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At least 811 records · Page 45Linked to original sources
PubMed1986

Epstein-Barr virus status and tumour cell phenotype in sporadic Burkitt's lymphoma.

Burkitt's lymphoma (BL) biopsy cells and derived cell lines can be grouped according to their patterns of reactivity with 6 selected monoclonal antibodies (MAbs) against B cell-associated surface antigens. Group I cells react only with MAbs J5 and 38.13, recognising the common acute lymphoblastic leukaemia antigen and a BL-associated antigen respectively; group II cells react with J5 and 38.13 and with one or more of a set of MAbs (Ki-24, MHM6, AC2, Ki-1) against "lymphoblastoid" antigens; group III cells react only with these anti-"lymphoblastoid" MAbs. Tumour biopsy cells from 17 cases of sporadic BL, 9 positive for the Epstein-Barr (EB) virus genome and 8 negative, have been analysed during the process of cell line establishment in vitro. In early passage the EB virus-negative BL cells showed either a group I phenotype or gave an additional reactivity with MAb Ki-24 which placed them in group II; these phenotypes remained essentially stable with continued growth of the cell lines for up to 50 passages. By contrast the EB virus-positive BL cells were much more susceptible to phenotypic change in vitro. Although such cells displayed a group I or group II phenotype in early passage, many of the lines soon moved into group III whilst retaining the karyotypic markers indicative of their malignant origin. These observations suggest that a resident EB virus genome can drive the in vitro progression of BL cells towards a more "lymphoblastoid" phenotype. This was confirmed in subsequent experiments where virus-negative BL cell lines were converted to EB virus positivity by in vitro infection. Clearly, therefore, phenotypic analysis of long-established lines can lead to false distinctions being drawn between the EB virus-positive and -negative forms of sporadic BL; both may derive from the same sub-population of target B cells in vivo.

Adolescent↗
PubMed1998

Use of chlorzoxazone as an in vivo probe of cytochrome P450 2E1: choice of dose and phenotypic trait measure.

Chlorzoxazone is being developed and proposed for use as a probe to measure in vivo cytochrome P4502E1 activity, but the phenotypic trait measures that are used vary. Although the doses proposed for phenotyping range from 250 mg to 750 mg, the effect of dose on chlorzoxazone hydroxylation has not previously been evaluated. The purpose of this study was to characterize the pharmacokinetics of chlorzoxazone in normal healthy volunteers (N = 6) after single randomized oral doses of 250 mg and 750 mg. An additional 10 volunteers underwent a detailed pharmacokinetic study using the 250-mg dose to further evaluate proposed phenotypic trait measures (N = 16). Timed blood and urine samples were obtained for 10 hours for chlorzoxazone and 6-hydroxychlorzoxazone determination by HPLC. Pharmacokinetic parameter estimates were estimated using noncompartmental methods. Evaluation of phenotypic trait measures show that 6-hydroxychlorzoxazone to chlorzoxazone plasma concentration ratios at 2 to 4 hours after drug administration demonstrated the highest correlations with metabolite formation clearance (r = 0.9; P < 0.001). Urine-based parameters (e.g., total recovery) were not significantly related to formation clearance (r = 0.5; P > 0.05). Dose dependency in chlorzoxazone metabolism was shown by a 30% increase (P < 0.05) in the dose-normalized area under the concentration-time curve (AUC) of chlorzoxazone and lower incremental dose-normalized urinary recovery of 6-hydroxychlorzoxazone at early timepoints after the 750-mg dose. In addition, the plasma ratio of 6-hydroxychlorzoxazone to chlorzoxazone at 4 hours was reduced by 48% in 5 of 6 subjects after the 750-mg dose (P > 0.05). These data suggest that 6-hydroxylation was saturated at the higher dose and illustrate the importance of dose selection in phenotyping. The results of this study indicate that a chlorzoxazone dose of 250 mg should be used and that a single plasma ratio obtained 2 to 4 hours after dosing is reflective of chlorzoxazone 6-hydroxylation and thus may serve as a cytochrome P4502E1 phenotypic trait measure.

Adolescent↗
PubMed2005

Phenotypic accommodation: adaptive innovation due to developmental plasticity.

