To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
In Klebsiella aerogenes strain V9A melibiose and raffinose fail to induce the lac operon and strongly repress its induction by isopropyl-β-d-thiogalactopyranoside (IPTG). This repression is specific to the lac system and is not released by cAMP, which releases the catabolite repression exerted by glucose and sucrose. It is concluded that melibiose and raffinose bind to the lac repressor molecule in Klebsiella V9A, competitively displacing IPTG, and that the resulting complex is able to repress the lac operon. Other Klebsiella strains tested show the same repression phenomenon.
The R-factor RP1, which carried the markers amp neo tet, confers resistance to penicillins by specifying the synthesis of Type IIIa β-lactamase. It was detected initially in a strain of Pseudomonas aeruginosa (Sykes & Richmond, 1970) and fragments spontaneously in Ps. aeruginosa strain Ps 18 to give clones which carry only the amp marker. Such clones are said to carry the element RP 1–1 since they are still capable of specifying the transfer of ampicillin and carbenicillin resistance to appropriate recipients in mating experiments. However, unlike lines carrying RP 1, they contain no detectable extrachromosomal DNA (Ingram et al. 1972), and the likely supposition is that the amp gene in these clones has become integrated into the bacterial chromosome together with the regions necessary to allow such strains to act as amp gene donors in mating experiments. It is probably cells of Ps. aeruginosa in which the amp gene has become integrated together with an RTF region that are responsible for the transfer of chromosomal markers reported by Holloway & Stanisich (1971).
The (I; II) duplication strain of Aspergillus nidulans contains a terminal segment of chromosome I twice, one copy being in the normal position, and the other one translocated to a tip of chromosome II. We show that in selfed cleistothecia (homozygous for the duplication) crossing-over between the two segments of the duplication followed by the appropriate disjunction and distribution of the meiotic chromosomes, results in segregation of recessive markers in the duplication. Alternative segregation mechanisms like the deletion mechanism responsible for mitotic non-conformity, cannot explain the observations. The average segregation frequency of the marker yA2 is 11%. Using the mathematical model outlined in the Appendix to this paper, we estimated the recombination frequency between the translocation breakpoint and the yA locus from the segregation frequency. The essential feature of the model is the computation of the probabilities of combinations of different tetrad types in quadrivalents. Application of the model leads to the qualitative conclusion that the meiotic recombination frequency within the duplication is increased over the normal level. Elsewhere in the genome the frequencies are either unchanged or decreased. Also in crosses heterozygous for the duplication, an increase by at least a factor of two is found. As judged from the appearance of certain recombinant classes, the quadrivalent frequency in homozygous and heterozygous crosses is 2/3 (random pairing) or slightly higher. The increased recombination is attributed to the same lesions that are responsible for the occurrence of deletions in duplication strains of A. nidulans.
Twelve FPA-resistant mutants were selected on medium containing p-fluorophenylalanine and ethionine. Dominance tests in heterozygous diploids showed that 8 out of 12 are dominant and 4 recessive to their wild-type alleles. One mutant, fpa60, showed a partial requirement for tyrosine and was found to be allelic to an fpaA mutant described previously. A tyrosine non-requirer, fpa65, was also assigned to this locus. The other 10 mutants did not show any growth requirement and were simultaneously resistant to ethionine and 3-amino-L-tyrosine. Of the 8 dominant mutants, 3 were allelic to the permease-mutants at the locus fpaD. Dominant mutants showed higher degrees of resistance than recessive ones. Six new loci, identified after preliminary genetic analysis, were located on 3 linkage groups: 3 on linkage group VI, and one each on linkage groups I, V, and VIII. The recombinant fpaD11; fpaK69 was found to be sensitive to FPA.
In Drosophila, the three yolk protein (yp) genes are transcribed in a sex-, tissue- and developmentally specific manner, providing an ideal system in which to investigate the factors involved in their regulation. The yolk proteins are synthesized in the fat body of adult females, and in the ovarian follicle cells surrounding the developing oocyte during stages 8–10 of oogenesis. We report here an analysis of the yolk protein 3 (yp3) gene and its flanking sequences by means of P-element mediated germ-line transformation and demonstrate that a 747 bp promoter region is sufficient to direct sex-specific expression in the female fat body and both the temporal- and cell-type-specificity of expression during oogenesis. Two elements that independently govern yp3 transcription in these tissues have been separated and no other sequences in the upstream, downstream or coding regions have been identified that are autonomously involved in yp3 expression.
Five polymorphic proteins, detected by two-dimensional electrophoresis, were analysed in the parents and progeny of a cross between two clones of the malaria parasite Plasmodium falciparum. The information obtained showed that different forms of each protein were determined by allelic variants of each respective gene. One protein was identified as the parasite enzyme adenosine deaminase. Recombinant parasites were produced at a higher than expected frequency.
