Chi is a sequence of eight nucleotide pairs which stimulate recBC-mediated recombination (Smith, 1983a, b). The effect of two linked Chis on recBC-mediated recombination was tested in bacteriophage lambda. It was noticed that the Chi element located on the right side of the phage chromosome is epistatic on the other Chi. These findings support a model proposed by Stahl et al. (1983) which suggests that the recombination machinery moves unidirectionaly in the phage chromosome from right to left. The results also suggest that in the presence of more than one Chi only the rightmost one stimulates recombination.

When grown on high-phosphate medium, the wild-type strain 74A of N. crassa synthesized two acid phosphatases, as shown by DEAE -cellulose chromatography. These purified enzymes showed heterogeneity on PAGE, low specific activities towards PNP-P, molecular weight values of at least 300000, no deviation from Michaelian behaviour, and great stability in 50 mM sodium acetate buffer, at pH 5·4, when kept at 54 °C. These acid phosphatases were synthesized in reduced amounts or not at all when the mould was grown under conditions of phosphate starvation, indicating that the level of phosphate also regulates the synthesis of the high molecular weight enzyme forms. When grown on high phosphate medium, the pho-3 mutant strain also synthesized two acid phosphatases, whose purified enzymes showed no pronounced differences when compared to those synthesized by the wild-type strain in terms of electrophoretic analysis, specific activities towards PNP-P, molecular weight values, and Michaelian behaviour. However, one enzyme form had a higher Km value and a lower heat stability than the corresponding enzyme of the wild-type strain. Even though the pho-3 locus might not be responsible for an alteration in the primary structure of the repressible acid phosphatase, it seems clear that the enzymes synthesized by the mould grown on low-or high-phosphate medium must share some structural features. Thus, the drastic differences observed in the molecular properties of the enzymes synthesized by the mould grown under conditions of phosphate starvation as opposed to phosphate repression might be due to an effect exerted by the level of inorganic phosphate in regulating the translation, post-translational modifications and/or excretion, but not necessarily the gene-directed synthesis of distinct mRNAs.

The transcriptional organization of the Tra2 region controlling conjugation by the narrow host range plasmid R91–5 of Pseudomonas aeruginosa has been determined. This region of 15·2 kilobase pairs of DNA encodes ten cistrons and specifies the synthesis and functionality of sex pili. The order of the cistrons was previously shown to be traW, (S, Z), U, (V, R), Q, T, Y, X (those within parentheses could not be ordered with respect to each other). The organization was determined by complementation tests for the restoration of plasmid transfer between transposon Tn7 or Tn501 induced insertion mutants and point mutants representative of the ten cistrons. Polarity mutations induced by Tn7 permitted the identification of three operons. Cistrons traW, Z, S, U, V, R and Q formed a large operon with transcription postulated to be in that order. The second consisted of tra T and tra Y also in that order and the third consisted of only one cistron, traX. Polarity was not observed with Tn501 insertions as they still permitted full expression of cistrons distal to the site of insertion with respect to the proposed promoter. Despite the unexpected behaviour of this transposon it nevertheless led to the identification of two previously unidentified cistrons, traO and traP being between traZ and S and traR and V, respectively.

I describe here a new screening procedure to isolate ribosomal suppressors in Podospora anserina. I have used the sporulation defect displayed by an antisuppressor mutation AS7–2. The revertants able to sporulate are due to either true reversions or external mutations. The mutations which restore most efficiently the sporulation show all the properties of ribosomal suppressors and are localized in two new suppressor loci su11 and su12.

