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PubMed2003

What friends are for! The use of routine standards in social comparison.

Social comparisons are frequently used for self-evaluation. As a consequence, judges have to be efficient in each comparison step. Standard selection, however, is traditionally seen as an elaborate process in which judges deliberately select similar standards. We propose that often judges do not engage in such deliberate selection processes. Instead, they use routine standards--standards that have frequently been used for self-evaluation. Consistent with this assumption, Studies 1-3 demonstrate that student participants activate knowledge about their best friend--a likely routine standard--during self-evaluation. In Study 1, lexical decisions for the best friend's name are facilitated after self-evaluation. In Study 2, participants judge their best friend faster after evaluating themselves on the same dimension. In Study 3, this is even the case if the best friend is dissimilar and consequently undiagnostic. Finally, in Study 4, self-evaluations are primarily influenced by comparison information about an experimentally created routine standard.

Adult↗
PubMed1978

Lengthening of the G1 phase is not strictly correlated with differentiation in Friend erythroleukemia cells.

Friend murine erythroleukemia cells (Friend cells) undergo erythroid differentiation in vitro with an increased probability when cells are cultured in the presence of dimethyl sulfoxide (Me2SO) or other agents. Exponentially growing Friend cells, after dilution into medium containing Me2SO, underwent a transient lengthening of the G1 phase of the cell cycle before they became committed to erythroid differentiation. For nine inducing agents, a positive correlation was found between the percentage of cells that had differentiated and synthesized heme, and the percentage of progenitor cells in which a lengthened G1 phase had previously been observed. This correlation was not found, however, with two other potent inducing agents, hypoxanthine and actinomycin D. Moreover, cells that underwent a lengthened G1 phase did not always terminally differentiate. One such example was a Me2SO-resistant, variant Friend cell line (520a) grown in the presence of Me2SO. These results imply that the prolonged G1 phase, although observed with many inducers, is not a prerequisite for erythroid differentiation with all inducers.

Animals↗
PubMed1979

Implantation of the isolated human erythrocyte anion channel into plasma membranes of Friend erythroleukemic cells by use of Sendai virus envelopes.

Sendai virus envelopes and human erythrocyte band 3 membrane polypeptides were isolated in detergent solutions and coreconstituted into detergent-free vesicle structurally resembling viral envelopes. Formation of hybrid viral envelope-band 3 vesicles (VB3) was demonstrated by immunoprecipitation of VB3 containing 4,4'-diisothiocyano-2,2'-ditritostilbenedisulfonic acid-labeled band 3 in the presence of antiviral antiserum. The hybrid VB3 vesicles displayed agglutination, fusion, and hemolytic properties similar to those of reconstituted viral envelopes. Incubation of VB3 with Friend erythroleukemic cells resulted in fusion-mediated insertion of viral antigens and of band 3 into the plasma membranes of the recipient cells. The presence of band 3 incorporated into Friend erythroleukemic cells was revealed structurally by electron microscopy after staining with ferritin-conjugated anti-human erythrocyte membrane antiserum. Incorporation of band 3, the putative erythrocyte antion channel, led to a marked and specific stimulation of anion exchange in Friend erythroleukemic cells. The viral-mediated insertion of an isolated membrane protein into viable Friend erythroleukemic cells provides a method for studying membrane protein turnover and for assaying reconstituted membrane components such as carriers or channels.

Animals↗
PubMed1990

Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.

The leukemogenic membrane glycoprotein (gp55) encoded by Friend spleen focus-forming virus appears to bind to erythropoietin receptors (EpoR) sto stimulate erythroblastosis [Li, J.-P., D'Andrea, A.D., Lodish, H.F. & Baltimore, D. (1990) Nature (London) 343, 762-764]. To directly compare the effects of gp55 with erythropoietin (Epo), we produced retrovirions that encode either gp55, Epo, or EpoR. After infection with EpoR virus, interleukin 3-dependent DA-3 cells bound 125I-labeled Epo and grew without interleukin 3 in the presence of Epo. These latter cells, but not parental DA-3 cells, became factor-independent after superinfection either with Epo virus or with Friend spleen focus-forming virus. In addition, Epo virus caused a disease in mice that mimicked Friend erythroleukemia. Although Fv-2r homozygotes are susceptible to all other retroviral diseases, they are resistant to both Epo viral and Friend viral erythroleukemias. These results indicate that both gp55 and Epo stimulate EpoR and that the Fv-2 gene encodes a protein that controls response to these ligands. However, the Fv-2 protein is not EpoR because the corresponding genes map to opposite ends of mouse chromosome 9. These results have important implications for understanding signal transduction by EpoR and the role of host genetic variation in controlling susceptibility to an oncogenic protein.