The Price (1970, 1972) equation is applied to the problem of describing the changes in the moments of allelic effects caused by selection, mutation and recombination at loci governing a quantitative genetic character. For comparable assumptions the resulting equations are the same as those obtained by different means by Barton & Turelli (1987; Turelli & Barton, 1989). The Price equation provides a natural framework within which to examine certain kinds of non-additive allelic effects, recombination and assortative mating. The use of the Price equation is illustrated by finding the equilibrium genetic variance under multiplicative dominance and epistasis and under assortative mating at an additive locus. The limitations of the use of recursion equations for the moments of allelic effects are also discussed.
The evolution of traits that affect genotypic responses to density regulated resources can be strongly affected by population dynamics in ways that are unpredictable from individual viability or reproduction potentials. Genotypes that are most efficient in utilizing energy may not always displace less efficient ones, and the evolution of energy allocation strategies may not always favour reproductive fitness because of their effects on destabilizing population growth rates. Furthermore, genetic polymorphisms in single loci that affect such traits can be maintained in populations with stable, periodic changes in population size and gene frequencies in the absence of heterozygote superiority. In fact, in the models investigated in this paper, the polymorphism is maintained, even in the absence of equilibrium genotypic frequencies.
(C57BL × CBA)F1 hybrid female mice were mated with hemizygous Rb(X.2)2Ad males to distinguish the paternal X chromosome. Homozygous tetraploids were produced by blastomere fusion at the 2-cell stage, and 161 of these were transferred to recipients and analysed on the 10th day of gestation. 59 implants contained resorptions and 76 contained either an embryo and/or extraembryonic membranes. 38 (20, XXXX and 18, XXYY) were analysed to investigate their X-inactivation pattern. Embryonic and yolk sac endodermally- and mesodermally-derived samples were analysed by G-banding and by Kanda analysis. In the XX and XY controls, the predicted pattern of X-inactivation was observed, though 12·2% of metaphases in the XX series displayed no X-inactivation. In the XY series the Y chromosome was seen in a high proportion of metaphases.
In the XXXX tetraploids, 8 cell lineages were recognized with regard to their X-inactivation pattern, though most belonged to the following 3 categories: (XmXm)XpXp, Xm(XmXp)Xp and XmXm(XpXp). The other categories were only rarely encountered. In the embryonic and mesodermally-derived tissue the ratio of these groups was close to 1:2:1, whereas in the endodermally-derived tissue it was 1:4·11:4·88, due to preferential paternal X-inactivation. A significant but small proportion of all 3 tissues analysed displayed no evidence of X-inactivation. Indirect evidence suggests that this represents a genuine group because of the high efficiency of the Kanda staining. The presence of the Xm(XmXp)Xp category is consistent with the expectation that X-inactivation occurs randomly in 2 of the 4 X chromosomes present. The presence of small numbers of preparations with no evidence of X-inactivation and other unexpected categories suggests that these are probably selected against during development.
The influence of sodium octanoate on the polymorphism at the loci G6PD and 6PGD in Drosophila melanogaster was investigated by studying its effect on egg hatchability, larval-to-adult survival and adult survival. The results demonstrate the existence of differences in fitness between the different genotypes of the two loci both for larval-to-adult survival and for adult survival. Furthermore, changes in enzyme activity of both enzymes, brought about by the sodium octanoate treatment, were observed. This makes it highly probable that the observed differences in fitness can be ascribed to the loci themselves and not to linked fitness genes. Finally, this study demonstrates the existence of strong interaction between the two loci with respect to fitness. Epistasis was demonstrated both in the larval-to-adult survival experiment and in the adult survival experiment.
In extracts of mature wheat grains, 13 hexokinase isozymes were distinguished by IEF. The genes controlling the production of five isozymes were located on chromosome arms 1BS, 1DS and 3BS by nullisomic analysis. The three loci, part of two homoeoallelic series (Hk-1 and Hk-2) are designated Hk-B1, Hk-D1 and Hk-B2 respectively. Analysis of chromosome 1D short-arm terminal deletions indicated the Hk-D1 locus to be located proximally to the glucose phosphate isomerase locus, Gpi-D1 on the shortarm. Three variant HK phenotypes were distinguished amongst 55 hexaploid wheats examined. Analysis of seven Chinese Spring/Agropyron elongatum chromosome addition lines showed that Ag. elongatum isozymes were expressed in the wheat background in additions IV and V.
In finite populations, loci maintained segregating by hétérozygote superiority will be disturbed from their equilibrium positions by genetic sampling and the mean fitness of individuals will consequently be reduced. A general expression for this reduction is obtained for the segregation of two alleles. If the probability of continued segregation at the locus is high, the reduction tends to 1/4N, irrespective of the strength of selection, where N is the effective population size. This will always be much less than the segregation load. If n alleles are segregating, so that all heterozygotes have the same fitness, the reduction tends to (n−1)/4N.