Recombination between the t6 complex, three allozyme-encoding loci, two antigen-encoding loci, and four molecular markers was studied. The allozyme-encoding loci were complement component-3 (C-3), kidney catalase (Ce-2), and glyoxalase-1 (Glo-1); the antigen-encoding loci were the H-2 Class I genes H-2K and H-2D; the four molecular markers were Tu66, an α-globin pseudogene (Hba-4ps), an unidentified H-2 Class I gene, and the H-2 Class II gene I-Aβ. The latter six loci were used as markers for the t complex. Recombination was detected between Glo-1, Ce-2 and C-3, but not between the markers for the t complex Tu66, Hba-4ps, and the H-2 loci. These data indicate that Ce-2 and C-3 are located outside the t6 complex, while the latter are located within. These data also indicate that the telomeric boundary of the t6 complex is located between H-2 and Ce-2. Recently published studies have shown that complete gametic disequilibrium exists between the t complex and loci located centromeric to the H-2 - Ce-2 interval, while disequilibrium was not detected between loci located telomeric to this interval. Loci included within the region of recombination suppression are also those in disequilibrium with the t complex. As a result, recombination suppression probably resulting from chromosomal rearrangements associated with the t complex appears to be a sufficient explanation for the gametic disequilibrium observed between certain loci and the t complex.

The zymogram phenotypes of triosephosphate isomerase (TPI) were determined for a large number of aneuploid derivatives of Triticum aestivum cv. ‘Chinese Spring’ and for six wheat-alien species chromosome addition series. Examination of the available compensating nullisomic-tetrasomic and homoeologous groups 3 and 5 ditelosomic lines of Chinese Spring disclosed that T. aestivum possesses two systems of dimeric TPI isozymes, designated TPI-1 and TPI-2. The genes TPI-A1, TPI-B1 and TPI-D1 were located in Chinese Spring chromosome arms 3Ap, 3Bp and 3Dp, respectively and the genes TPI-A2, TPI-B2 and TPI-D2 in chromosome arms 5Aq, 5Bq and 5Dq, respectively. TPI-1 genes were also located in Hordeum vulgare cv. Betzes chromosome 3H, T. longissimum chromosome G, Elytrigia elongata chromosome 3E, and Secale cereale cvs. Imperial and Dakold chromosome 3R. TPI-2 genes were found in Betzes chromosome 5H, T. umbellulatum chromosome 5U, T. longissimum chromosome F, and Imperial and Dakold chromosome 5R. These gene locations provide evidence of homoeology between the alien chromosomes in which the genes are located and the chromosomes of homoeologous groups 3 and 5 of Chinese Spring, respectively. Evidence was obtained for the presence of a TPI-R2 gene in each of the T. aestivum cv. Kharkov -S. cereale cv. Dakold chromosome addition lines studied suggesting that this gene is present in the wheat genome in each member of this addition series.

Three acid phosphatase allozyme strains (Acph-1, Acph-2 and Acph-4) of Drosophila virilis show large differences of enzyme activity when examined by means of starch gel electrophoretic technique, Acph-4 strain showing approximately four times the activity of Acph-1 and twice that of Acph-2, as reported previously (Narise, 1976). Crude extract difference between Acph-4 and Acph-1 strains is less than twofold and this compared with larger differences in supernatants. Cell fractionation and density gradient centrifugation demonstrated that the acid phosphatase resides mainly in lysosomes and becomes soluble in part during preparation without structural damage to lysosomes. The solubility of the allozymes from lysosomes was variable among the three strains. ACPH4 allozyme was released in the highest degree. However, the release-rate of other lyso-somalenzymes, such as α-glucosidase, β-galactosidase and β-glucuronidase was similar among these strains. These results suggest that the strain variation in ability of the allozymes to be incorporated into lysosomes is due to the allozymes themselves, not due to alteration in the lysosomes.

Mutants of Chinese hamster ovary (CHO) cell resistant to cytosine arabinoside (ara-C), an inhibitor of DNA synthesis and antitumour drug, have been isolated and characterized both biochemically and genetically. Mutants occurring spontaneously and those induced by treatment with N-methyl-N′-Nitro-N-nitrosoguanidine (MNG), were obtained at a frequency of 0·24 × 10−6 and 3·4 10−6 respectively. The mutants showed a stable ara-C resistant phenotype which was inherited as a dominant trait in genetic crosses. The wild type (CHO K-1) and the mutant (103, 002 and 003) cells showed no differences in the levels of the uptake of ara-C or of its degradation. Results of biochemical studies further excluded the involvement of deaminase, kinase and ribonucleotide reductase as the possible factor(s) in conferring drug resistance to the mutant cells. However, the wild type and mutant DNA polymerases differed in the level of the in vitro incorporation of specific dNMP in the presence of ara-CTP. These data suggested that the wild-type DNA polymerase which becomes error prone in the presence of ara-CTP may cause the drug sensitivity of the wild-type cells and that a change in the mutant enzyme making it resistant (or less prone) to ara-CTP induced errors in dNMP incorporation may control the drug resistance of the mutant cells.

