogenase showed that alnA and dad are alternative names for the same locus. dad was shown to be a single gene which codes for a protein of 55000–60000 mol. wt. Study of thermosensitive mutants of dad indicated that its product is a structural component of D-alanine dehydrogenase. The regulatory gene alnR was shown to be involved in positive control of dad expression. This was concluded from (i) the absence of constitutive strains among Dad+ revertants of alnR– mutations, (ii) the trans dominance of alnR+ to alnR–, and (iii) the failure to isolate fully constitutive strains by any means. To obtain a uniform nomenclature it is proposed to re-name dad as dadB and alnR as dadQ.

Using a mouse cDNA probe encoding for the major part of peripherin, a type III intermediate filament protein, we have assigned, by in situ hybridization, the mouse and human peripherin genes, Prph, to the E–F region of chromosome 15 and to the q12–q13 region of chromosome 12, respectively. These regions are known as homologous chromosomal segments containing other intermediate filament genes (keratins) and also other genes which could be co-ordinately regulated.

Two series of 12½ day mouse chimaeric conceptuses were produced by aggregating (C57BL × CBA)F2 strain preimplantation embryos with embryos that differed at the Gpi-1s locus that encodes glucose phosphate isomerase, GPI-1. The composition of individual issues was evaluated by quantitative electrophoresis to estimate the % GPI-1A in the chimaeric tissue containing GPI-1A and GPI-1B. In one series of chimaeras, the GPI-1A cells were derived from a backcross between inbred BALB/c strain females and (BC × BALB/c)F1 males, where BC is the partly congenic strain C57BL/Ola.AKR-Gpi-lsa,c/Ws. In the other series of chimaeras, the GPI-1A cells were derived from the reciprocal backcross between (BC × BALB/c)F1 females and inbred BALB/c strain males. The [(BC × BALB/c)F1 female × BALB/c male] ↔ (C57BL × CBA)F2 series of chimaeras was reasonably balanced so that GPI-1 A and GPI-1B cells were fairly equally represented in the foetuses, placentas and extraembryonic membranes (tissue means: 37–51 % GPI-1A). This series did not differ significantly in composition from an earlier series of (BC × BALB/c)F2 ↔ (C57BL × CBA)F2 chimaeras. However, the [BALB/c female × (BC × BALB/c)F1 male] ↔ (C57BL × CBA)F2 series of chimaeras was unbalanced, with mean tissue compositions (28–33% GPI-1A) that were intermediate between the above two balanced series and the unbalanced (BALB/c × BALB/c) ↔ (C57BL × CBA)F2 series (tissue means: 14–22% GPI-1 A), that was studied previously. Thus, both (BALB/c×BALB/c) and [BALB/c×(BC x BALB/c)F1 embryos contributed less to the tissues of chimaeric conceptuses than either (BC × BALB/c)F2or [(BC × BALB/c)F1 × BALB/c] embryos. This implies that embryos from BALB/c mothers contributed less to the tissues of chimaeric conceptuses than embryos from (BC × BALB/c)F1 mothers. We, therefore, conclude that a maternal genetic effect is responsible for some of the differences in composition among the four groups of chimaeras. This maternal effect must act before the 8-cell stage but it is not yet known whether it is mediated via cytoplasmic inheritance, genomic imprinting or by the reproductive tract. Evidence that a maternal effect retards preimplantation development of embryos from BALB/c females is reviewed and the possibility that this might cause them to contribute poorly to chimaeric conceptuses when aggregated with more precociously developing embryos is discussed.

The effect of ultraviolet radiation (u.v.) on λ lysogens of exrA strains of Escherichia coli was studied. exrA strains could be lysogenized with, as well as support the vegetative reproduction of, λ. However, though spontaneous induction of λ occurred in exrA(λ) strain at 10% the frequency of exrA+(λ) strain, exrA(λ) strains were not induced by u.v. Because λ was not induced in exrA(λ) strains, lysogens of these strains were no more sensitive to u.v. than were non-lysogens.

The heat-inducible mutant λhcI857 could be induced in exrA strains at elevated temperatures. Furthermore, u.v. irradiation of exrA (λhcI857) strain did not prevent the heat induction of this λ mutant. The exrA mutation appeared to interfere only with the inactivation of λ repressor by u.v.

Among the exrA strains studied was strain Bs1(exr A uvrB). Whereas the λ lysogen of strain Bsl could not be induced by u.v. and was no more sensitive to u.v. than its non-lysogen, the exrA+uvrB(λ) derivative of strain Bsl could be induced by u.v. and was more sensitive to u.v. than its non-lysogen.

The autosomal recessive gene muted, mu, which arose spontaneously, dilutes coat and eye colour and causes absence of otoliths in some but not all homozygotes. Its locus is in linkage group XIV of the mouse, and the order of loci was shown to be bg–Xt–sa–mu–f–pe.