Phenotypic accommodation is adaptive adjustment, without genetic change, of variable aspects of the phenotype following a novel input during development. Phenotypic accommodation can facilitate the evolution of novel morphology by alleviating the negative effects of change, and by giving a head start to adaptive evolution in a new direction. Whether induced by a mutation or a novel environmental factor, innovative morphological form comes from ancestral developmental responses, not from the novel inducing factor itself. Phenotypic accommodation is the result of adaptive developmental responses, so the novel morphologies that result are not "random" variants, but to some degree reflect past functionality. Phenotypic accommodation is the first step in a process of Darwinian adaptive evolution, or evolution by natural selection, where fitness differences among genetically variable developmental variants cause phenotype-frequency change due to gene-frequency change.

Adaptation, Physiological↗
PubMed2004

Phenotypic variability associated with Arg26Gln mutation in caveolin3.

Caveolin3 (CAV3) is a protein associated with dystrophin, dystrophin-associated glycoproteins, and dysferlin. Mutations in the CAV3 gene result in certain autosomal-dominant inherited diseases, namely, rippling muscle disease (RMD), limb-girdle muscular dystrophy type 1C (LGMD1C), distal myopathy, and hyperCKemia. In this report we show that a previously reported family with RMD has a mutation in the CAV3 gene. Affected individuals had either a characteristic RMD phenotype, a combination of RMD and LGMD1C phenotypes, or a LGMD1C phenotype, but one mutation carrier was asymptomatic at age 86 years. This phenotypic variability associated with mutations in CAV3 has been reported previously but only in a few families. It is important to remember the significant phenotypic variability associated with CAV3 mutations when counseling families with these mutations. These observations also suggest the presence of factors independent of the CAV3 gene locus that modify phenotype.

Aged↗
PubMed1992

Cellular interactions determine neuronal phenotypes in rodent retinal cultures.

Progenitor cells isolated from early rat embryo retinas differentiate into phenotypes normally generated early in retinal development (e.g., ganglion cells), whereas progenitors isolated from postnatal retinas differentiate into later-generated retinal cell types (e.g., rod photoreceptors; Reh and Kljavin, J. Neurosci. 9:4179-4189; 1989; Adler and Hatlee, 1989; Science 243:391-393; Sparrow, Hicks, and Barnstable, 1990, Dev. Brain Res. 51:69-84). To determine whether this change in committment is intrinsic to the progenitor cells, or alternatively can be modified by interactions with their developing environment, I co-cultured mouse and rat retinal cells, from different developmental stages, and identified the resulting phenotypes with species-specific and cell class-specific antibodies. I found that the phenotypes into which mouse neuroepithelial cells differentiate depends on the phenotypes of the rat cells that surround them. Retinal precursor cells from embryonic day (E) 10-12 will adopt the rod photoreceptor phenotype only when close to cells expressing this phenotype. By contrast, when the E10-12 retinal progenitor cells are cultured with cells from the cerebral cortex, they differentiate primarily into large multipolar neurons, similar in their morphology and antigen expression to retinal ganglion cells. These results indicate that interactions among the cells of the developing retina are important in the determination of cell fate.

Animals↗
PubMed2003

Absence of either gastric or intestinal phenotype in microscopic differentiated gastric carcinomas.

Differentiated gastric carcinoma (DGC) corresponds roughly to the intestinal type of gastric carcinoma described by Laurén. It has been suggested that DGCs arise from intestinalized gastric mucosa, but recent findings regarding their mucin expression do not support this hypothesis. To evaluate the histogenetic relationship between DGCs and intestinal metaplasia, lesions that are as small as possible should be examined. Twenty-five DGCs, ranging in their greatest dimension from 0.4 to 2.7 mm, were collected and divided into two groups by size. Group A consisted of 13 lesions less than 1.4 mm across, and group B of 12 lesions 1.4 mm or more. The presence of mucin and a brush border was assessed by immunostaining with antibodies against human gastric mucin, pyloric-gland-type mucin, Muc-2 glycoprotein, and CD10 antigen, and the lesions were classified as having the gastric phenotype (G-type), intestinal phenotype (I-type), mixed gastric and intestinal phenotype (M-type), or null phenotype (N-type). Thirteen (52%) of the 25 lesions were N-type, 5 (20%) lesions were G-type, 5 (20%) were I-type, and 2 (8%) were M-type. Group A had a larger proportion of N-type lesions than B (10/13, or 77%, vs. 3/12, or 25%; p = 0.027, chi-square test for proportions). Group B had a larger proportion of G-type lesions than A (5/12, or 42%, vs. 0/13, or 0%; p = 0.033). The phenotypes of the carcinomas and their surrounding mucosa were unrelated. Therefore, DGCs may arise from gastric mucosa affected by intestinal metaplasia or not, without having either the gastric or intestinal phenotype.