Haploid amoebae of Physarum polycephalum may form plasmodia by crossing, a sexual process that involves cellular and nuclear fusions, or by selfing, an asexual process in which the development of a single amoeba into a plasmodium may involve neither cellular nor nuclear fusion. Mutant strains (npf) in which selfing is suppressed were previously assigned to several functional groups on the basis of their ability to cross with one another in certain combinations. In the present study hybrid, diploid amoebae were isolated from both crossing-compatible and incompatible mixtures of npf mutants. The diploid amoebae from mixtures of compatible strains readily formed plasmodia by selfing, but selfing was suppressed in the diploids from incompatible mixtures. Thus the crossing tests between npf mutants may be viewed as complementation tests: their results reflect the differing selfing abilities of the hybrid, diploid amoebae that formed in each mixture. Genetical and environmental factors affecting the efficiency of formation of diploid amoebae were studied, and the diploids were shown to be stable during repeated subcultures. Although diploid amoebae carrying complementing npf mutations readily formed plasmodia by selfing at 26 δC, they could be cultured without plasmodium formation at 30 δC, a temperature that also inhibited selfing of the haploid npf+ strains. Ways are discussed of exploiting this combination of properties in a general procedure for isolating and testing diploids for dominance and complementation of amoebal mutations in P. polycephalum.

Inferences on the mechanism of chiasma maintenance can be drawn from study of the distribution and frequency of chiasma-like associations between bridges and fragments and between normal chromatids and fragments in meiotic material heterozygous for paracentric inversions. These bridges and fragments are the result of crossing over within the inverted region so that differing predictions for the associations are generated by the various models for chiasma maintenance mechanism. Results of such a study in material heterozygous for a large paracentric inversion in the long arm of chromosome 1 in maize are reported here. Findings are generally consistent with predictions of the ‘generalized sister chromatid cohesiveness model’, but are markedly at odds with the ‘binder only at specific crossover sites model’, and with the ‘late effective doubling of telomeres model’. Some of the results do not conform quantitatively to predictions of the ‘generalized sister chromatid cohesiveness model’ for a linear relationship between potential extent of sister chromatid cohesiveness and frequency of maintained association, suggesting additional complexity.

Data from Neurospora, Drosophila, and the mouse support the mapping parameter conventionally used for man, exclude the Haldane, Kosambi, and Carter—Falconer functions, and suggest a refinement for centromere mapping. Different sexes, chromosome arms, and types of data are surprisingly consistent. Double recombination frequencies are accurately predicted, but triple recombination frequencies are overestimated. The centromere appears to act on interference as an obligatory chiasma. Recombination across the centromere conforms to a simple approximation, based on the interval Markov assumption with a common mapping parameter. These results imply that mapping of n loci requires estimation of at most n parameters, and the relation between map distances and all recombination frequencies is explicit.

We have employed stocks bearing clonally derived X chromosomes to investigate several features of the bobbed mutant syndrome, and the amplification of rDNA genes in D. melanogaster. We report that posterior macroscutellar bristle length correlates well with the rDNA content (i.e. dose of ivs–, or uninterrupted genes) in cloned X derivative strains. X/O males and X/X females with statistically indistinguishable rDNA contents have virtually identical bristle lengths. This indicates that (with respect to this phenotypic character) the rDNAs in these two genotypes are expressed equally, without apparent sexual dimorphism or dosage compensation. However, the severity of bobbed phenotype in terms of bristle morphology, turgite etching, and delayed eclosion is greater in the Xbb/XNO− female than in the Xbb/O male genotype for the alleles examined. We estimate the minimum dose of functioning rRNA genes required for viability at 26 δC to be 70 genes per diploid genome. We have examined the capacity of several X chromosomes which bear bobbed mutant alleles to compensate in X/O males, and find that disproportionate replication of these rDNAs does not take place. In contrast, at least one of the non-compensating bobbed alleles does appear to undergo rDNA magnification.

