1. Complex hybrids were produced having twenty-nine chromosomes, consisting of one telocentric and twenty complete chromosomes of T. aestivum (2n = 6x = 42), seven complete chromosomes of Ae. speltoides (2n = 2x = 14) and one telocentric chromosome derived from A. elongatum (2n = 10x = 70). The presence of the Ae. speltoides genome permitted pairing between homoeologous chromosomes at meiosis and the behaviour of the two telocentric chromosomes was observed.

2. The A. elongatum chromosome was seen to pair with chromosomes homoeologous to those of group 6. There was no evidence that it paired with chromosomes of any other group.

3. When the A. elongatum telocentric and those of 6A and 6D occurred in the same configuration it was evident that the telocentrics 6A and 6D were for corresponding chromosome arms, and the A. elongatum telocentric for the opposite arm.

4. The average rate of pairing was much lower for the A. elongatum telocentric than for wheat telocentrics. Previous studies had indicated very good genetic compensation of the A. elongatum chromosome for chromosomes 6A and 6D. It was therefore indicated that genetic equivalence and pairing affinity were not closely related in this case. Some implications of this are discussed.

An extension of two-way selection (i.e. selection of mutant from wild-type and vice versa within the same locus and with the same efficiency) to four different mutational or segregational situations was made possible by using acetate, fluoro-acetate and other substances related to their metabolism.

Two types of mutants resistant to fluoro-acetate were selected, the first of which (designated fac) cannot grow on acetate as the sole carbon source, while the second (designated fan) can.

Commencing with either a fac or a fan strain a double fac fan strain may be isolated, which is much more resistant to fluoro-acetate than either single mutant strain. Such double mutant strains may also be obtained by crossing a fac to a fan strain. Various characteristics of growth response of these strains on various media were observed.

fac mutants are recessive and map in three meiotically unlinked loci, one in linkage group V and two in linkage group VIII.

fan mutants are recessive and map in five loci, one in each of the linkage groups V, VII and VIII, and two linked in linkage group VI.

Most fac mutants isolated did not revert and this failure is considered genuine. Of the revertants tested, most resulted from extra-cistron suppressors, while revertants of two fac mutants resulted from very closely linked or intra-cistron suppressors.

It is argued that the findings indicate the existence of two pathways for acetate utilization in Aspergillus nidulans, a major and a minor; fac mutants are blocked in the major pathway, fan mutants in the minor pathway.

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.

It is argued that the primary break-points for meiotic recombination arise from the replication of regions in which DNA synthesis is delayed until meiotic prophase. The gaps would be in nucleotide chains of opposite polarity in sister chromatids. This would place a restriction on the recombination models of Holliday and of Whitehouse, so that neither is able to explain observed chromatid interference. It follows that if the primary breaks originate in the manner proposed here, the Whitehouse and Holliday models are either both wrong or both right.

Several genes expressed in kidney and other tissues determine phosphate homeostasis in extracellular fluid. The major form of inherited hypophosphatemia in humans involves an X-linked locus (HPDR, Xp22.31-p21.3). It has two murine homologues (Hyp and Gy) which map to closely-linked but separate loci (crossover value 0·4%–0·8%). Both murine mutations impair Na+-phosphate cotransport in renal brush border membrane; an associated renal disorder of 1, 25-dihydroxyvitamin D3 (1, 25(OH)2D) metabolism has been characterized in Hyp mice. Whereas experiments with cultured Hyp renal epithelium indicate that the gene is expressed in kidney, studies showing the development of the mutant renal phenotype in normal mice parabiosed to Hyp mice implicate a circulating factor; these findings can be reconciled if the humoral factor is of renal origin. The gene dose effect of HPDR, Hyp and Gy on serum phosphorus values is consistently deviant and heterozygotes resemble affected hemizygotes. The deviant effect is also seen on renal phosphate transport; all mutant females (Hyp/Hyp and Hyp/+) have similar phenotypes. On the other hand, there is a normal gene dose effect of HPDR in mineralized tissue; tooth PRATIO (pulp area/tooth area) values for heterozygotes are distributed between those for affected males and normals. The tooth data imply that the X chromosome locus is expressed in both renal and non-renal cells. The polypeptide product of the X chromosome gene(s) is still unknown.