Aged↗
PubMed1993

Expression of the IV (reversed and/or heterotaxic) phenotype in SWV mice.

Approximately 50% of iv/iv mice have situs inversus (mirror image reversal of viscera) and 40% have heterotaxia (anomalous arrangement of viscera). The occurrence of heterotaxia is independent of situs. Using the cross-intercross breeding system to put the iv gene on the SWV background, an occasional presumed iv/+ mouse was found that had an IV (situs inversus and/or heterotaxic) phenotype. Testcrosses of these reversed animals indicated an iv/+ genotype. Since iv is linked tightly to Igh-C on chromosome 12, we inferred the genotype with a polymorphism of Igh-C demonstrated using the polymerase chain reaction (PCR). This confirmed them to be iv/+. The expression of the IV phenotype in animals heterozygous for the iv gene may be due to an interaction of iv with an autosomal recessive gene found in SWV. We have not found the IV phenotype in heterozygous iv/+ mice following placement of the iv gene on six other inbred strains. Rarely, we also found that presumed SWV +/+ mice had the IV phenotype. Test matings of these phenodeviants, corroborated by PCR, have confirmed them to be +/+. Although the phenotypes of the affected SWV +/+ and iv/+ mice resembled those found in iv/iv mice, the occurrence of situs inversus and heterotaxia were not independent of each other, and most of the SWV mice with the IV phenotype had heterotaxia with situs solitus. This infrequent dominant expression of the iv gene has so far only been seen when iv is on the SWV background. These findings are consistent with the idea that this phenomenon is due to the interaction of the iv gene with another gene found so far only in the SWV strain.

Animals↗
PubMed2003

Automated screening in environmental arrays allows analysis of quantitative phenotypic profiles in Saccharomyces cerevisiae.

A methodology for large-scale automated phenotypic profiling utilizing quantitative changes in yeast growth has been tested and applied to the analysis of some commonly used laboratory strains. This yeast-adjusted methodology is based on microcultivation in 350 microl liquid medium, where growth is frequently optically recorded, followed by automated extraction of relevant variables from obtained growth curves. We report that cultivation at this micro-scale displayed overall growth features and protein expression pattern highly similar to growth in well aerated medium-scale (10 ml) culture. However, differences were also encountered, mainly relating to the respiratory potential and the production of stress-induced proteins. Quantitative phenotypic profiles for the laboratory yeast strains W303, FY1679 and CEN-PK.2 were screened for in environmental arrays, including 98 different conditions composed of low, medium and high concentrations of 33 growth inhibitors. We introduce the concepts phenotypic index(rate) and phenotypic index(stationary), which relate to changes in rate of growth and the stationary phase optical density increment, respectively, in a particular environment relative a reference strain. The laboratory strains presented selective phenotypic profiles in both phenotypic indexes and the two features appeared in many cases to be independent characteristics. We propose the utilization of this methodology in large-scale screening of the complete collection of yeast deletion mutants.

Fungal Proteins↗
PubMed1996

Expression of MyoD in cultured primary myotubes is dependent on contractile activity: correlation with phenotype-specific expression of a sarcoplasmic reticulum Ca(2+)-ATPase isoform.

Myogenic determination factors (MDF) have been implicated in the establishment and maintenance of the fast or slow phenotype in skeletal muscle, with MyoD favoring the fast and myogenin favoring the slow phenotype. Accordingly, contractility-induced changes in muscle phenotype should be accompanied by a change in the MyoD/myogenin ratio. Some reports show such changes, but limitations inherent to in vivo studies complicate interpretation of these data. Here we tested whether a relationship can be found between contractility, MDF expression, and the expression of phenotype-specific muscle proteins in a simple in vitro system of cultured primary myotubes. We show that contractions reduce the MyoD/myogenin ratio by specifically repressing MyoD mRNA expression. This is accompanied by a selective repression at a pretranslational level of the expression of fast-type sarcoplasmic reticulum Ca(2+)-ATPase. These in vitro results support a phenotype-determining role of MDFs as a function of contractile activity and show that cultured myotubes can be a useful model for the analysis of the molecular mechanism of such regulation of muscle phenotype.