A special screening procedure for the detection of induced Y-autosome translocations with centric breakpoints was applied. A series of Experimental stocks was constructed, each containing a different half of one of the induced T(Y; 2)'s (T element). The three other elements that were involved in the segregation experiments in each stock were a sex chromosome (X element), an inverted chromosome 2 (A element), and a free arm of chromosome 2 (F element). It is not feasible to determine the relative frequencies of all the 16 possible gamete types by mating an Experimental stock to one tester, nor to different testers that have each at least one class of progeny of the same genotype. Each Experimental stock was mated to four different Tester stocks and the data were calibrated so that a coherent segregation pattern could be obtained.

Segregation patterns in meiosis of males from 15 Experimental stocks, each with a different T element were studied. In most Experimental stocks the T element was of the left autosomal arm, while the F element was of the right autosomal arm. In four Experimental stocks the X element segregated independently of the A, F and T elements. In these Group 1 stocks, both the F and the T elements disjoined regularly from the A element. It was concluded that the T element of these stocks had no sex-chromosome disjunction determinants (‘S-determinants’) to interact with the determinants on the X element. Both the T elements and the F elements carried autosomal disjunction determinants (‘H-determinants’) that secured the segregation of the autosomal elements. The H-determinants of the left autosomal arm were qualitatively different from those of the right arm.

In the remaining 11 Group-2 Experimental stocks the X and T elements disjoined regularly, indicating the presence of S-determinants on the T elements of these stocks. The segregation of the T and the A elements in these stocks varied from nearly complete dependence to complete independence. It was concluded that this gradation reflected differences in the quantity of H-determinants present on the T elements of these Experimental stocks. It was impossible to discriminate between a model of continuous H determinants activity and one of a finite discrete number of determinants. The results do not agree with the claim that there are no autosomal disjunction determinants in the proximal heterochromatin of chromosome 2.

The S-determinants on the BsYy+ chromosome were located both adjacent to the centromere and distally on the long arm. The latter were probably translocated to the Y chromosome together with the Bs marker.

Genetic variation in hormone-sensitive cyclic AMP production was investigated among inbred strains of mice. Significant strain differences were observed in β-adrenergic- and glucagon-stimulated adenylate cyclase activity. Comparable differences were also found in membrane methyl-transferase I activity in these strains. Our results of studies using F1 progeny of high and low strains suggest a dominance of high MT I activity over low MT I activity. Investigation of recombinant inbred lines between the high and low strains indicates that MT I activity is regulated by at least two major genes; H-2-congenic lines of several inbred strains were then used to identify an association between hormone-stimulated MT I activity and the mouse major histocompatibility complex.

Covariance between direct and maternal genetic effects on body weight in random-bred ICR mice at 2 through 10 weeks of age was estimated from cross-fostering experiments. The covariance contributes only a few percent of phenotypic variance at 2 weeks, but increases to 10–15% at later ages. Nearly all estimates are positive. We suggest that genes active during later parts of growth affect maternal performance more than those active during early growth, causing increased covariance at later ages. A model of combined genetic and persistent environmental effects on maternal performance is presented. Persistent effects of genetic or environmental variation in recent ancestors can influence covariance between relatives and response to selection.

This is a study of the chromosomal segregation patterns in females of 15 Experimental stocks of Drosophila melanogaster, each carrying one element of a T (Y; 2) with a centric break-point. In each Experimental stock the relative frequency of all eight possible meiotic configurations of four relevant chromosomal elements was followed: an attached-X chromosome, a multiply-inverted chromosome 2, a free arm of chromosome 2, and a half-translocation element. Although the 15 translocation elements were broken at different sites, there were no basic differences among the Experimental stocks in their segregation patterns. The three two-by-two configurations were the most common. Comparison of this pattern with that of the segregation pattern of stocks similar but for an inversion-free chromosome 2, showed that in the Experimental stocks exchange pairing did not play a significant role in the determination of the segregation pattern.