Animals↗
PubMed1974

In situ localization of globin messenger RNA formation. II. After treatment of Friend virus-transformed mouse cells with dimethyl sulfoxide.

Globin messenger RNA (mRNA) levels in Friend virus-transformed mouse cells have been estimated by in situ hybridization of DNA copy (cDNA) to fixed preparations of cells and by hybridization of cDNA to extracted cytoplasmic RNA in true solution. The results obtained by both methods agree in showing that a low level of globin mRNA can be detected in untreated Friend cells. The levels of hemoglobin and globin mRNA have also been correlated after treatment of Friend cells with dimethyl sulfoxide (DMSO). The results obtained by both experimental approaches show that there is a minimum period of treatment with DMSO required in order that Friend cells may become hemoglobinized, and that this period coincides with the time when globin mRNA accumulates. Moreover, bromodeoxyuridine prevents both hemoglobin and globin mRNA accumulation.

Animals↗
PubMed1980

Hypomethylation of DNA during differentiation of Friend erythroleukemia cells.

DNA from mammalian cells has been shown to contain significant amounts of 5-methyl cytosine resulting from enzymatic transfer of methyl groups from s-adenosylmethionine to cytosine residues in the DNA polymer. The function of this modification is not known. We have found that DNA synthesized during chemically induced differentiation of friend erythroleukemia cells is hypomethylated, as measured by its ability to accept methyl groups transferred by homologous DNA methyltransferases in vitro. The extent of hypomethylation detected by this sensitive method is small, a decrease of less than 1.6 percent in 5-methylcytosine content. Hypomethylated DNA can be isolated from friend erythroleukemia cells grown in the presence of dimethyl sulfoxide, butyrate, hexamethylene-bis- acetamide, pentamethylene-bis acetamide, and ethionine. However, hypomethylated DNA is found only under conditions where differentiation is actually induced. DNA isolated from cells of a dimethyl sulfoxide- resistant subclone grown in the presence of that agent is not hypomethylated, although DNA of these cells becomes hypomethylated after growth in the presence of inducers that can trigger their differentiation. We also find that the DNA of friend erythroleukemia cells does not become hypomethylated when the cells are exposed to inducing agents in the presence of substances that inhibit differentiation. These results suggest a close link between genome modification by methylation and differentiation of friend erythroleukemia cells.

Animals↗
PubMed1976

Mechanisms of genetic resistance to Friend virus leukemia in mice. II. Resistance of mitogen-responsive lymphocytes mediated by marrow-dependent cells.

Friend leukemia virus suppresses the proliferative responses of normal thymus-dependent (T) and bursa equivalent-dependent (B) lymphocytes from spleen, thymus, lymph node, and bone marrow to mitogens. The suppressive effect of Friend virus complex (FV) requires fully infectious virions. Friend erythroleukemic cells, washed to removed extracellular virus, fail to suppress concanavalin A (Con-A)-induced mitogenesis of normal spleen cells. This indicates that FV does not mediate its immunosuppressive effect via transformed erythropoietic cells. The in vitro suppressive effect of FV on lymphocyte mitogenesis is under host genetic control. Spleen, bone marrow, and thymus cells from strains of mice susceptible to FV-induced leukemogenesis in vivo were quite susceptible to the suppressive effects of FV in vitro. On the other hand, similar cells from strains of mice such as C57BL/6 resistant to Friend erythroleukemia, were quite resistant to in virto immunosuppression by FV. Mitogenesis of splenic T cells from resistant B6 mice, previously treated with 89Sr, became susceptible to suppression by FV. This indicated that the in vitro resistance of lymphocytes to FV-induced suppression is not an intrinsic property of T cells, but is controlled by marrow-dependent (M) cells which are selectively eliminated by treatment with 89Sr. M-cell function does not develop in mice less than 3-wk old. The Con A response by thymus cells from 2-wk-old B6 mice was susceptible to suppression by FV, further supporting the concept that M cells may regulate the genetic resistance to FV.

Age Factors↗
PubMed1979

Friend erythroleukemia antigen. A viral antigen specified by spleen focus-forming virus and differentiation antigen controlled by the Fv-2 locus.

