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Using four independent late mutants, obtained by treatment of the early cultivar Dijon-G with N-methyl-N-nitrosourea, it was found that their delayed flowering has a monogenic genetic basis, the mutant alleles appearing to be incompletely dominant. All these mutants display a positive reaction to the graded vernalisation; the vernalisation requirement of the individual mutants is, however, both quantitatively and qualitatively different and hence specific for each of the mutant genotypes. lodoacetic acid is found to inhibit the vernalisation of the mutants to some extent only when the duration of the vernalisation is relatively short (20 days). A hypothesis is advanced, assuming a potential existence of a complete genetic apparatus for vernalisation already in the Dijon-G cultivar, where it is, however, blocked by suppressor or epistatic genes.

A double mutant A1G82 of the su III + tyrosine gene in Escherichia coli was constructed by genetic cross. This mutant is a stronger glutamine-inserting amber suppressor than either of the single mutants A1 or G82.

Three distinguishable aleurone-color-suppressing alleles at the C locus have been identified. They are differentiated on the basis of potency in suppressing color. The tester line showing the least suppression is the more efficient substrate to distinguish the color-suppressing alleles. A model is proposed on the nature of dominant suppression of aleurone color.

The effects of a suppressor variable on subjects' achievement, consistency, and matching in a MCPL task were examined at two levels of system predictability; r e = .52 (Expt 1) and r e = .92 (Expt 2). Labeled stimuli were presented in two environments: meaningful and abstract. Three types of control conditions were employed to assess the suppressor effect. Results showed that subjects were able to utilize the suppressor effect in making their predictions, but only at the lower level of system predictability involving a meaningful environment. The difficulty of developing a consistent strategy when the meaningfully labeled stimuli were semantically illogical was evidenced. The results were discussed in the framework of the Brunswik normative model involving meaningful versus abstract decision making tasks.

The mixed leukocyte reaction stimulatory M-locus product of DBA/2 spleen cells was absent from thymus cells. The absence of stimulation was not a result of suppressor T cells. These findings are discussed in relation to the divergent specificity found for the inductive and effector phases of cell-mediated responses.

SummaryCattle with Johne's Disease, a chronic mycobacterial infection, often have a cutaneous anergy. The lymphocytes from a Johne's Disease affected animal responded poorly to phytohemagglutinin (PHA) when incubated in autologous plasma. When the cells were washed and incubated in normal plasma, the PHA responses returned to normal values. Sera from these cattle also were found to inhibit PHA-induced transformation of normal peripheral blood lymphocytes. When the immunosuppressive serum from one of these animals was fractionated by ion-exchange chromatography the suppressor of lymphocyte transformation was recovered in the fractions containing immunoglobulins G1 and G2.

The nature of the defect in patients with common variable hypogammaglobulinaemia has been investigated using a technique established to study terminal differentiation of B lymphocytes into immunoglobulin synthesising and secreting cells. The peripheral-blood lymphocytes from normal individuals had geometric mean synthetic rates of 1641 ng. for IgG, 1698 ng. for IgA, and 3715 ng. for IgM per 2×10 6 cells when cultured for seven days in the presence of pokeweed mitogen. In contrast, the lymphocytes from all 13 patients with hypogammaglobulinaemia studied synthesised and secreted less than 100 ng. of each class of immunoglobulin during this period. When lymphocytes from 5 of the 8 hypogammaglobulinaemic patients studied were co-cultured with normal lymphocytes and pokeweed mitogen, the synthesis of immunoglobulin by normal lymphocytes was depressed by 84 to 100%. A comparable suppression of immunoglobulin synthesis by normal lymphocytes was observed when they were co-cultured with purified thymus-derived lymphocytes (T cells) from a hypogammaglobulinaemic patient. In control studies, suppression of immunoglobulin synthesis was not seen when normal cells were co-cultured with lymphocytes from unrelated normal individuals or from patients with the Sezary syndrome, nor were they inhibited when incubated with purified T cells from normal individuals. In addition, no suppression of immuno-globulin synthesis by normal lymphocytes was observed when they were cultured in serum from the hypogammaglobulinaemic patients. Theses studies suggest that in some patients the disease common variable hypogammaglobulinaemia may be caused or perpetuated by an abnormality of regulatory T cells which act to suppress B-cell maturation and antibody production.