1. The effects of long-continued selection for body weight in two lines of mice, one large and one small, are described.

2. The large line showed a sharp increase in weight after remaining at an apparent limit for twenty generations. A rare combinational event is suggested as the most likely explanation.

3. Reversed and relaxed selection from the large line at the limit failed to yield any response. This indicates that effectively, the additive genetic variance in this line had been exhausted.

4. In contrast, the small line at the limit regressed slightly towards the base population when selection was relaxed. Reversed selection yielded a ready response until a new limit was apparently reached. Loci affecting body weight in this line had therefore not been fixed by selection.

5. Natural selection, operating on viability between conception and the time when the selection was made, appears to explain best the lack of fixation in the small line.

6. Attention is drawn to the necessity of more experimental work to elucidate the genetic nature of the limits to artificial selection.

The gene pfpr-10 in Coprinus confers resistance to p-fluorophenylalanine. The resistance of the heterozygote pfpr-10/pfp8-10 is completely recessive, both in diploids and dikaryons. A dominance modifier Mod+ makes pfpr-10 dominant in a dikaryon but not in a cliploid. It also enhances the degree of resistance in r homozygotes. These results are explained on a hypothetical model based upon a hexameric product of the pfpr-10 gene, with resistance to PFP being proportional to the percentage of homo r hexamers. The Mod+ is presumed to act by keeping the r and s products separate so that hybrid multimers are reduced to a minimum. Critical threshold concentrations of PFP for diploid/haploid dikaryons in 40 different combinations of pfpr and Mod+ genes cover a wide range of gene doses and percentage of homo r multimers. The relationship between the critical threshold concentrations and the calculated percentage of homo r multimers supports the model.

Transformation studies in pneumococcus had shown that loci determining the resistance to erythromycin and streptomycin were unlinked when strain Cl3 was recipient but linked when strain SIII-I was recipient. This phenomenon also applies to other pairs of markers studied in these two recipients, no matter whether the transforming DNA was derived from strain Cl3 or strain SIII-I. Other differences between the two recipient strains were also revealed. Whereas competent cultures of strain Cl3 were composed of all competent cells, which was in agreement with previous reports of pneumococcal cultures, strain SIII-I normally gave a maximum average of 28% competent cells. Strain SIII-I was unstable, since on repeated sub-culturing the competence peak profile changed and the value of ‘fcq’ increased. These properties were reflected in the two hex− strains 401 and R6x which were found to be similar to the ‘altered SIII-I’ strain. The results from the linkage studies have been applied to the chromosome map and have placed the opt-r2 gene in the str-r41-containing chromosome arm.

Pseudomonas aeruginosa carries polar pili which act as receptors for RNA-containing bacteriophages. In order to confirm, that these pili were not involved in the transfer of the sex factor FP 2, eleven bacterial strains, both FP 2+ and FP 2−, were examined in the electron microscope for the presence of pili and tested for sensitivity to the RNA phage PP7. Pili were found on all strains save one which was resistant to phage PP7. It was also found by electron microscopy that about 25 times more pili per cell were present after PP7 adsorption than before it. This result is discussed with reference to the pilus retraction theory, providing further evidence that some kinds of pili retract instead of acting as simple tubes for the transfer of genetic material. The strong supporting evidence provided by the infective processes of male-specific coliphages is discussed and compared to current knowledge of P. aeruginosa RNA phages.

It was also found that pili were present on the host strain for the P. aeruginosa filamentous phage Pf. Although similar in appearance to RNA phage pili, these differed in that they did not adsorb phage PP7. However, it seemed likely that they were receptors for Pf. A structural comparison is made between P. aeruginosa pili and Escherichia coli F-pili. It is possible that P. aeruginosa pili could be coded for by a plasmid other than FP 2.

Until 1960 all the chromosome counts performed on cells of this species were done on histologically prepared specimens of testicular tissue. In January 1960, Chiarelli et al. published the results of their experiments to grow renal tissue in culture. Their specimens were obtained from male and female calves. They confirmed that 2n = 60 and described the chromosomes as being all acrocentric except the X chromosome, which was submetacentric.

