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Results for “genetic interaction”

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At least 73 records · Page 4Linked to original sources
PubMed1979

Macrophage-lymphocyte clusters in the immune response to soluble protein antigen in vitro. VII. Genetically restricted and nonrestricted physical interactions.

We have assessed the genetic restrictions on physical interactions between macrophages and central lymphocytes and between central and peripheral lymphocytes in antigen-specific macrophage-lymphocyte clusters with respect to I-region differences of inbred strains 2 and 13 guinea pigs. When using lymphocytes from guinea pigs immunized with DNP-OVA or DNP-GL in CFA, the antigen-specific interaction between central lymphocyte and macrophage requires that both cells be derived from animals syngeneic at the I-region of the major histocompatibility complex. In studies using antigens, the responses to which is under the control of MHC-linked Ir genes, macrophages from the responder, but not from the nonresponder parental strain support cluster formation with responder x nonresponder F1(2 X 13) T cells. In contrast, the physical interactions between central and peripheral T lymphocytes are not restricted by the I-region of the MHC and the peripheral lymphocyte need not be from an animal immune to the antigen used to drive macrophage central lymphocyte interactions.

Animals↗
PubMed2026

Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.

Down syndrome (DS), associated with trisomy 21, is the most common genetic cause of developmental delay and intellectual disability, yet the specific dosage-sensitive genes and the associated genetic mechanisms underlying these phenotypes remain incompletely defined. Here, we applied an additive genetic strategy to dissect the Down syndrome critical region (DSCR) by generating 2 complementary mouse models using Cre/loxP-mediated chromosome engineering that together span the entire DSCR on mouse chromosome 16: Dp(16)5Yey, duplicating the Setd4-Kcnj6 interval, and Dp(16)6Yey, duplicating the Kcnj15-Mx2 interval. In addition, we engineered a third duplication model, Dp(16)7Yey, carrying a selective duplication of the Dyrk1a-Kcnj6 interval containing only these 2 genes. Building upon our previously reported results, cognitive behavioral analyses of these 3 models reveal a complex functional genetic architecture of the DSCR, including dosage-sensitive genetic elements, interactions among these elements, and their contributions to DS-associated cognitive deficits. Together, these findings highlight the complexity of dosage-dependent genetic interactions, which provide important insights into DSCR functional organization and have major implications for the development of effective therapeutic strategies for DS-associated cognitive deficits. In addition, these duplication mouse models represent valuable resources for further genetic dissection of DS phenotypes beyond cognition.

Animals↗
PubMed1976

Interaction of genes and metals in development.

Examples are presented in interactions between genetic factors and certain trace during development in experimental animals. One type of interaction irenatal nutritional manipulation. The other involved strain differences, which lead differential responses to dietary deficiency. The mutant gene pallid in mice produces abnormal development of the inner ear similar to that resulting from intrauterine manganese deficiency. This abnormality is prevented by manganese supplementation of prenant mutant mice, and as in manganese deficiency, appears to result from depressed synthesis of mucopolysaccharides. Are interaction between copper and the mutant gene cribkled in mice is describes. High dietary copper curing prenatal and abnormal life doubled postnatal survival of mutants and brought about alterations in other parameters. In A/J mice, which have a significant incidence of spontaneous cleft lip and palate, a marginal deficiency prenetally of dietary zinc did not cause an increased incidence of this anomaly. However, the incidence of other malformations was greatly increased in this strain but not in hybird controls. It is proposed that in man as in animals teratogenesis might involve genetic-nutritional interactions as well as multifractorial interactions including genes, nutrients, drugs, and other environmental agents.

Animals↗
PubMed1977

Genetic controls and cellular interactions in antibody formation.

Both thymus-derived lymphocytes (T cells) and bone marrow--derived lymphocytes (B cells) play critical roles in specific antibody responses to antigens. Genetic controls of the antibody response in mammals have been found to reside largely within the major histocompatibility complex where different genes appear to code for immune response (Ir), immune suppression (Is), and cell interaction (CI) molecules.

Animals↗
PubMed1978

Diet, genetics, and mental retardation interaction between phenylketonuric heterozygous mother and fetus to produce nonspecific diminution of IQ: evidence in support of the justification hypothesis.

The justification hypothesis postulates that an individual genetically deficient in the synthesis of any of the 12 nonessential amino acids requires that amino acid in the diet just as a normal individual requires any essential amino acid. The deficiency of that single amino acid causes diminished protein synthesis. The hypothesis proposes that mental retardation develops during the late stage of fetal development, when the brain is growing most rapidly, as a result of the inability of the mother to deliver an appropriate amount of that nonessential amino acid to her fetus who, in turn, is unable to correct for this deficiency due to his genetic constitution. A paradigm is provided by the disease phenylketonuria in which the homozygote lacks the enzyme for synthesis of the nonessential amino acid tyrosine. By measuring the appearance of tyrosine in the plasma after an oral dose of phenylalanine, it is possible to show differential capability among siblings of known phenylketonuric children, in the expected Mendelian ratio. The mean IQ of the two-thirds of the siblings who were least able to convert phenylalanine to tyrosine (presumably heterozygotes) was 10 points lower than the mean IQ of the "normals," who were most able to synthesize tyrosine. The difference is statistically significant (P <0.01). The mean maternal IQ was halfway between that of the heterozygote group and that of the normal group, confirming the prediction of maternal-fetal interaction.