1. Twenty-three mutations, mapping at eight different loci, were shown to prevent detectable suppression of ade2-1 and can1-100 by the ochre suppressor, ocSUPQ2. 2. Some reduce the efficiency of suppression of his5-2 and lys1-1 also. 3. Mutants from each of the eight loci prevented the lethal phenotype of ocSUPQ2 in [psi+] strains. They are, therefore, antisuppressor mutations. 4. One of the loci, asu3, is centromere-linked; two of the loci, asu2 and asu6, are linked to each other.

SUMMARY A mutant induced by nitrosoguanidine in the Challis (group H) strain of Streptococcus contains a number of separable mutations linked to each other and to the locus governing sensitivity to streptomycin. One suppresses the level of resistance conferred by mutations in the streptomycin-sensitivity locus, two confer sensitivity to mitomycin and one confers sensitivity to ultraviolet radiation. None of these mutations affects transformability with either homologous or heterologous DNA. However, with the suppressor in the recipient strain there is a loss of streptomycin-resistant transformants, dependent upon the level of resistance conferred by the donor streptomycin-resistance marker and the degree of linkage between the suppressor and that marker.

This study confirms the finding that washed thymocytes from rats given 100 mg of BGG 48 h earlier, when transferred to syngeneic recipients, exert a specific suppressor effect on immunological responses to BGG in the latter. The active cells are found in a subpopulation of low density, making up less than 10% of the total thymocytes, and are partially resistant to hydrocortisone.

Recent studies support the concept of thymic regulatory or suppressor function. Such regulatory function appears to be present in the first month of life in NZB and NZB/W mice, but is rapidly lost with age. Evidence is presented to support the hypothesis that loss of suppressor function may play an important pathogenetic role in the development of autoimmunity.

Suppressor-sensitive mutants of phage Φ29 have been isolated and classified in 13 complementation groups. These mutants have been complemented with the temperature-sensitive mutants of Talavera et al. (1971) and mutant tsQ1360 reported in this paper; all together they make a total of 17 complementation groups. Two- and three-factor crosses have been carried out with sus and ts mutants, and 16 cistrons have been arranged in a linear genetic map. This map, integrating suppressor- and temperature-sensitive mutants, has a total of 24.2 recombination units.

The action of eight suppersuppressors has been tested on 76 ad-3B mutants which were induced by base-pair transition mutagens. Thirteen mutants were found to be suppressible by at least one ssu gene. Most of the suppressible mutants were found to belong to a class in which one would expect to find nonsense mutants (polar complementing or noncomplementing classes, with AT at the mutant site). However, suppression was observed in other classes, including those containing presumed missense mutants. The specificity of the suppressors and the criteria for molecular classification of the mutants are discussed.

In this work we show that the wild-type ( su − 7) progenitor of the recessivelethal suppressors of UAG ( su + 7(UAG)) and of UAA/G ( su + 7(UAA/G)) is the structural gene for transfer RNA Trp , the adaptor for translating the codon UGG. The su + 7(UAG) suppressor form of the tRNA has a C for U substitution in the middle base of the anticodon; in the su + 7(UAA/G) suppressor tRNA both C residues of the anticodon are replaced by U. Our data establish that the mutational change altering the tRNA Trp to a UAG suppressor is accompanied by a loss of tryptophan-accepting specificity and the acquisition of glutamine-acceptor activity.

SUMMARYThe melanotic tumour genetu bwofDrosophila melanogasterhas a specific suppressorsu-tu. The genotypestu bw; +su-tuandtu bw; su-tushow opposite responses, as measured by tumour penetrance, to increasing choline levels in the defined axenic medium. The three major metabolic functions of choline have been examined using additions to the axenic medium to determine which biochemical pathway(s) are different in the two genotypes. It is concluded that the opposite strain responses are due to changes in the pattern of phospholipid synthesis, and that the gene product of thesu-tugene probably functions in this area of metabolism.

