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Results for “Locus Control Region”

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PubMed1976

Guinea pig histocompatibility antigens. III. Analysis of normal lymphocyte transfer (NLT) reactions among guinea pigs with serologically defined phenotypes (GPL-AB locus and I region).

The normal lymphocyte transfer (NLT) reaction occurring upon intradermal injection of lymphocytes into a normal recipient may be considered as a kind of mixed lymphocyte reaction in vivo. In previous experiments, we have defined serologically a number of guinea pig lymphocyte antigens, controlled either by a GPL-A locus (equivalent of H-2 D locus in mice) or by a so-called I region (equivalent to the I region in mice). The I region also appears to control a number of immune response genes in the guinea pig. Using guinea pig inbred strains (such as 2, 13, OM3, BE), guinea pig families homozygous for their GPL-A antigens and serologically characterized outbreds, it has been possible to show that antigens of the I region probably play a higher role in NLT reactions. No NLT reactions occur among outbred animals of a closed colony which have been bred to homozygozity for their GPL-A antigens and thereby probably possess haplotype homozygozity for their major histocompatibility complex. The NLT reaction among serologically characterized guinea pigs may become a convenient way to detect new specificities and recombinant progeny.

Animals↗

PubMed1981

Fine structure of the 21S ribosomal RNA region on yeast mitochondrial DNA. IV. Characterization of the omega neutral allele.

The omega locus controls the polarity of recombination and transmission of genetic markers in the 21S ribosomal RNA region in yeast mtDNA. Polarity is observed in crosses between omega+ and omega- strains. These two strains differ by the presence of an intervening sequence in the 21S ribosomal RNA gene of omega+ strains. Mutations of the omega- allele, omega neutral (omegan), can eliminate the polarity effect. We have made DNA:RNA hybrids containing ribosomal RNA from an omegan strain and mtDNA from Saccharomyces carlsbergensis (identical to omega- in the nucleotide sequence of the omega region). These hybrids contain no mismatch at the omega region detectable by digestion with S1 nuclease. We conclude that omegan differs from omega- only in a point mutation or analogous small alteration and that the omegan mutation can result either in a Cr phenotype (omeganCr) or in the phenotypic suppression of pre-existing Cr mutations (omegenCs). All results can be explained by a model which postulates interaction in the ribosome between the Cr and omegan regions of the ribosomal RNA and interference of the omegan mutation with splicing of the precursor ribosomal RNA in omega+ strains. The mechanism of omega-directed polarity is discussed.

Alleles↗

PubMed1990

Neurospora crassa A mating-type region.

The mating-type locus of the haploid filamentous fungus Neurospora crassa is a regulatory region that controls entry into the sexual cycle and prevents formation of mixed mating-type heterokaryons in the vegetative phase. The locus consists of alternative sequences called A and a. The A mating-type DNA sequence of Neurospora crassa is composed of a region of 5301 base pairs that has little similarity to the sequence present at the mating-type locus in an a mating-type strain. However, the sequences flanking the mating-type locus in the A haploid and a haploid genome are essentially identical. The region of the A mating-type sequence required for expression of the heterokaryon incompatibility and sexual functions has been localized to a single open reading frame (ORF) encoding a polypeptide of 288 amino acids. Sequence analysis of sterile, heterokaryon-compatible mutants reveals frameshift mutations in this same ORF. The putative 288-amino acid product has a region of similarity to the MAT alpha 1 polypeptide of Saccharomyces cerevisiae.

Amino Acid Sequence↗

PubMed1986

Assignment of symbiotic developmental phenotypes to common and specific nodulation (nod) genetic loci of Rhizobium meliloti.

Rhizobium meliloti nodulation (nod) genes required for specific infection and nodulation of alfalfa have been cloned. Transposon Tn5 mutagenesis defined three nod regions spanning 16 kilobases of the pSym megaplasmid. Genetic and cytological studies of 62 nodulation-defective mutants allowed the assignment of symbiotic developmental phenotypes to common and specific nod loci. Root hair curling was determined by both common (region I) and specific (region III) nod transcription units; locus IIIb (nodH gene) positively controlled curling on the homologous host alfalfa, whereas loci IIIa (nodFE) and IIIb (nodH) negatively controlled curling on heterologous hosts. Region I (nodABC) was required for bacterial penetration and infection thread initiation in shepherd's crooks, and the nodFE transcription unit controlled infection thread development within the alfalfa root hair. In contrast, induction of nodule organogenesis, which can be triggered from a distance, seemed to be controlled by common nodABC genes and not to require specific nod genes nodFE and nodH. Region II affected the efficiency of hair curling and infection thread formation.