Animals↗
PubMed1999

The genomic organization of the partial D category DVa: the presence of a new partial D associated with the DVa phenotype.

Within the Rh blood group, the partial D phenotype is a well known RhD variant, that induces Rh-incompatible blood transfusion and hemolytic diseases in the newborn. The partial D category DVa phenotype (DVa Kou.) results from a hybrid of RhD-CE-D transcript. We demonstrated a genomic organization of the hybrid RHD-CE-D gene leading to the DVa phenotype, and showed that the DVa gene were generated from gene conversion between the RHD and the RHCE genes in relatively small regions. This study also revealed that the presence of a new partial D associated with the DVa phenotype, which we termed the DVa-like phenotype. In this phenotype, five RHD-specific nucleotides were replaced with the corresponding RHCE-derived nucleotides on the exon 5 of the RHD gene. In addition, two variants of the mutated RHD genes at nucleotide 697 were revealed in the RhD variant samples. These results will provide useful information for future research into the diversification of the Rh polypeptides.

Alleles↗
PubMed2000

Distinct phenotypic expression associated with a new hyperunstable alpha globin variant (Hb heraklion, alpha1cd37(C2)Pro>0): comparison to other alpha-thalassemic hemoglobinopathies.

Clinical phenotypes associated with abnormal globin chain biosynthesis may result in thalassemia (deficient quantity) or hemolytic anemia (abnormal hemoglobins). However, the phenotypic expression of hyperunstable hemoglobin variants often includes features of thalassemia, along with variable peripheral hemolysis. Hemoglobinopathies caused by highly unstable beta-chain variants have a dominant thalassemia-like phenotype, in which carriers have a clinical expression of thalassemia intermedia, but highly unstable alpha-globin variants are usually only phenotypically apparent when they interact with other alpha-thalassemia mutations. In a child with clinical and hematological features consistent with beta-thalassemia intermedia, DNA analysis excluded any beta-globin gene mutations but characterized a novel deletion cd37(C2)Pro>0 (Hb Heraklion) in the alpha1 globin gene, in trans to a common Mediterranean nondeletion alpha-thalassemia mutation (alpha(Hph)alpha). The deletion of proline at alpha37(C2) is predicted to result in severe instability of the variant hemoglobin, which on interaction with a synthesis-deficient alpha-thalassemia mutation causes a relatively severe dyserythropoietic anemia, representing an alternative phenotype associated with highly unstable alpha-chain variants. Hb Heraklion is the fourth highly unstable alpha-globin variant that we have observed in patients from Greece and Albania. Two variants involve the alpha2-globin gene: Hb Agrinio (alpha29(B10)Leu>Pro) and Hb Adana (alpha59(E8)Gly>Asp), and two the alpha1-gene: Hb Aghia Sophia (alpha62(E11)Val>0) and (Hb Heraklion a37(C2)Pro>0). Each has been observed on interaction with a different alpha-thalassemia mutation and the phenotypes associated with these highly unstable alpha-variants are presented.

Adolescent↗
PubMed1997

Bacterial phenotypes mediated by mviA and their relationship to the mouse virulence of Salmonella typhimurium.

The focus of this study was the phenotypic characterization of Salmonella typhimurium mutants lacking the function of the response regulator mviA. The inactivation of mviA+ (mviA::kan) is shown to induce a significant change in the growth of most virulent strains, as reflected in the size of the colonies formed on agar plates. The colony phenotype observed in these strains has been designated as the small colony morphology (Scm+) phenotype. Mutants exhibiting the Scm+ phenotype are shown to be significantly attenuated for virulence in susceptible (ItyB) mice. The Scm+ phenotype therefore provides an in vitro phenotypic marker for mviA+ activity. Further examination of Scm+ mutants has revealed that they lack expression of a 55 kDa periplasmic protein which is detected in isogenic mviA+ strains. This protein has been designated mviA+ related protein A (MrpA) and was expressed in direct correlation with virulence in all S. typhimurium strains examined.