Mutants in a tRNA methylase gene, supK, of Salmonella typhimurium give suppression of UGA and certain frameshift mutants. In addition suppressors which do not suppress UGA, but which suppress frameshift mutants of opposite (effective) signs are described.

Hydroxylamine-induced amber and opal mutants are localized on the map of gene 47 of bacteriophage T4B. The matched map of amber and opal mutations showed the presence of four paired sites which seemed to have arisen in the triplet coding for tryptophan. In growth studies o opal mutants in gene 47 in a series of Su + strains the number of strains bearing a gene-suppressor for amber or ochre mutations also had a weak suppressor activity for some opal mutants. This suppressor acitivity is supposedly due to a second mutation in gene Su uga . A comparative study of the phage yield with amber and opal mutations located in the same (paired) triplet in gene 47 has shown that the suppressor activity depends on the location of the mutant site along the gene. Experiments dealing with the induction of reversions by nitrous acid in amber and opal mutants with mutational sites located in the same triplet of gene 47 (mutant pairs) have shown the essential influence of the nucleotide sequence in the triplet on the frequency of induced reverse mutations at the given site.

SummaryNZB/W mice 4 weeks or older are not easily made tolerant by ultracentrifuged BGG. Younger mice can be made tolerant, but they escape rapidly. Recent studies have suggested a loss of regulatory or suppressor cells in the pathogenesis of immunologic abnormalities early in life in NZB/W mice. Several reports indicate that Concanavalin A (Con A) is capable of activating suppressor cells in normal mice. We found that Con A could prolong the period of tolerance in NZB/W mice when ultracentrifuged BGG was given at 20 days of age. NZB/W mice given ultracentrifuged BGG at 4 weeks of age were not tolerant to subsequent challenge with BGG in adjuvant unless they also received Con A. These studies are compatable with the hypothesis that Con A activates suppressor cell activity which is deficient in NZB/W mice. Alternative explanations of these phenomena are discussed.

It was previously shown that the ochre suppressor mutation sup15B in Escherichia coli determines the accumulation of altered 30 S ribosomal subunits and the presence of altered transfer ribonucleic acid (tRNA) capable of suppressing in vitro the UAG codon. This mutation has been mapped in the present study by means of conjugation and transduction experiments. After establishing the location of sup15B near argH , the following order was determined for the markers tested: metB-argH -( sup15B, supA36 )- rif-thi . A comparison of location, growth rate, and suppressor pattern determined by sup15B and supM indicates the high probability that both suppressor mutations are identical. This study has also yielded a more precise location for the rifampin resistance gene. The most interesting finding is the very close (if not adjacent) location of the suppressor mutations sup15B and supA36 , both of which determine tRNA alterations.

Some physicochemical properties of several aspartate transcarbamylases extracted from pyr3 su-arg2 strains of Neurospora crassa have been studied. It was found that there are differences between these enzymes and the wild-type aspartate transcarbamylase. The principal alteration which is always present is a variable lower affinity of the enzymes for one of the substrates, l -aspartate. This fact could explain the mechanism of the suppressor effect.

Amino acid substitutions in alkaline phosphatase are shown to result from suppression of nonsense mutations in the phosphatase structural gene. The suppressor gene involved in the experiments was Su-1 , one of several that act on nonsense mutations. With one phosphatase mutant the substitution was serine for tryptophan, and with two other mutants the substitution was serine for glutamine. Thus, the original amino acid that is affected by a nonsense mutation can vary, but the amino acid inserted by the Su-1 suppressor gene is in all cases serine.

ABS>It was shown that a large number of isoleucine revertant result from suppressor mutation. Three types of suppressors of isoleucine requirements have been encountered. One kind of suppressor specifically suppresses the allele is/ sub 1-1/ and none of the other three alleles. The second type is nonspecific and suppresses all of the alleles. Both of these kinds of suppressors are dominant. Whereas mutation at any one of the five loci indicated can give rise to specific suppressors, all of the four nonspecific suppressors analyzed are the result of mutation at a single locus. The third type of suppressor, which is also nonspecific, permits the utilization of threonine as a substitute for the isoleucine requirement for growth. This property seems to be under the control of two recessive but complementar linked genes. Growth studies indicate that the presence of specific suppressor (S/sub 1-/is/sub 1-1/) in a haploid culture with any one of the isoleucine alleles (is/sub 1-1/, is/sub 1-2/ or IS) stimulates the growth to some extent. There is also some evidence, although not conclusive, that in some cases a haploid strain possessing two suppressor genes gives poor growth. It is suggested that the nonspecific suppressors act by making available anmore » alternative pathway of synthesis for isoleucine, and that the specific suppressors act by repairing the primary defect in some way or by controlling some environmental factor. (auth)« less