Diet↗
PubMed1979

A dnaB analog ban, specified by bacteriophage P1: genetic and physiological evidence for functional analogy and interactions between the two products.

Bacteriophage P1 has been shown previously to determine a product ban that can substitute in DNA replication for the protein specified by cis-tron dnaB of Escherichia coli. However, ban product furnished by P1 bac prophage (ban constitutive) substitutes only poorly for DNA replication in the absence of dnaB product in a strain bearing an unsuppressed amber mutation, dnaB266, as shown by the cryosensitivity of the dnaB266 (P1 bac) lysogen and its unability to support lambda growth. An additional mutation (termed crr) in the P1 bac prophage has been obtained which confers cryoresistance to the sup+ dnaB266 (P1 bac crr) lysogen and restores its ability to support lambda growth. ban product produced in P1 bac crr lysogen fulfills all dnaB roles in vivo, especially in the various instances in which ban product expressed in P1 bac lysogens does not. The ban product is expressed constitutively in P1 crr prophage. The crr-1 mutation is tightly linied to the bac-1 and ban-1 mutations and is dominant over crr+. The nature of the crr mutation is discussed: two hypotheses are considered, that of a mutation in the ban gene rendering the ban product more active or that of a site mutation in the ban operon increasing the level of ban expression. Expression of ban product (wild type or altered) leads to interactions with the variously altered dnaB product. Both positive and negative interactions are described. Genetic results presented here suggest that ban and dnaB subunits interact to form hybrid dnaB-like molecules; the average composition of which depends on the relative quantities of ban and dnaB subunits in the cell.

Coliphages↗
PubMed1976

The genetic instability and mutagenic interaction of chromosomal duplications present together in haploid strains of Aspergillus nidulans.

Previous work has shown that strains of Aspergillus nidulans with a chromosome segment in duplicate (one in normal position, one translocated to another chromosome) are unstable. Deletions occur from either duplicate segment. The present work has shown that when a chromosome I duplication and a chromosome III duplication are together in a haploid, deletions from the intact III duplication generally precede deletions from particular sections of the I duplication. Furthermore, the III duplication can enhance to some (but not major) extent the frequency of deletions from the I duplication. After the III duplication becomes reduced in size as a result of the loss of chromosomal material from the translocated duplicate III segment, such a reduced III duplication can greatly enhance the frequency of deletions from the I duplication. In other words, a III duplication of reduced size can promote far more deletions from the I duplication than the intact III duplication. The major increase in the deletional instability of the I duplication as promoted by the reduced III duplication is confined to the translocated duplicate I segment. The reduced III duplication can induce deletions from a section of the translocated duplicate I segment in accord with a temporal programme, and it appears that a particular region of the I duplication is far more under the mutagenic influence of the reduced III duplication than another region. Moreover, there is indication that there is a differential effect of two generally different genetic backgrounds on the susceptibility of duplication-regions to deletion. Possible mechanisms involved in such chromosomal instability are proposed. A manner in which genetic instability may be related to development is also proposed.

Aspergillus nidulans↗
PubMed1979

Genetic evidence for possible interaction between a ribonucleic acid polymerase subunit and the spo0C gene product of Bacillus subtilis.

Spontaneous rifampin-resistant mutants (9V Rifr) were isolated from a mutant strain of Bacillus subtilis, 9V, which has a spo0C mutation. Whereas 90% of the 9V Rifr double mutants maintained the Spo0C phenotype (Spo- Abs +/-), the remaining 10% had the Spo0A phenotype (Spo- Abs-). The latter mutants, termed 9V Rifr Spo- Abs-, were revealed to have other Spo0A characters, such as reduced transformability, higher sensitivity to phage phi 2, and reduced frequency of lysogenization by phage phi 105. The rif mutation of these 9V Rifr Spo- Abs- strains was mapped near the cysA locus. The phenotype of the Rifr transformants of strain 9V by deoxyribonucleic acid derived from these 9V Rifr Spo- Abs- strains was Spo0A, and that of the Rifr transformants of strain 168 was Spo+ Abs+. The ribonucleic acid polymerase of the 9V Rifr Spo- Abs- strains was shown to be resistant to rifampin.

Bacillus subtilis↗
PubMed1978

[Studies on possible interactions of thalidomide and genetic material from chicken embryos (author's transl)].

Tritium labelled thalidomide was applied to chicken embryos of various stages and the distribution of the readioactive label was investigated. No specific binding tendency to components of the cell could be found, especially no affinity to nucleic acids and to the chromosomal proteins (histones and non-histones) could be observed, which had been discussed hypothetically. An influence on DNA replication and transcription rate could also not be detected.

Animals↗