Animals↗
PubMed2003

Phenotypic variability (heterogeneity) of peroxisomal disorders.

Peroxisomes perform a multitude of biosynthetic and catabolic functions, many of which are related to lipid metabolism. Peroxisomal disorders result either from deficiency of a single peroxisomal enzyme or protein, or from a defect in the complex mechanism of peroxisomal biogenesis, resulting in deficiency of several or multiple peroxisomal functions. These can be assessed by a battery of biochemical assays, enabling a biochemical phenotype to be defined that is specific and diagnostic for each of the peroxisomal disorders. Some peroxisomal disorders have unique and specific clinical phenotypes, which may be diagnostic. Others share patterns of clinical abnormalities (particularly neurological dysfunction, craniofacial dysmorphism, skeletal defects, sensory deafness, retinopathy) consistent with defined clinical phenotypes, but with considerable overlap and heterogeneity. To a certain extent, the clinical features of a particular disorder reflect the accumulation or deficiency of specific metabolites. Thus, the same clinical phenotypes may be caused by both single enzyme defects and PBDs. Furthermore, the same defect may present with different clinical phenotypes. In general, the severity of the clinical phenotype correlates with the degree of biochemical dysfunction. The clinical heterogeneity of peroxisomal disorders constitutes a diagnostic challenge demanding a high index of suspicion on the clinician's part.

Chondrodysplasia Punctata, Rhizomelic↗
PubMed1984

Generation of phenotypic diversity and progression in metastatic tumor cells.

The emergence of diversified tumor cell subpopulations in malignant neoplasms accounts for their heterogeneous cellular phenotypes and virtually ensures that some tumor cells will ultimately evolve with the most favorable properties for their enhanced abilities to survive, grow, invade and metastasize (tumor progression). The rates of cellular phenotypic diversification appear to vary greatly among different tumors and within the same tumor, and they are probably controlled, at least in part, by cellular instability due to chromosomal defects and random somatic mutational events, the rates of which are known to be higher in more malignant cells, and by epigenetic events, which may vary widely depending on the nature of the tumor cells and their microenvironments. As tumor progression proceeds, the most malignant cell subpopulations appear to lose their responsiveness to changes in tumor microenvironment while maintaining their high rates of phenotypic diversification. Tumor and normal cell-cell and cell-extracellular matrix interactions, as well as tumor cell nutrients, oxygen, hormones, growth factors, inducers and other regulatory molecules provide individual malignant cells with microenvironmental signals that could act through epigenetic cellular modifications, such as DNA methylation, and transcriptional, posttranscriptional, translational and posttranslational controls, or combinations of these. In addition, integration of viral gene sequences or viral modification of host DNA in critical regions could affect phenotypic stability. Finally, manipulation of tumor cells by antitumor therapy can also have profound effects on the rates of phenotypic diversification of the surviving tumor cells. A model for generating cellular phenotypic diversity based on the proposed mechanism for rapid generation of immunoglobulin molecular diversity in B cells may be applicable to malignant cells and to cells in general. In this model the expression and activity of gene products from multigene families are affected by a variety of genetic and epigenetic controlling mechanisms, and alterations in regulatory genes caused by recombination, methylation, mutation, or other changes could lead to differences in gene expression, resulting in widespread quantitative (and perhaps some qualitative) changes in particular gene products or their activities. As they proceed down different pathways of gene expression, each cell would be exposed to continual host selection pressures creating diverse, ever-changing malignant cell-populations.

Animals↗
PubMed1981

Circadian clock phenotypes of chromosome aberrations with a breakpoint at the per locus.

The circadian rhythm phenotypes of eight chromosome aberrations with a breakpoint in the region of the per locus (3B1-2) were analyzed. Two duplications and five deficiencies with a 3B1-2 breakpoint produce either a wild-type or an arrhythmic clock phenotype while one translocation with a 3B1-2 breakpoint. T(1;4)JC43, produces locomotor-activity rhythms with either very-long period (31--39 h), rhythms that grade into arrhythmicity, or completely arrhythmic phenotypes. This is a unique phenotype that had not previously been observed for mutants at the per locus. An extensive complementation analysis of 3B1-2 chromosome aberrations and per mutant alleles provided no compelling evidence for genetic complexity at the per locus. This is in contrast to the report of Young and Judd (1978). Analysis of both the locomotor-activity and eclosion phenotypes of 3B1-2 chromosome aberrations did not uncover differences in the genetic control of these two rhythms. The clock phenotypes of 3B1-2 chromosome aberrations, the three per mutant alleles, and per+ duplications suggest that mutations at the per locus shorten, lengthen, or eliminate periodicity by respectively increasing, decreasing, or eliminating per activity.