Studies presented in this report are concerned with the effect of endotoxin upon the release of bactericidal antibodies as determined by the agar plaque technique. We found that shortly after the injection of mice with small amounts of endotoxin the number of plaque-forming cells in the spleen was substantially reduced and remained low for about 12 hr. At the same time the titer of specific bactericidal antibodies in the circulation was increased, 6-mercaptopurine was shown to be an effective suppressor of the immune response by inhibiting the multiplication of bactericidin-forming cells. However, administration of this drug did not modify the initial responses of antibodies and plaque-forming cells to endotoxin. Thus, we postulate that endotoxin does not induce destruction and subsequent reconstitution of bactericidin-forming cells, but that the observed changes represent a release of preformed antibodies from competent cells. For a limited time, thereafter, these cells become inactive, but soon resume their normal function of releasing bactericidal antibodies.

Certain constitutive mutations in the two regulator genes for alkaline phosphatase respond to an external suppressor. This result suggests that the products of the regulator genes, and therefore the repressor for alkaline phosphatase, are protein molecules.

During the genetic mapping of a mutation in the pheS gene which confers temperature sensitivity on a strain of Escherichia coli K-12, an extragenic suppressor was discovered which restores ability to grow at the restrictive temperature. The suppressor, which has been named supQ , is cotransduced by bacteriophage P1 with the purE marker. SupQ does not suppress a number of amber or ochre mutations. SupQ − is carried by the prototrophic Hfr Hayes strain AB259, and the presence of the supQ − allele impairs the growth of this strain at 42 C.

In Drosophila recessive mutations have been observed which suppress the effect of specific mutations at other loci. Thus an individual, homozygous for a suppressor gene in the mutant form and for the mutant gene upon which the suppressor acts, is phenotypically wild type, or nearly so. Suppressors of black,(1) purple,(2,3) sable(4) and vermilion(4, 5) are among those, which have been reported. In the vermilion case there is evidence(5) which shows that the action of the suppressor is to restore v+ substance (kynurenine), the formation of which is prevented when the mutant gene vermilion is present in the homozygous condition.

Spleen and lymph nodes of rats, in which a state of transplantation tolerance has been deliberately abolished by adoptive transfer, contain cells which can inhibit syngeneic lymphocytes from normal donors in the initiation of a graft versus host reaction. The suppressive effect shows immunologic specificity. Suppressor cells were not detected in tolerant chimeras.

SUMMARYForty-one suppressors obtained after NG and EMS mutagenesis of two ‘polar’ mutants of segment ‘29’ inPodospora anserinawere genetically analysed. Three classes of suppressor could be distinguished on spectrum pattern criteria. One representative suppressor of each class was demonstrated to be non-gene specific. The class I suppressor was dominant and only suppressed polar mutants in segment ‘29’ and non-ICR-induced ones in genes where polarity cannot be determined. Class II and III suppressors were partially dominant and they suppressed polar, non-polar and even ICR-induced mutants. The difference between classes II and III seems to be only quantitative. According to whether class II and III suppressors are considered strongly or weakly allele-specific, two hypotheses are considered. First,tRNAs could be involved in all three classes of suppression: class I would be nonsense-specific and classes II and III would be nonsense-missense suppressors. Secondly,tRNA could be involved only in class I suppression, while ribosomal ambiguity could be responsible for class II and III suppression.

