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.

Pyruvate kinase activity was studied in kidney extracts of mice from various sources. One C57BL/6J female among several hundred examined expressed activity approximately one half of the normal level. This animal transmitted the trait, and a single gene responsible for the activity difference was identified and mapped to chromosome 9. Linkage with Mod-1 and dilute was established. A spontaneous mutation in the C57BL/6J strain apparently was responsible for the variant pyruvate kinase.

In order to understand the evolution of genetic systems in which two genes are tandemly repeated (small multigene family) such as has been recently found in the haemoglobin α loci of primates, haemoglobin β loci of mouse and rarbit and other proteins, a population genetics approach was used. Special reference was made to the probarility of gene identity (identity coefficient), when unequal crossing-over is continuously occurring as well as random genetic drift, inter-chromosomal recombination and mutation. Two models were studied, cycle and selection models. The former assumes that unequal crossing-over occurs in cycles of duplication and deletion, and that the equilibrium identity coefficients were obtained. The latter is based on more realistic biological phenomena, and in this model it is assumed that natural selection is responsible for eliminating chromosomes with extra or deficient gene dose. Unequal crossing-over, inter-chromosomal recombination and natural selection lead to a duplication-deletion balance, which can then be treated as though it were a cycle model. The basic parameter is the rate of duplication-deletion which is shown to be approximately equal to 2(u + 2β)X, where u is the unequal crossing-over rate, 2β is the inter-chromosomal recombination rate and X is the frequency of chromosomes with three genes or of that with one gene. Genetic variation of the globin gene family, of which gene organization is known in most detail, is discussed in the light of the present analyses.

The non-random X chromosome expression that has been observed with coat markers in female mice heterozygous for the Xce alleles, Xcea and Xceb, has now been investigated with the electrophoretic enzyme marker, Pgk-1. Because the Xce status of the Pgk-1a marked chromosome was not known, PGK expression was assessed in Pgk-1a/Pgk-lb heterozygotes which carried either Xcea or Xceb on their Pgk-1b chromosome. The PGK-1A allozyme was found to predominate in both genotypes but when Xceb was present on the Pgk-lb chromosome the expression of the two allo-zymes was less unequal. This effect was seen in both liver and kidney of adults and to at least the same degree in embryos aged 13·5 and 7·5 days. The results have been interpreted to mean that the non-random X expression derives from a primary non-randomness of the X inactivation process and that a new and more extreme Xce allele, designated Xcec, was present on the Pgr-1a-marked X chromosome.

Cockerels singly or doubly heterozygous (t1/ +, t2/ + and tl/t2, respectively; collectively heterokaryotypic, HTK) for two different Z-autosome translocations (t1, t2) produce an array of chromosomally balanced and unbalanced spermatozoa owing to adjacent segregation and nondisjunction at the first meiotic division. This study addresses the developmental capacity of embryos derived from matings of control ( + / + ) and HTK (tl/ +, t2/ +, tl/t2) cockerels with hens bearing normal chromosome complements (+ /W).

Estimates of the hatchability of fertile eggs sired by + / +, tl/ +, t2/ + and tl/t2 cockerels were 82·8%, 43·0%, 41·3% and 10·9%, respectively. Approximately 75% of the mortality observed in embryos sired by HTK cockerels occurred by four days of incubation. Developmental arrest generally occurred earlier in embryos sired by t2/+ and tl/t2 cockerels than in those by tl/ + cockerels. These differences reflect variation in the degree of embryonic chromosome unbalance expected among embryos of the different sire groups. The pattern of mortality after three days was similar in embryos sired by HTK cockerels. In control embryos, mortality was highest on days 20–21 of incubation.

Chromosome analysis of 16/18 h embryos, day 1/5 embryos and hatched chicks sired by HTK cockerels revealed that most, if not all, chromosomally unbalanced embryos died during development; the majority before three days of incubation. Partial monosomy for chromosome one was found to be more deleterious to embryonic development than partial trisomy.

Mutants of [psi] a cytoplasmically inherited factor in the yeast Saccharomyces cerevisiae were isolated after treatment with a variety of agents including conventional mutagens and a number of compounds which cause loss of [psi] at high frequencies, namely methanol, KCl, dimethyl sulphoxide and guanidine hydrochloride. In [psi−] mutants the suppressor SUQ5 does not suppress ochre mutations such as ade.2.1.