Serum from C57BL/6 (B6) mice hyperimmunized with NB-tropic Friend virus complex (FV) was cytotoxic for FV-induced erythroleukemic spleen cells and B6 Friend-murine leukemia virus (F-MuLV) lymphoma cells. Cytotoxic activity for erythroleukemia cells remained after repeated absorption of B6 anti-FV antiserum with Friend-Moloney-Rauscher MuLV lymphoma cells but was removed by absorption with erythroleukemia cells induced by FV or Rauscher Vrus. This serologic test system identified a previously unrecognized cell-surface antigen of mouse leukemia, designated Friend Erythroleukemia (FE) antigen to signify its appearance as a determinant of virally induced erythroleukemic differentiation. FE antigen was not detected on 15 transplanted or primary hematopoietic neoplasms, nor was it detected on cells infected with ecotropic, xenotropic, or dualtropic MuLV isolates in tissue culture. Two spleen focus-forming virus (SFFV) nonproducer cells of rats and one of mice express FE antigen in amounts comparable to primary erythroleukemia cells. Absorption tests with FE typing serum indicated that FE antigen was expressed on bone marrow and spleen but not thymus, lymph node, or peripheral blood of uninfected AKR, BALB/c, DBA, and SWR mice; all five tissues from B6 and C57L were negative. Quantitiative absorption tests indicated that the expression of FE antigen, though much lower than on erythroleukemic cells, was greatest on fetal liver, less on bone marrow, and lowest on spleen from BALB and SWR mice. Treatment of BALB/c or SWR fetal liver, bone marrow, spleen, thymus, or lymph node cells with FE typing serum did not result in significant lysis. These observations are consistent with the interpretation that FE antigen is expressed by a minor cell population present in fetal liver, bone marrow, and spleen. Expression of FE antigen, determined by absorption with bone marrow cells, cosegregated with inheritance of the Fv-2s allele in the 17 inbred, 7 recombinant inbred, and 4 congenic mouse strains tested. In summary, the FE antigenic system identifies a cell-surface determinant that has the properties of a SFFV-specified antigen and hematopoietic differentiation alloantigen controlled by the Fv-2 locus. The similarity of FE antigen to Abelson antigen may provide insight into the pathogenic properties of defective transforming MuLV.

Animals↗
PubMed1980

Erythroleukemia induction by replication-competent type C viruses cloned from the anemia- and polycythemia-inducing isolates of Friend leukemia virus.

In this study, the biological properties of the replication-competent viruses, F-MuLVA, present in the anemia-inducing isolate of Friend leukemia virus complex (FV-A); and F-MuLVP, present in the polycythemia-inducing isolate of Friend leukemia virus complex (FV-P) have been examined. BALB/c mice infected as newborns with clonal isolates of F-MuLVA or F-MuLVP become anemic and show splenic enlargement characterized by an increased proportion of cells that resemble immature nucleated erythroid cells. In addition, the spleens of these F-MuLVA- or F-MuLVP-infected mice contain a markedly increased proportion of both erythropoietin-dependent erythroid progenitor cells and spectrin-containing erythroid cells. These results suggest that Friend murine leukemia virus (F-MuLV) by itself can induce an erythroleukemic transformation in newborn BALB/c mice similar to that induced by the anemia-inducing spleen focus-forming virus (SFFVA) in newborn or adult mice. Kinetic studies indicated that the alterations in hemopoietic cell populations induced by F-MuLVA or F-MuLVP in newborn BALB/c mice occurred more slowly than the rapid changes observed after infection with FV-A. In addition, adult BALB/c mice were fully susceptible to the erythroleukemic transformation induced by either SFFVA or SFFVP, whereas only newborn mice were susceptible to F-MuLV. Taken together, these results suggest that, although the replication-defective Friend spleen focus-forming viruses appear to be the major determinant of erythroleukemia induction in adults, the replication-competent helper F-MuLV also have erythroleukemic potential when assayed in newborn animals.

Anemia↗
PubMed1978

Frequency distribution of mRNA and pre-mRNA in growing and differentiated Friend cells.

The frequency distribution of poly(A)+-mRNA in growing and in differentiated Friend cells has been measured by mRNA-cDNA hybridization and their differences established by heterologous hybridization of mRNA of one type and cDNA of the other. It was shown that induction of Friend cells involves an increase in abundance of a small number of mRNAs, while no specific pattern of messenger disappearance could be detected. The frequency distribution of pre-mRNA was determined by hybridizing nuclear RNA with the cDNA probes complementary to mRNA. In uninduced Friend cells, it was shown that most precursor messenger sequences are present at a single frequency of about 3 molecules per nucleus, independently of their final frequency in polysomal mRNA. In induced Friend cells, the frequency distribution of pre-mRNA is more heterogeneous and correlated to some extent with the corresponding mRNA frequency distribution.

