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PubMed2006

Gastric and intestinal phenotypes and histogenesis of advanced glandular stomach cancers in carcinogen-treated, Helicobacter pylori-infected Mongolian gerbils.

The Helicobacter pylori-infected Mongolian gerbil (MG) has been established as an appropriate animal model for studies of stomach cancer development. However, there have hitherto been no data on the phenotypic classification of glandular stomach cancers in H. pylori-infected and non-infected MG. We therefore examined the phenotypes of 50 and six advanced glandular stomach cancers in H. pylori-infected and non-infected MG, respectively, as well as adjacent non-neoplastic mucosa, using several gastrointestinal epithelial phenotypic markers. The lesions were divided phenotypically into 21 gastric, 24 gastric-and-intestinal mixed, four intestinal and one null types, with 90.0% of the lesions harboring gastric elements and 56.0% demonstrating intestinal phenotypic expression in H. pylori-infected MG. All six lesions were classified as gastric type in non-infected MG. There was no clear correlation with the presence of intestinal metaplasia in surrounding mucosa. In conclusion, our data suggest that most advanced adenocarcinomas retain a gastric cellular phenotype in the glandular MG stomach. Thus, it might be proposed that intestinal metaplasia is a paracancerous phenomenon rather than a premalignant condition. H. pylori infection may trigger intestinalization of both stomach cancers and non-neoplastic mucosa.

Animals↗
PubMed1979

Hereditary acanthocytosis associated with the McLeod phenotype of the Kell blood group system.

Some boys with X-linked chronic granulomatous disease (CGD) have red cells of the rare McLeod phenotype in the Kell blood group system. Only one example of this phenotype has previously been described in a non-CGD subject. We have studied a 10-year-old boy and a maternal brother who do not have CGD and whose red cells are of the McLeod type . The boy presented as a haematological problem with red-cell abnormalities. These were acanthocytosis, anisocytosis and 'tailing' in the osmotic fragility curve, changes now known to occur with the McLeod phenotype. Subsequent studies revealed his rare blood group. A family study has established that an uncle also has acanthocytic red cells and the McLeod phenotype. In addition the boy's sister, mother and maternal grandmother all show red-cell mosaicism with double populations of McLeod acanthocytes and normal red cells of common Kell type. The gene that determines inheritance of the McLeod phenotype is X-linked and the mosaicism present in female carriers is believed to result from X chromosome inactivation by the Lyon effect. The study provides further evidence that the McLeod phenotype arises by inheritance of a variant X-linked modifying gene and not through inheritance of a variant gene at the Kell autosomal locus. It also represents the first occasion that a person of rare blood group has been recognized because of an associated anomaly in red cell morphology.

Acanthocytes↗
PubMed2004

Are there clinical phenotypes of homozygous sickle cell disease?

The distribution of clinical features was examined in subjects with homozygous sickle cell (SS) disease in the Jamaican Cohort Study to determine whether there is evidence of distinct clustering of symptoms or clinical phenotypes. A twofold model yielded groups that could be interpreted as painful crisis or leg ulcer phenotypes and 78% of patients were classified with 95% confidence into one of these. The painful crisis phenotype also manifested higher frequencies of dactylitis, meningitis/septicaemia, acute chest syndrome and stroke. Attempts to define a three-group model were less convincing although 43% of patients could be allocated with 95% confidence. The three-group model essentially divided subjects with the leg ulcer phenotype into subgroups with higher and lower frequencies of painful crisis, dactylitis, meningitis/septicaemia and acute chest syndrome. In the three-group model, the painful crisis phenotype had lower total haemoglobin, fetal haemoglobin, mean cell volume and higher reticulocytes but there was no apparent influence of alpha thalassaemia or beta globin haplotype. Both environmental and genetic factors are likely to contribute to most manifestations of SS disease and the evidence for different clinical phenotypes suggests that a search for associated genetic polymorphisms may provide insights into the mechanisms of clinical variability in SS disease.

Acute Disease↗
PubMed1989

Nickel deficiency gives rise to the defective hydrogenase phenotype of hydC and fnr mutants in Escherichia coli.