Cloning, Molecular↗

PubMed1987

MAT alpha 1 protein, a yeast transcription activator, binds synergistically with a second protein to a set of cell-type-specific genes.

We show by electrophoresis mobility shift and by DNAase I footprinting assays that the alpha 1 product of the yeast alpha mating-type locus binds to homologous sequences within the control regions of the three known alpha-specific genes. Binding requires both alpha 1 and a second yeast protein(s) (called PRTF) that is present in all three cell types (a, alpha, and a/alpha); neither protein binds alone. Binding and competition experiments using synthetic oligonucleotides indicate that PRTF binds to only part of the homology found at alpha-specific genes and imply that alpha 1 binds to the remainder. Our results suggest that alpha 1 renders gene expression alpha-specific by creating a binding site for PRTF. Similar experiments lead to the idea that PRTF also plays a role in transcription of a-specific genes. Perhaps a-specificity is achieved through the occlusion of the PRTF binding site by alpha 2, the negative regulator encoded by the alpha mating-type locus.

Base Sequence↗

PubMed1976

Regulatory mechanisms in cell-mediated immune responses. III. I-region control of suppressor cell interaction with responder cells in mixed lymphocyte reactions.

Active suppression of mixed lymphocyte reaction (MLR) response is mediated by a soluble factor released by alloantigen-activated murine suppressor cells. Genetic restrictions controlling suppressor factor interaction with MLR responder cells were elucidated in this study. Non-H-2 genetic background was irrelevant to effective interaction. Using congenic strains and strains with intra-H-2 recombinants the genetic locus controlling suppressor T-cell-responder cell interaction was mapped in the I-C or S regions of the H-2 complex. Similarly, recombinant strains were used to exclude the presence of another suppressor cell-responder cell interaction locus in K,I-A, and I-B regions. It thus appears that the I-C subregion of the H-2 complex controls suppressive cell interactions in this T-cell-mediated immune response.

Animals↗

PubMed1985

Defective responsiveness of adenylate cyclase to forskolin in the Drosophila memory mutant rutabaga.

The Drosophila memory mutant rutabaga (rut) has been previously shown to have a defective subpopulation (or functional state) of the enzyme adenylate cyclase. We report here that the reduced adenylate cyclase activity is also associated with a defective responsiveness of the enzyme to forskolin. Forskolin activation isotherms of the enzyme in normal membranes reveal low- and high-affinity forskolin-interacting components; the residual enzyme in the mutant shows a smaller proportion of the high-affinity response. In addition, in mutant membrane preparations, forskolin fails to shift the Km of the enzyme for free Mg2+ and for MgATP, in contrast to the situation in the normal tissue. The defect in the responsiveness to forskolin in rut is even more pronounced in a Lubrol-solubilized enzyme preparation, and is due to intrinsic properties of the cyclase system rather than to the absence (or presence) of a soluble, or detergent solubilized, factor in rut. The reduced forskolin responsiveness maps to the X chromosomal segment 12F5-6 to 13A1-5, within the region previously reported to span the locus that controls both the abortive memory and the lack of Ca2+-stimulation of adenylate cyclase in rut17. The possible relevance of the findings to postulated molecular mechanisms of short-term memory formation is discussed.

Adenylyl Cyclases↗

PubMed1983

Characterization of T lymphocyte subsets with monoclonal antibodies: discovery of a distinct marker, Ly-m22, of T suppressor cells.