The results of these experiments, together with the analysis of results from other published studies provide evidence against the model that had been forwarded by Grell. According to this model, chromosomes that did not participate in exchange pairing undergo another pairing cycle, in which total chromosome length is a factor in the determination of segregation.

We support a modified version of Novitski's model of premetaphase chromocenter-like chromosome aggregation. Disjunction of non-exchange chromosomes is regulated by determinants located in the proximal heterochromatin of the sex chromosomes and the autosomes. However, the specificity, especially that of the autosomal determinants, is not high. Thus, if an autosome and a sex chromosome are available, their determinants may interact-to-disjoin by default. More frequently, the determinants of the left-arm autosomal element may interact-to-disjoin with those of the right-arm chromosomal element.

The lack of robustness of models of the maintenance of polymorphism in a heterogeneous environment which has been pointed out by Maynard Smith & Hoekstra (1980), applies also to models based on habitat selection, on temporal variation and on density-regulated selection. Only if (partial) dominance ‘switches’ between environments such that the fitness of the heterozygote is always close to the favoured homozygote, is there reasonable robustness. This is true for all models considered. It is argued that there are good reasons for supposing that the favourable allele at a locus may show dominance, although the experimental evidence is still scanty.

A ‘two locus two allele’ model is developed with special reference to the introgression of extranuclear genomes between two species of finite size. The model assumes that one locus, coded by a nuclear genome, causes the reproductive barrier while the other locus, coded by an extranuclear genome, causes nucleo-cytoplasmic incompatibility in particular genotypes. To fully study this model, simulations are conducted, and a diffusion equation is derived when introgression or extranuclear gene flow occurs in one direction. It is shown that although selection against the nuclear genome can reduce the levels of extranuclear gene flow and retard the introgression process, the dynamics are very similar to those without such selection. In contrast, the nucleo-cytoplasmic incompatibility directly affects the dynamics of introgressing extranuclear genomes: in large populations the ability of incompatibility to overcome extranuclear gene flow is conspicuous, but in small populations it is overshadowed by random sampling drift. Paternal leakage of extranuclear genomes, if present, is of evolutionary importance only when the male's migration rate is much larger than the female's. When the sizes of two populations are unequal, the introgression is most likely to occur from the larger population to the smaller one in the absence of mating preferences of backcross progeny. Recent observations on interspecific mitochondrial transfer in various species do not support the ubiquitousness of nucleo-cytoplasmic incompatibility as an efficient reproductive barrier.

Using mice that were mosaics for both Xce and phosphoglycerate kinase (Pgk-1) alleles, we have established that the parental source of the Xce gene may affect the probability with which the X chromosome carrying it will remain active. This effect was seen in one allelic combination of Xce but not in another. The relationship between these effects and other phenomena of maternal ‘imprinting’ is discussed.

Relationships between protein genetic distance (D) and protein heterozygosity (H) were studied using allele frequency data for 42 proteins derived from multilocus electrophoretic surveys of genetic variation in over 200 invertebrate and over 300 vertebrate species. D¯ and H¯ values for the different proteins (mostly enzymes) were calculated, and large and significant correlations between D¯ and H¯ were found in comparisons of both intraspecific and interspecific populations. Empirical relationships between D¯ and H¯ were compared with neutral expectations under the stepwise model of neutral mutation with the assumption that populations are in equilibrium with respect to the effects of mutation and genetic drift.

At low divergence levels, a linear relationship of D¯ on H¯ was observed, but at high levels of divergence D tended towards an asymptote at high H¯. The results at high divergence cannot be explained using the approximate relationship D = 2ut (where u = mutation rate, t = time). However, computer simulations of neutral models showed that changes of this nature in the relationship between D¯ and H¯ were to be expected as divergence increases, the equation D = 2ut being a poor approximation at high D We therefore conclude that the observed relationships between D¯ and H¯ are, in fact, compatible with equilibrium neutral theory.