Hydrogenase activity and other hydrogenase-related functions can be restored to hydC mutants by the specific addition of nickel salts to the growth medium. These mutants are defective in all three hydrogenase isoenzymes and the restoration is dependent upon protein synthesis. The cellular nickel content of the mutant when grown in LB medium is less than 1% of that of the parental strain. Partial suppression of the hydrogenase phenotype of hydC mutants occurs when growth takes place in a different medium. This correlates with an increased cellular nickel content. The phenotype of the mutant is also fully suppressed by growth in media of very low magnesium content. Such media facilitate nickel uptake via the magnesium transport system, which leads to the acquisition of a normal cellular nickel content. Mutations in the fnr gene, which encodes a transcriptional regulator for several anaerobically expressed enzymes, abolishes hydC expression and gives rise to a defective hydrogenase phenotype. The hydrogenase phenotype of fnr is closely similar to that of hydC in all respects examined. The hydrogenase activity of fnr strains can be restored by the presence of a functional hydC gene on a multicopy plasmid. The hydrogenase phenotype of fnr strains therefore arises indirectly via suppression of hydC, which leads to a low cellular nickel content. Nickel has no influence on fumarate reductase or nitrate reductase activities in fnr strains. The hydrogen-metabolism phenotype of fnr strains is, therefore, dependent upon their ability to acquire nickel from growth media. It is likely that hydC encodes a specific transport system for nickel.

Escherichia coli↗
PubMed1990

Lung-phase immunity to Schistosoma mansoni: definition of alveolar macrophage phenotypes after vaccination and challenge of mice.

Phenotypic changes in murine alveolar macrophages have been described in response to vaccination with irradiated cercariae and to a subsequent challenge with normal parasites. Flow cytometric analysis was used to quantify the proportions of cells strongly positive for a number of macrophage surface markers, detected by a panel of monoclonal primary antibodies and fluorescent secondary antibodies. The proportion of Ia+ macrophages sampled by bronchoalveolar lavage increased 5-fold over days 14 to 28 post-vaccination. This upregulation of Ia was accompanied by a sharp decrease in F4/80 expression between days 14 and 21. The low percentage of F4/80+ cells persisted for several weeks after vaccination, and no further change was stimulated by challenge parasites. These altered characteristics are consistent with the 'activation phenotype' induced by other infectious agents. After challenge of immune mice, further changes in macrophage phenotype were slight compared to the responses elicited by vaccination, or to those induced in the challenge control group; Ia expression increased to about three times normal levels. The phenotypic changes correspond both in magnitude and timing with the pattern of alveolar macrophage activation determined in a previous study. The limited changes in phenotype of alveolar macrophages from immunized mice after challenge could indicate that these cells become refractory to reactivation. Overall, the altered macrophage phenotype after vaccination and challenge provides circumstantial evidence for the action of cytokines, particularly interferon-gamma, in lung-phase immunity to schistosomes.

Animals↗
PubMed2005

How stress selects for reversible phenotypic plasticity.

Stress occurring in periods shorter than life span strongly selects for reversible phenotypic plasticity, for maximum reliability of stress indicating cues and for minimal response delays. The selective advantage of genotypes that are able to produce adaptive reversible plastic phenotypes is calculated by using the concept of environmental tolerance. Analytic expressions are given for optimal values of mode and breadth of tolerance functions for stress induced and non-induced phenotypes depending on (1) length of stress periods, (2) response delay for switching into the induced phenotype, (3) response delay for rebuilding the non-induced phenotype, (4) intensity of stress, i.e. mean value of the stress inducing environment, (5) coefficient of variation of the stress environment and (6) completeness of information available to the stressed organism. Adaptively reversible phenotypic plastic traits will most probably affect fitness in a way that can be described by simultaneous reversible plasticity in mode and breadth of tolerance functions.

Computer Simulation↗
PubMed2006

Predator-induced phenotypic plasticity in tadpoles: extension or innovation?