Animals↗
PubMed1981

Transcriptional activity of globin genes in uninducible variants of Friend leukemic cells.

Transcriptional activity of globin genes in inducible and uninducible Friend leukemic cells was studied by two different approaches in an attempt to identify the biochemical basis for the loss of inducibility. (1) Nuclei were isolated, and transcripts synthesized endogenously were purified by the Hg-UTP/sulfhydryl-Sepharose method. Globin mRNA sequences were quantitated by hybridization with [32P]globin cDNA. The results showed that the transcription of globin genes was stimulated in DMSO-treated inducible cell nuclei, whereas there was no activation of globin gene transcription in nuclei of uninducible variants cultured with DMSO. (2) Nuclei were prepared from inducible and uninducible Friend cells cultured in the presence or absence of DMSO, and were then subjected to limited digestion with DNase I. DNA was isolated from the nuclei after about 10% of total DNA had become acid-soluble, and was hybridized with globin cDNA. Globin genes either in inducible or in uninducible Friend cells were specifically susceptible to DNase I irrespective of the addition of inducer. From these studies, it was concluded that globin genes of uninducible Friend cells retained the "active conformation" but were not actively transcribed even in the presence of inducers.

Animals↗
PubMed1985

The Fv-2 gene controls induction of erythroid burst formation by Friend virus infection in vitro: studies of growth regulators and viral replication.

When infected in vitro with Friend virus complex, the bone marrow cells of susceptible mice form large colonies (bursts) of erythroblasts after 5 days of culture in semi-solid medium. This virus-induced burst growth occurs without the addition of erythropoietin (EP) which is normally required for erythroid progenitor growth in vitro. Erythroid progenitor cells from C57BL/6 mice infected in vitro with Friend virus are resistant to virus-induced burst growth, while cells from the B6.S mouse strain, which is congenic with C57BL/6 but possesses the 'Friend virus sensitivity' alleles at the Fv-2 locus, are susceptible. This susceptibility of the B6.S cells demonstrates that virus-induced burst growth is regulated by the Fv-2 gene. Two mechanisms by which the Fv-2 locus could control virus resistance were analysed. The possible modulation of the erythroproliferative effect of the virus by soluble substances which either promote burst growth in the sensitive strains or inhibit growth in the resistant strain was examined. Also, the possible restriction of virus infection or replication in resistant (Fv-2rr) haemopoietic cells was investigated. In a variety of experimental conditions designed to test the effects of soluble growth promoters on bone marrow cells infected in vitro, the resistance of C57BL/6 cells to erythroid burst formation could not be overcome. Neither could resistance be transferred to co-cultured sensitive cells by any soluble substances produced in culture by C57BL/6 cells. Use of haemopoietic cells from C57BL/6 animals in various physiological states of haemopoiesis also did not overcome the resistance to virus-induced burst growth. Quantification of several parameters of viral replication in whole marrow cultures or in erythroblasts from bursts of the Fv-2 sensitive and Fv-2 resistant congenic mouse strains showed that haemopoietic cells of both strains support virus growth equally well. These data suggest that Fv-2rr-mediated resistance to the erythroproliferative effect of Friend virus infection in vitro is an inherent property of an erythroid progenitor target cell and is not determined by external factors. The resistance is also not due to restriction of virus replication.

Animals↗
PubMed1980

Transcription of Friend virus proviral sequences in isolated nuclei.

Transcription studies using isolated Friend nuclei and Escherichia coli polymerase are presented. Combination of the techniques of thiol-Sepharose chromatography and cDNA-Sepharose hybridisation has resulted in a system in which the transcription of the Friend virus proviral sequences with endogenous and E. coli polymerase can be examined. The results show that the percentage of Friend viral-specific sequences in RNA transcribed by E. coli RNA polymerase and by endogenous RNA polymerase in isolated nuclei are similar. The percentage of viral-specific sequences synthesized in isolated nuclei is similar to that found in Friend cell nuclear RNA.

Animals↗
PubMed1986

T-lymphocyte priming and protection against Friend leukemia by vaccinia-retrovirus env gene recombinant.

The current prevalence of the acquired immune deficiency syndrome in humans has provoked renewed interest in methods of protective immunization against retrovirus-induced diseases. In this study, a vaccinia-retrovirus recombinant vector was constructed to study mechanisms of immune protection against Friend virus leukemia in mice. The envelope (env) gene from Friend murine leukemia virus (F-MuLV) was inserted into the genome of a vaccinia virus expression vector. Infected cells synthesized gp85, the glycosylated primary product of the env gene. Processing to gp70 and p15E, and cell surface localization, were similar to that occurring in cells infected with F-MuLV. Mice inoculated with live recombinant vaccinia virus had an envelope-specific T-cell proliferative response and, after challenge with Friend virus complex, developed neutralizing antibody and cytotoxic T cells (CTL) and were protected against leukemia. In contrast, unimmunized and control groups developed a delayed neutralizing antibody response, but no detectable CTL, and succumbed to leukemia. Genes of the major histocompatibility complex influenced protection induced by the vaccinia recombinant but not that induced by attenuated N-tropic Friend virus.