The study of cell surface antigens has accelerated in the few years since the advent of hybridoma technology to the point where many dozens of such markers have now been described. The functional heterogeneity of post-thymic T cells in the immune response, however, still exhibit complexities beyond the resolving power of our current repertoire of marker antigens. In this study, we investigated the surface phenotype of three types of effector T cells: helper cells, nonspecific suppressor cells, and cytotoxic T cells, using four recently discovered alloantigen systems of T cells: Ly-m10, Ly-m18, Ly-m19, and Ly-m22. SRBC-primed spleen cells were used as a source of specific helper T cells, and they were tested by their ability to promote antibody synthesis by B lymphocytes. Concanavalin A-activated suppressor cells were assayed by their ability to inhibit that response. Cytotoxic T cells were activated by alloantigen. We found Ly-m10 to be expressed on all three cell types tested, whereas Ly-m18 and Ly-m19 were absent from all three. Ly-m22, whose controlling locus is closely linked to the Mls region, had a unique distribution, being present solely on suppressor cells. Thus Ly-m22 emerged as a new marker that distinguishes nonspecific T suppressor cells (Ly-m22+) from T helper as well as cytotoxic T cells (Ly-m22-). Ly-m22 is the only antigen besides I-J so far known to be restricted to suppressor cells.

Animals↗

PubMed1978

Two-gene control of the expression of a murine Ia antigen.

Two dimensional polyacrylamide gel electrophoresis of Non-Idet P-40 extracts and of specific Ia immunoprecipitates from [35S]methionine-labeled mouse spleen lymphocytes has revealed that the cell surface expression of some Ia antigens appears to be controlled by two genes. One locus, which maps in the I-A subregion, is probably the structural gene for an Ia polypeptide chain. The second locus, which maps between the I-J and H-2D regions, controls whether this I-A encoded molecule (Ae) remains in the cytoplasm or is modified and expressed on the cell surface. Complementation between these two loci allowing surface expression of Ae can occur in the cis or trans chromosomal position. Both the I-A molecule and a polypeptide chain coded for by a locus in I-E are coprecipitated by anti-I-E antibodies, suggesting that these two chains are associated with each other as a multisubunit complex in the cell. Because the ability to complement I-A for Ae expression is a property only of those strains which synthesize an I-E-encoded protein, it is likely that the I-E product itself is regulating the expression of Ae. These observations suggest several mechanisms by which interaction between two I region loci can generate new cell surface molecules. As a result, they may have important implications for understanding the molecular basis of two gene control of immune responsiveness and immune suppression.

Animals↗

PubMed1985

Genes controlling gp25/30 cell-surface molecules map to chromosomes X and Y and escape X-inactivation.

The monoclonal antibody AbO13 defines a cell-surface antigen that is expressed on most cultured human cells, but not on rodent cells. AbO13 precipitates glycoproteins of 25,000 and 30,000 mol. wt. from lysates of [3H]glucosamine-labeled human cells. Results of the serological typing of a panel of 25 rodent-human somatic cell hybrid clones show that reactivity with AbO13 segregates with the human X and Y chromosomes. The presence of either of these chromosomes is sufficient for O13 expression on the hybrid cell surface. Analysis of hybrid clones containing human X chromosomes with karyotypically defined deletions permitted the regional assignment of the X-linked gene locus controlling the expression of O13 to Xp22-pter. In addition, AbO13 is reactive with Chinese hamster-human hybrids derived from fibroblasts of a 49,XXXXX individual that contained only inactivated copies of the human X chromosome. These results suggest that the X-linked locus determining the expression of O13 is not subject to X-inactivation.

ABO Blood-Group System↗

PubMed1981

Genetic control of the expression of allelic Ig genes at the VH a locus in a1/a2 heterozygous rabbits.

Heterozygous rabbits representing 9 of 15 possible a1 and a2 heavy chain haplotype gene combinations among rabbits in the University of Illinois colony were analyzed for ratios of a1 to a2 in serum immunoglobulin (Ig). The Ig from rabbits of the a1x-y-n81f73g74de12,15 heavy chain haplotype in combination with any of three a2-associated heavy chain haplotypes have higher ratios of a1 to a2 than Ig from rabbits in which a1 is encoded by 4 other heavy haplotypes. For example, the mean a1:a2 ratio for adult a1x-y-n81f73g74de12,15/a2x32y33,- n82,f71g75de12,15 rabbits was 12:1 compared to 5:1 for a1x-y33,30n83,f71g75de12,15/a2x32y33,- n82,f71g75de12,15 heterozygous rabbits. Family studies indicated that the a1:a2 ratio was under the control of the heavy chain chromosomal region or a locus closely linked to it. Whether the regulation is due to varying numbers of VH genes and/or J gene segments, a separate regulator gene, or more efficient joining of certain gene segments, has yet to be determined.