Phenotypic plasticity, the ability of a trait to change as a function of the environment, is central to many ideas in evolutionary biology. A special case of phenotypic plasticity observed in many organisms is mediated by their natural predators. Here, we used a predator-prey system of dragonfly larvae and tadpoles to determine if predator-mediated phenotypic plasticity provides a novel way of surviving in the presence of predators (an innovation) or if it represents a simple extension of the way noninduced tadpoles survive predation. Tadpoles of Limnodynastes peronii were raised in the presence and absence of predation, which then entered a survival experiment. Induced morphological traits, primarily tail height and tail muscle height, were found to be under selection, indicating that predator-mediated phenotypic plasticity may be adaptive. Although predator-induced animals survived better, the multivariate linear selection gradients were similar between the two tadpole groups, suggesting that predator-mediated phenotypic plasticity is an extension of existing survival strategies. In addition, nonlinear selection gradients indicated a cost of predator-induced plasticity that may limit the ability of phenotypic plasticity to enhance survival in the presence of predators.

Animals↗
PubMed1990

Collagen synthesis by cultured arterial smooth muscle cells during spontaneous phenotypic modulation.

Quantitative and qualitative changes in collagen synthetic activity by rabbit arterial smooth muscle cells were monitored during spontaneous phenotypic modulation from days 2-15 of culture. The cultured smooth muscle cells transformed into a synthetic phenotype, reaching a maximum of 94.6% on day 4, and then gradually returned to a contractile phenotype accounting for 59.3% on day 15 of culture. The maximum collagen synthesis was found on day 7 when the cells were in early quiescent phase and showed a 91.7% synthetic phenotype. With an increasing proportion of cells in a contractile state, total collagen synthesis per cell decreased in parallel with the reduction in total protein synthesis. Synthesis of type I collagen was predominant, and the proportion of type I + III collagen was over 85% during the entire period of culture. Synthetic activity of type IV collagen, however, was relatively increased, and reached 3.8 +/- 0.4% at day 15 in comparison with 0.8 +/- 0.1% in the late logarithmic growth phase on day 4. This significant increment of type IV collagen in vitro seems to be correlated with the phenotypic modulation of cultured smooth muscle cells into a contractile phenotype.

Animals↗
PubMed1994

Heterogeneity in the phenotypic expression of the mutation in the mitochondrial tRNA(Leu) (UUR) gene generally associated with the MELAS subset of mitochondrial encephalomyopathies.

BACKGROUND: Point mutations in the mitochondrial (mt) genome underlie a number of neurological disorders. Some are well defined including the myoclonus epilepsy ragged red fibre syndrome (MERRF) and the mitochondrial encephalopathy lactic acidosis stroke like episode syndrome (MELAS). However, other clinical phenotypes are less distinctive and mitochondrial studies are often included in the workup in complex neurological syndromes of uncertain aetiology. AIMS: We investigated 27 consecutive patients with varied clinical phenotypes referred to our laboratory for mtDNA studies to determine the incidence of recognised point mutations in a patient group with a range of phenotypes including many where mt disease was possible but did not fall into a classical syndrome. METHODS: The recognised point mutations were detected by amplification of the appropriate DNA fragment by PCR followed by restriction-endonuclease digestion of the normal and mutant species. RESULTS: The A-G base substitution mutation at nucleotide (nt)3243 in the tRNA(Leu) gene of mtDNA which is present in the majority of cases of MELAS syndrome, was detected in four cases, only one of whom had typical MELAS symptoms. Their clinical manifestations ranged from mild deafness to a mixture of chronic progressive external ophthalmoplegia symptoms (CPEO) and stroke like episodes. The nt3243 mutation was also identified in one of seven mtDNA deletion negative CPEO cases. CONCLUSIONS: The presentation of the mtDNA mutation at nt3243 appears therefore to be quite variable with some mild phenotypes as well as severe phenotypes observed. In general, the chance of finding a mitochondrial point mutation in a patient with an atypical clinical phenotype is small.

Adult↗
PubMed2005

Evolution of phenotypic plasticity: patterns of plasticity and the emergence of ecotypes.

Phenotypic plasticity itself evolves, as does any other quantitative trait. A very different question is whether phenotypic plasticity causes evolution or is a major evolutionary mechanism. Existing models of the evolution of phenotypic plasticity cover many of the proposals in the literature about the role of phenotypic plasticity in evolution. I will extend existing models to cover adaptation to a novel environment, the appearance of ecotypes and possible covariation between phenotypic plasticity and mean trait value of ecotypes. Genetic assimilation does not sufficiently explain details of observed patterns. Phenotypic plasticity as a major mechanism for evolution--such as, invading new niches, speciation or macroevolution--has, at present, neither empirical nor model support.