Protocols employing the mutagens ethyl methanesulfonate and nitrous acid, the base analogs 5-bromouracil and 2,6-diaminopurine, and ultraviolet light have been used in the selection of nonsense suppressors in Saccharomyces cerevisiae . The examination of 1843 revertants obtained in two haploid strains each bearing 12 or 13 suppressible alleles gave 10 phenotypically different suppressors. The classification scheme based on 19 ochre and 3 amber alleles contains 5 ochre-specific, 3 ochre-amber, and 2 amber-specific suppressor classes. The ethyl methanesulfonate protocol, the most effective treatment, resulted in the enhancement of 2 ochre-specific, 1 ochre-amber, and 2 amber-specific suppressor classes. It is assumed that, like the amber and ochre suppressors in E. coli , the nonsense suppressors in yeast are genes coding for transfer-RNA's and that the mutational event giving rise to a suppressor is a change in the bases of the triplet specifying the anticodon. Therefore, from a consideration of the genetic code and the mutagenic specificity of ethyl methanesulfonate, one can predict the amino acids being substituted in the translation of the nonsense codons by the above suppressors: tyrosine by the ochre-specific suppressors, glutamine by the ochre-amber suppressor, and tryptophan and glutamine by the two classes of amber-specific suppressors.

The N1 class of phosphatase nonsense mutations is suppressible by either the Su-1, Su-2 or Su-3 suppressor genes of Escherichia coli . It was previously shown that suppression by the Su-1 gene results in the incorporation of a serine residue into the phosphatase molecule at the position specified by a nonsense codon. The present experiments demonstrate that the amino acid incorporated is glutamine when Su-2 is the suppressor gene, and is tyrosine when Su-3 is the suppressor gene. Thus, the same nonsense codon can be translated in three ways, as serine, glutamine or tyrosine, depending on which of the three suppressor genes is responsible for suppression.

Single subcutaneous injections of supernatant, the equivalent of that from one spleen obtained from either normal or 3-week postburn rat donors and homogenized in phosphate buffer, were given to normal recipient rats in three weight groups, 45–60 gm, 73–84 gm and 245–295 gm. Phosphate buffer controls were injected concomitantly. Effects on the recipients' hematocrits and circulating reticulocyte percentages were observed. Both ‘burned’ and ‘normal’ spleen supernatant depressed hematocrits and reticulocytes. The greatest effect was noted in the 73–84-gm weight class. In a second series of experiments, repeated injections were given for 5 days to normal animals weighing between 190 and 210 gm. The effects of supernatant from both ‘burned’ and ‘normal’ spleens on hematocrits and reticulocyte numbers were compared with those from similarly prepared supernatants of liver and kidney and sera injections. The tissue extracts were given on the basis of 1 gm of the initial wet weight of tissue or serum per 100 gm of body weight of recipient. Only the splenic injections resulted in a progressively sustained hematocrit and reticulocyte depression, with the greatest effect produced by the ‘burned’ spleen extract.

A reciprocal suppression of rough phenotype was found in rough mutants of two prototrophic strains ofSaccharomyces cerevisiae on medium containing 1 % glucose. Suppression affects at least three independent rough loci and is strongly influenced by the genetic background. It is accompanied by suppression of red pigmentation inade2-1 mutants, and this too responds similarly to the genetic background. There is evidence for at least two independent loci that modify the action of the suppressor of both rough and red. The suppressor segregates regularly and is linked to one of the tested rough loci. It is not a super-suppressor and probably is not involved in the regulatory mechanism of purine biosynthesis either. An involvement of glucose metabolism in the suppression can be assumed from the lifting of the suppression of rough phenotype on lactate medium.

Two frameshift mutations located at different genetic sites respond with high specificity to the same outside suppressors. These frameshifts contain similar altered (+1) messenger RNA sequences. In each case the suppressors appear to act by translating the altered (+1) mRNA sequence as the correct (0) sequence.

Greater genetic complexity has been revealed for the control of bivalency in hexaploid wheat. A suppressor of homoeologous pairing has been detected on chromosome 3A. Thus, there are two suppressors in homoeologous group 3. The 3A suppressor may be homoeoallelic to either the suppressor on 3Dβ or the promoter, detected in this study, on 3Dα. Individually these two suppressors are less effective than the suppressor on the long arm of chromosome 5B; however, their combined effect is yet to be studied. This greater complexity suggests that hexaploid wheat may not be too dissimilar to other polyploids as regards genetic control of bivalency. The mode of action of these suppressors appears to be consistent with a heteromultimeric hypothesis.