Alleles↗

PubMed1988

The nature of hemopoietic histocompatibility determinants. Differential sensitivity of Hh-1b and H-2b determinants to tunicamycin.

NK cell-dependent resistance of F1 hybrid mice to parental H-2b hemopoietic allografts is directed to cell surface structures controlled by the Hh-1 locus in or near the H-2D region. Crucial to an understanding of this enigmatic phenomenon is the information on the biochemical nature of the Hh-1 locus-controlled structures. Therefore, we examined the effect of tunicamycin (TM), an inhibitor of asparagine-linked glycosylation and ganglioside biosynthesis, on the expression of Hh-1 determinants in H-2b/Hh-1b lymphomas. The Hh-1b determinants on EL-4 and RBL-5 cells were no longer detectable after TM treatment, as demonstrated by the failure of the treated cells to inhibit hybrid resistance to parental H-2b bone marrow cells in vivo. This interpretation was supported by the unaltered ability of the TM-treated cells to localize in the spleens of irradiated F1 hybrid recipients. In contrast, TM caused only moderate reduction in H-2Kb and H-2Db expression as measured by binding of specific antibodies. This was accompanied by reduced susceptibility to alloimmune anti-H-2Db CTL, but not to anti-H-2Kb CTL. No decrease was found in the susceptibility to NK cell cytotoxicity in vitro. These data indicate that N-linked glycosylation or ganglioside synthesis is crucial for the expression of the Hh-1 locus-controlled target structures, but not for the H-2 class I molecules. The data also show that the Hh-1b determinants are substantially different from those which confer the susceptibility to NK cell-mediated in vitro cytotoxicity.

Animals↗

PubMed1992

Spontaneous malignant transformation of melanocytes explanted from Wf/Wf mice with a Kit kinase-domain mutation.

The W/Kit mouse locus, affecting proliferation and survival of pigment cells, blood cells, and germ cells, is known to encode a tyrosine kinase growth factor receptor and is considered a protooncogene; yet it has not heretofore been causally implicated in any malignancies of those cells. The Wf/Wf mutant mouse coat comprises viable and inviable melanoblast clones, seen ultimately as pigmented and white transverse stripes--the latter more prominent. Judging from the pattern, all clones initially expand, and the inviable ones then undergo programmed cell death prenatally. To observe skin melanocytes of the viable clones during extended proliferation, the cells were explanted from individual young mice. An unusually large number of primary explants failed to survive--a result consistent with a growth handicap. In 3 of the 10 surviving cell lines, many cells spontaneously underwent a series of striking changes with the classic features of transformation. The two transformed lines that have been tested by grafting to immunosuppressed hosts formed undifferentiated invasive tumors compatible with malignant amelanotic melanoma. None of our 52 other melanocyte lines of the coisogenic wild-type strain and 13 other natural genotypes have become transformed under the same culture conditions. Molecular analysis of the Wf gene revealed a single change from wild-type: a point mutation affecting the catalytic region in the kinase domain of the Kit protein. The apparent growth disadvantage due to the mutation may allow selection for melanocytes mobilizing more efficient pathways, thus leading to neoplasia. Production of both viable and inviable melanoblast clones is unlikely to be due only to the kinase mutation; possibly the degree, duration, and consistency of expression of this locus may be controlled by cis elements outside the coding region.

Animals↗

PubMed1990

Detailed structure of the Drosophila melanogaster stellate genes and their transcripts.

The X-linked Stellate locus contains two major size classes of a tandemly repeated gene. An example of each class has been sequenced. The steady-state level of Stellate RNA is much higher in XO testis than in XY testis. Sequencing of six cDNA clones derived from XO testis RNA shows that there are two major introns in the Stellate genes. Primer extension and RNase protection analyses show that these introns are spliced much more efficiently in XO than in XY testis. These results also indicate the major transcriptional start site for Stellate RNA. P element transformation results with a marked Stellate gene demonstrate that at least one of the genes sequenced contains a functional promoter, which generates low levels of RNA in XY testis and high levels of RNA in XO testis. This promoter does not contain a TATA element in the -30 region relative to the transcriptional start. Previous results had implicated a specific region of the Y chromosome, designated here as the Su(Ste) locus, in the control of the Stellate genes on the X. Analysis using segmental Y deficiencies shows that the Su(Ste) region suppresses both the high levels and efficient splicing of Stellate RNA.