Animals↗
PubMed1991

Complete reversion of the abo phenotype in D. melanogaster occurs only when the blood transposon is lost from region 32E.

The abnormal oocyte phenotype is characterized by instability, as shown by the loss and reappearance of the abo maternal effect under specific genetic conditions. Our previous finding that a correlation exists between the abo phenotype and the presence of a blood transposon in region 32E, led us to perform an extensive genetic and molecular analysis of the most significant aspects of the abo phenotype in different genetic backgrounds. The results of these experiments can be summarized as follows: Complete reversion occurs only when the blood trnasposon is lost, thus definitively demonstrating that the insertion of the blood transposon in region 32E is the molecular event that causes the pleiotropic abo phenotype. Partial reversion can also occur without loss of the transposon indicating that different molecular pathways may be involved in the loss of the abo phenotype. Reappearance of the full abo phenotype can occur only in heterozygous lines constructed from partially revertant abo homozygous lines that have not lost the blood transposon.

Animals↗
PubMed1983

Alloreactive T-cell clones. Ly phenotypes predict both function and specificity for major histocompatibility complex products.

We have studied the association of Ly phenotype with function and specificity for major histocompatibility complex (MHC) products by examining the properties of 21 T-cell clones derived from B10 anti-B10.D2 and B10.A anti-B10.D2 mixed lymphocyte cultures (MLC). T cells were selected after MLC solely on the basis of Ly phenotype, cloned by limiting dilution, and tested for stability of Ly phenotype, function and specificity for class I or class II MHC products. Sixteen Ly-1+2- and five Ly-1-2+ T-cell clones were tested. The clones selected for the Ly-1+2- phenotype maintained this phenotype, expressed helper but not lytic function, and recognized class II MHC products (I-Ad or I-Ed). All Ly-1-2+ clones maintained this phenotype, possessed cytolytic but not helper activity, and recognized class I MHC products (Dd and Ld). Our data therefore confirm at the clonal level the original observations of a remarkably consistent correlation between Ly markers, MHC specificity, and function. They suggest that the expression of Ly antigens on T-cell clones forms part of a genetic program for each of these specialized cells that also determines their function and MHC specificity.

Animals↗
PubMed1984

Polymorphism of human liver alcohol dehydrogenase: identification of ADH2 2-1 and ADH2 2-2 phenotypes in the Japanese by isoelectric focusing.

Liver homogenate-supernatants from most Japanese exhibit an "atypical" pH optimum for ethanol oxidation at pH 8.8 instead of 10.5, the "typical" pH-activity optimum. It has been proposed that atypical livers contain alcohol dehydrogenase isozymes with beta 2 subunits while typical livers contain isozymes with beta 1 subunits, both produced by the ADH2 gene. Because it is difficult to differentiate the atypical ADH2 2-2 phenotype from the ADH2 2-1 phenotype by starch gel electrophoresis, an agarose isoelectric focusing procedure was developed that clearly separated the atypical Japanese livers into two groups, A1 and A2. The beta beta isozymes in A1 and A2 livers were purified. Type A1 livers contained a single beta beta isozyme with an atypical pH-rate profile; it was designated beta 2 beta 2. Three beta beta isozymes were isolated from A2 livers, two of which corresponded to beta 1 beta 1 and beta 2 beta 2. A third, absent from the typical and the atypical A1 livers, had an intermediate mobility; it was designated beta 2 beta 1. Type A1 livers are, therefore, the homozygous ADH2 2-2 phenotype, and type A2 livers, the heterozygous ADH2 2-1 phenotype. The ADH2 2-2 phenotype was found in 53% of 194 Japanese livers, and the ADH2 2-1 phenotype, in 31%. Accordingly, the frequency of ADH2(2) was 0.68.

Adult↗