Reversion analysis of the [psi−] mutants revealed three classes: (1) a class of agents producing [psi−] mutations which could readily revert to [psi+] (methanol, KCl and dimethyl sulphoxide belong to this class), (2) those which could not be shown to revert (GuHCl) and (3) the conventional mutagens which produced both revertible and apparently non-revertible [psi−] mutations. We conclude that GuHCl causes a deletion or loss of the [psi] factor. Methanol may cause an alteration of ‘state’ for example, of a promoter, and KCl may be selecting or inducing low copy number variants of [psi+] strains. It is possible that DMSO may be involved in regulation of [psi].

The electrophoretic variants of the X-chromosome-linked enzyme phosphoglycerate kinase (PGK-1) have been used to investigate the randomness of X chromosome expression in the fetus and various extra-embryonic membranes of the mouse conceptus. The amnion shows essentially random expression of the maternally derived X chromosome (Xm) and the paternally derived X chromosome (Xp). The parietal endoderm, however, shows exclusive or preferential expression of Xm. The results support the idea that the randomness of X chromosome expression is correlated with embryonic cell lineage such that Xm is preferentially (perhaps exclusively) expressed in derivatives of the primitive endoderm and trophectoderm but that Xm and Xp are randomly expressed in the derivatives of the primitive ectoderm.

Experiments involving ovary transplants, embryo transfers or crosses with heterozygous mothers confirm previous findings that Xm is preferentially expressed regardless of the X chromosome expressed in the reproductive tract. Additional experiments show that the preferentially expressed X chromosome in the parietal endoderm and visceral yolk sac endoderm of a normal XmXp conceptus is always Xm regardless of grand-parental origin of Xm and regardless of whether the mother is a normal XX female or an XO female. Xp is, however, expressed in these tissues hi XpO female conceptuses. It is argued that a form of chromosome imprinting occurs at each generation to mark Xm and Xp as different and that this difference influences the choice of which X chromosomes are expressed in each cell lineage.

The rudimentary locus of Drosophila melanogaster contains the structural information for the first three enzymes of the de novo pyrimidine pathway. Two new rudimentary (r) mutants have been isolated following mutagenesis with ICR-170. From complementation analysis and cyto-genetical observation both were shown to be deficiencies which expose the r locus. Df(1)r19 is deleted from band 14D1 to 15D1 and Df(1)r1D from band 14B6 to 15A2. These deficiencies were combined with several characterized r alleles each giving a single enzymatic defect in one of the first three enzymes of the pyrimidine pathway. An unusual semilethal trans effect was observed in some but not all the combinations. The effect was not observed with a third smaller deficiency which also exposes the rudimentary locus.

The major type I insert sequence for the 28S rRNA genes of Drosophila melanogaster has been mapped within the chromosomes using a probe synthesized from a cloned sequence containing the entire 5·4 kb segment. The genomic distribution was shown to be complex in that the insert sequence occurred next to many different types of sequences, in addition to occurring as an insert in the 28S rRNA genes of the X chromosome. In situ hybridization of mitotic chromosomes showed most of the insert units not contained in the ribosomal genes to be located near the ribosomal gene cluster on the X chromosome. Additional sites were detected in polytene chromosomes in region 102C, 8–12 and in the hetero-chromatin of the autosomes.

The possibility of using Hordeum bulbosum Crosses to facilitate production of disomic wheat–barley addition lines from monosomic additions was investigated. Aneuhaploids with 22 chromosomes were obtained in the expected gametic frequencies after crossing monosomic, disomio and monotelo-disomic addition lines, involving four different barley chromosomes, as the female parent with tetraploid H. bulbosum. Thus the added barley chromosomes were not eliminated when preferential elimination of the bulbosum chromosomes took place in the hybrid embryos. Disomic addition lines were obtained after treating the aneuhaploids with colchicine. This method could have wider application in the production of other wheat–alien chromosome disomic addition lines, especially where the transmission frequency of the alien chromosome through the pollen is very low, but its use will depend on the wheat parent being crossarle with H. bulbosum and the alien chromosome being retained during the elimination of bulbosum chromosomes.