Amino Acid Sequence↗

PubMed1989

[Restriction analysis of deletions and deletion mapping of point mutations in the ADE2 gene of Saccharomyces cerevisiae yeasts].

The method of restriction analysis has been used to study the length of 10 deletion mutations in ADE2 locus of Saccharomyces cerevisiae. We showed that 7 deletions overlapped the whole transcribed region of the gene ADE2, while 3 deletions have one of the ends situated in this region. Four controlled sites were fixed on the genetic map of ADE2 locus, based on these results. Deletion mapping of great number of point mutations demonstrated non-random distribution of mutations of different types on the map of ADE2 locus.

Chromosome Deletion↗

PubMed1976

A new I subregion (I-J) marked by a locus (Ia-4) controlling surface determinants on suppressor T lymphocytes.

In an accompanying publication we show that a subpopulation of T lymphocytes, which includes allotype suppressor T cells, selectively expresses I-region determinants. In this report, we show that these determinants are controlled by a new locus, Ia-4. Unlike the classically defined Ia antigens, they are not found on B lymphocytes. Antibody against Ia-4 determinants cannot be detected by conventional dye exclusion cytoxicity assays, suggesting that they are present on a small subpopulation (less than 10%) of peripheral T lymphocytes. The Ia-4 locus marks a new I subregion, provisionally designated I-J. This chromosomal segment is defined by the crossover positions in strains B10.A(5R) (K-end boundary) and B10.HTT (D-end boundary), and maps between the I-B and I-C subregions.

B-Lymphocytes↗

PubMed1990

A transgenic mouse model of sickle cell disorder.

A single base-pair mutation (beta s) in codon 6 of the human beta-globin gene, causing a single amino-acid substitution, is the cause of sickle cell anaemia. The mutant haemoglobin molecule, HbS, polymerizes when deoxygenated and causes deformation of the erythrocytes to a characteristic 'sickled' shape. Sickling of cells in small vessels causes painful crises and other life-threatening complications. Although the molecular basis for sickle cell anaemia has been known for 30 years, no definitive treatment is available. An animal model of sickle cell anaemia would not only allow a detailed analysis of the factors that initiate erythrocyte sickling in vivo and of the pathophysiology of the disease, but would also permit the development of novel approaches to the treatment of the disease. By using the dominant control region sequences from the human beta-globin locus, together with human alpha- and beta s-globin genes, we have obtained three transgenic mice with HbS levels ranging from 10 to 80% of total haemoglobin in their red cells. As observed in homozygous and heterozygous Hbs patients, the erythrocytes of this mouse sickle readily on deoxygenation. Irreversibly sickled cells, which are characteristic of sickle-cell patients homozygous for beta s, are also observed in the peripheral blood of the mouse with high levels of HbS.

Anemia, Sickle Cell↗

PubMed1984

Induction of interferon gamma in mouse spleen cells by culture supernatants of mycoplasma arthritidis.

Factor(s) in the supernatant of cultured mycoplasma arthritidis (MAS) represented potent inducers of interferon (IFN) in cultures of mouse spleen cells. Responding mouse strains included A/J, BALB/c, CBA, C3H, and DBA/2 whereas spleen cells of C57BL/6 and C57BL/10 mice were nonresponders. Interferon production was controlled by the I region of the H-2 locus. Treatment of CBA spleen cells by anti-thy-1 antibody plus C abolished IFN production. A similar effect was seen when CBA spleen cells were freed of macrophages by passage through Sephadex G-10 columns. Pure macrophages themselves, however, were not producing IFN when treated by MAS. Macrophage-depleted CBA spleen cells could be reconstituted to produce IFN by the addition of 2-ME. Interferon induction by CBA spleen cells was independent of lymphoproliferation as evidenced by experiments utilizing mitomycin C. The IFN induced by MAS represented IFN gamma (gamma), since it was acid-labile and neutralized by a specific antiserum.

Animals↗