The purpose of the work described below was to try to apply the peripheral-blood culture technique of Moorhead to bovine blood, and to attempt to grow bovine muscle cells in a tissue culture.

A new spontaneous mutant bubble (bu) with a marked effect on early morphogenesis in the multicellular green alga, Ulva mutabilis is described. It behaves as a recessive chromosomal mutant. The bu+ gene product formed in heterozygous sporophytes exerts a predetermining effect on morphogenesis of haploid gametophytes with the bu genotype. It is suggested that the product of the bu+ gene affects the orientation of the mitotic spindles during early development.

A mechanism for gene conversion is proposed which overcomes many of the difficulties that any copy choice model encounters. It is suggested that along with general genetic pairing of homologous genomes at meiosis, effective pairing over short regions of the genetic material occurs at the molecular level by the separation of the strands of the DNA double helices, followed by the annealing of strands from two homologous chromatids. If the annealed region happens to span a heterozygous site, mispairing of bases will occur. Such a situation may be analogous to that in DNA which is damaged by mutagens; the same or similar repair mechanisms may operate, and these, by adjusting the base sequences in order to restore normal base pairing, would bring about gene conversion in the absence of any genetic replication. The model indicates how precise breakage and rejoining of chromatids could occur in the vicinity of the conversion, so that conversion would frequently be accompanied by the recombination of outside markers. The model also proposes that the distance between two mutant sites on a fine structure map depends not so much on the frequency of a recombinational event occurring between them, but rather on the degree of inhibition of the processes of genetic pairing by the mutants themselves.

The model will explain almost all the data in a formal way, and it has the advantage over copy choice mechanisms for gene conversion in (1) being compatible with semi-conservative replication of DNA, (2) not invoking DNA synthesis during or after genetic pairing, (3) providing a molecular mechanism for close specific pairing, (4) making it unnecessary to postulate sister strand exchange or a process akin to this, (5) suggesting why rates of gene conversion in opposite directions are sometimes unequal and (6) providing an explanation of the clustering of mutant sites, a basis for map expansion and for the apparently capricious departure of fine structure maps from additivity. Although the model proposed is a general rather than a specific one, it suggests that the process of conversion and intragenic recombination is more complex than is usually believed, since it depends on several interacting factors. Nevertheless, it is hoped that the introduction of a model with this complexity will help to stimulate specific experiments, and that these will provide definitive information which would never be obtained if simpler models of conversion and intragenic recombination were believed to explain the genetic data sufficiently well.

Chlosyne lacinia (Geyer) is a nymphalid butterfly ranging from the Southwestern United States and thence southward to Argentina (Ehrlich & Ehrlich, 1961). The insect is multibrooded and preferably feeds on sunflower (Helianthus annuus L.), although high populations have also been observed to be maintained on cocklebur (Xanthium saccharatum Wallr.).

Strain Bs8 is a u.v.-sensitive derivative of strain B. It is unable to reactivate irradiated phage (HCR) and it cannot be induced to form filaments. The HCR properties are attributable to a gene, uvr8, cotransducible with gal+. When uvr8 was transduced into radiation-resistant strain B/r the resulting phenotype was indistinguishable from Bs8. When transduced into a lon K-12 strain the phenotype was more sensitive than Bs8, filament-inducible and mucoid. When PI-Bs8 was used to transduce proC+ into a proC K-12 strain, 4% of the transductants were lon, i.e. about as u.v.-sensitive as Ion K-12, filament-inducible and mucoid. Radiation resistance could not be transduced from strain Bs8 with proC+ into a proC lon K-12 derivative. Nor did Bs8 show any evidence of being exr. Bs8 is a double mutant of strain B, behaving as though it were HCE, in a B/r background.

Previous studies had shown that haploid strains of Aspergillus nidulans which have a chromosome segment in duplicate are unstable at mitosis. Through the study of various haploid and diploid strains, with and without translocations and with balanced and unbalanced genomes, it has been shown: (1) that imbalance of chromosome segments is responsible for instability, and (2) that the chromosomal deletions produced are confined solely or largely to the segments which provoke instability.

The term ‘mitotic non-conformity’ has been proposed for this instability phenomenon. An explanation for it has been sought in terms of attachment sites, limited in number and specific for chromosome segments, at which replication is initiated.