An elementary echo suppressor is described which consists of a single voice-operated switch located at each end of a four-wire toll connection. It is shown that this circuit is unsuitable for telephone conversations if there is an appreciable delay between the speakers. Modifications and additions to the elementary echo suppressor are made in an effort to improve its performance. Action in the presence of break-in speech is discussed in some detail. The operation of four present-day echo suppressors is described

The “suppressor A” allele facilitates the survival of the untranslated mRNA immediately distal to nonsense codons in the tryptophan operon of E. coli. This may be associated with lack of an endonuclease which is thought to degrade the exposed mRNA.

Normal rat spleen cell synthesis of DNA in response to stimulation with PHA is inhibited at high doses of PHA (≥ 1 μliter/ml) and with cell concentrations ≥ 106/ml. Inhibition is removed when the subpopulation adherent to glass wool is removed and is not restored by reconstituting with purified splenic or peritoneal macrophages. Since the inhibitory or “suppressor” cells do not adhere to plasic and can be recovered from glass wool by simple agitation, they are considered to be weakly adherent spleen cells. Removal of suppressor cells on glass wool does not affect the time course of DNA synthesis by the remaining cells in response to PHA; the peak at 2–3 days is followed by the usual rapid fall to low levels by the fifth day. Spleen cells exert suppressor activity on lymph node cells, in mixtures stimulated with moderate doses of PHA. A new hypothesis, based on a comparison of the present results with recent findings in other laboratories, is proposed: that the regulatory unit in spleen is a suppressor T-cell-macrophage complex.

SUMMARY: Forward mutations at the pyr locus in Neurospora, and back mutations at arg, were scored by using the ‘suppressor method’. This method is efficient and well suited for mutagen screening. Nitrous acid, ethyl-methane sulphonate and ultraviolet radiation were effective as mutagens; 8-ethoxycaffeine yielded inconclusive results. The same pattern of forward mutations at pyr, but different frequencies of back mutations at the arg locus, were obtained with the three agents. In this Neurospora system, nitrous acid appeared to induce mutations which affected simultaneously both DNA strands.

The prime purpose of this paper is to describe the advances in Zener diode transient suppressors for ground vehicle and aircraft application. The evolution of the transient suppressor development for the U.S. Army is presented with emphasis on space, weight, and cost considerations. Improvements including an electronic thermal switch and a "battle override" switch are also described. A futuristic transient suppressor of modular design developed for use as an integral part of the equipment being protected is functionally described.

The cross resistance of intermediate resistant mutants to streptomycin (SM) and kanamycin (KM) was studied genetically by several investigators. The present author attempted to observe the cross resistance of one-step highly SM resistant mutants and SM dependent mutants against KM, and to analyze the genetics of the cross resistance using SM dependent mutants. Strains used were Escherichia coli, strain B/r and its mutants. Phage P 1 was used for transduction technique.One-step highly SM resistant mutants showed the slightly increased resistance to KM, but SM dependent mutants showed various resistant levels, increased or decreased, to KM.From the results of reciprocal transduction between SM dependent mutants and original strain, it was clearly shown that a resistance level to KM was controlled by SM dependent mutation itself or by a closely linked mutation not separable from SM dependent mutation through transduction.The analysis of non-dependent (suppressor) mutants derived from SM dependent mutants indicated that resistance level to KM was also controlled by the suppressor mutation.

SUMMARY: About 200 forward mutants of Neurospora obtained as suppressors of arg were studied. All fell in the pyr region, and all appeared deficient in aspartic transcarbamylase (ATC) to various degrees: extreme deficiencies in ATC (pyr-N alleles) resulted in pyrimidine-dependence as well as suppression of arg, while partial ATC deficiencies (pyr su-arg lleles) led only to suppression. Five different complementation groups were represented among the pyr-N alleles studied. Evidence is presented which suggests that pyr-N and pyr su-arg lleles affect ATC via different mechanisms.