Animals↗
PubMed1976

Inhibition of friend murine leukemia virus production by low-ionic-strength medium.

The effect of medium of low ionic strength on the release of virus from Friend leukemia cells has been studied. The release of infectious Friend leukemia virus is almost completely inhibited in medium of low ionic strength, as measured by a focus-forming assay (XC assay), by endogenous RNA-dependent DNA polymerase activity of released virus particles, and by electron microscope studies of the production of C-type particles. Friend leukemia virus-transformed proerythroblasts undergo extensive morphological changes in low-ionic-strength medium. The cells are viable in this medium, but they can no longer be stimulated with dimethyl sulfoxide to produce hemoglobin and increase virus production. Infectious virus is released between 30 and 120 min of resuspension of inhibited cells in normal medium. The rate of virus release after reversal of the inhibition is much greater than the rate of virus release during normal cell growth. The morphological changes occurring after dimethyl sulfoxide stimulation of Friend leukemia cells are compared with those resulting from resuspension in normal medium of cells inhibited by low ionic strength.

Cell Membrane↗
PubMed1977

Friend strain of spleen focus-forming virus: a recombinant between mouse type C ecotropic viral sequences and sequences related to xenotropic virus.

The genome of the Friend strain of the spleen focus-forming virus (SFFV) has been analyzed by molecular hybridization. SFFV is composed of genetic sequences homologous to Friend type C helper virus (F-MuLV) and SFFV-specific sequences not present in F-MuLV. These SFFV-specific sequences are present in both the Friend and Rauscher strains of murine erythroleukemia virus. The SFFV-specific sequences are partially homologous to three separate strains of mouse xenotropic virus but not to several cloned mouse ecotropic viruses. Thus, the Friend strain of SFFV appears to be a recombinant between a portion of the F-MuLV genome and RNA sequences that are highly related to murine xenotropic viruses. The implications of the acquisition of the xenotropic virus-related sequences are discussed in relation to the leukemogenicity of SFFV, and a model for the pathogenicity of other murine leukemia-inducing viruses is proposed.

Animals↗
PubMed1983

Expression of a transformation-related protein (p53) in the malignant stage of Friend virus-induced diseases.

Stage 1 (pre-malignant) and stage 2 (malignant) cells derived from mice infected with Friend murine leukemia virus or polycythemia-inducing Friend virus complex were examined and compared for the expression of a transformation-related cellular protein, p53. Stage 2 cells were found to express high levels of p53, whereas stage 1 cells did not express detectable levels of this protein. These results indicate that p53 may be a marker for transformed cells present in the second stage of diseases induced by Friend murine leukemia virus or polycythemia-inducing Friend virus complex.

Animals↗
PubMed1983

Molecular cloning of Friend mink cell focus-inducing virus: identification of mink cell focus-inducing virus-like messages in normal and transformed cells.

Friend mink cell focus-inducing virus (Fr-MCF) is a leukemogenic murine retrovirus that was isolated from a leukemic NIH Swiss mouse. We molecularly cloned the genome of this virus into pBR322. Restriction enzyme mapping of this cloned Fr-MCF DNA revealed a 1.0-kilobase-pair region in the envelope gene which differs from the restriction map of the Friend ecotropic virus (Friend murine leukemia virus). A 400-base-pair Fr-MCF envelope gene fragment was subcloned from this region and designated pLEK. Probes made with pLEK hybridize to Fr-MCF DNA but do not hybridize to either Friend or amphotropic murine leukemia virus DNA. Polyadenylic acid-selected RNA was prepared from the hematopoietic tissues of normal NIH Swiss mice, Fr-MCF-infected erythroleukemia cells (TP-1), and uninfected chemically transformed T lymphocytes (RB-1). The pLEK probe identified 34S and 22S messages in the TP-1 cells and in the normal hematopoietic tissues. RB-1 cells contain 32S and 26S messages that hybridize to pLEK. However, the pLEK-like RNAs found in the normal hematopoietic tissues and in the RB-1 cells were 400-fold less abundant than the RNAs found in the TP-1 cells.

Animals↗