Adaptation, Physiological↗
PubMed1997

Antibody-mediated selection of a Mycoplasma gallisepticum phenotype expressing variable proteins.

A variant phenotype of Mycoplasma gallisepticum S6 was isolated from an in vitro antibody-culture system utilizing metabolism-inhibiting antibodies against the 64 kDa lipoprotein (LP64). M. gallisepticum populations grown in medium alone or medium containing normal rabbit serum maintained expression of the parental phenotype. This paper describes the identification of proteins which undergo variable expression. Several of these were integral membrane proteins, with estimated molecular masses of 91, 43, 41, 38, 37, and 18 kDa, which were expressed in the variant phenotype but not in the parental phenotype. Three proteins (LP64, p63 and p47) were expressed in the parental phenotype, but not in the variant phenotype. The data suggest that the interaction of specific immunoglobulins with target epitopes resulted in the selection of a subpopulation of organisms expressing an alternative array of membrane proteins which, lacking the target epitopes, was able to escape the metabolism-inhibiting effects of the specific antibodies.

Animals↗
PubMed1997

Genetic and phenotypic analysis of the genes of the elbow-no-ocelli region of chromosome 2L of Drosophila melanogaster.

The elbow locus is found to be two genes elA and elB, each of which has a distinct phenotype when mutant. Mutations of the elA gene have a strong phenotype where the wing is markedly disrupted. Mutations of elB are weak, mainly affecting the alula and the wing bristles. The two genes are dominant enhancers of each other. Homozygous deletion of the complete elbow region results in lethality. Situated between the elbow genes is the pupal gene and a locus which when deleted causes a crippled leg phenotype. This locus may be a control region for elbow. Immediately adjacent on the proximal side of elA is the no-ocelli locus. The phenotypes of noc alleles vary from extreme, where the ocelli and associated bristles are absent, to weak where these structures are disrupted. The various noc phenotypes are associated with genetically distinct gene regions, mutations of which act as enhancers of each other. Alleles of el and noc show partial failure of complementation, heterozygotes having weak el or weak noc phenotypes. Alleles of both these genes interact with the antimorphic noc allele Sco.

Alleles↗
PubMed1999

Phenotypes and genotypes of erythromycin-resistant Streptococcus pyogenes strains in Italy and heterogeneity of inducibly resistant strains.

A total of 387 clinical strains of erythromycin-resistant (MIC, >/=1 microg/ml) Streptococcus pyogenes, all isolated in Italian laboratories from 1995 to 1998, were examined. By the erythromycin-clindamycin double-disk test, 203 (52.5%) strains were assigned to the recently described M phenotype, 120 (31.0%) were assigned to the inducible macrolide, lincosamide, and streptogramin B resistance (iMLS) phenotype, and 64 (16.5%) were assigned to the constitutive MLS resistance (cMLS) phenotype. The inducible character of the resistance of the iMLS strains was confirmed by comparing the clindamycin MICs determined under normal testing conditions and those determined after induction by pregrowth in 0.05 microg of erythromycin per ml. The MICs of erythromycin, clarithromycin, azithromycin, josamycin, spiramycin, and the ketolide HMR3004 were then determined and compared. Homogeneous susceptibility patterns were observed for the isolates of the cMLS phenotype (for all but one of the strains, HMR3004 MICs were 0.5 to 8 microg/ml and the MICs of the other drugs were >128 microg/ml) and those of the M phenotype (resistance only to the 14- and 15-membered macrolides was recorded, with MICs of 2 to 32 microg/ml). Conversely, heterogeneous susceptibility patterns were observed in the isolates of the iMLS phenotype, which were subdivided into three distinct subtypes designated iMLS-A, iMLS-B, and iMLS-C. The iMLS-A strains (n = 84) were highly resistant to the 14-, 15-, and 16-membered macrolides and demonstrated reduced susceptibility to low-level resistance to HMR3004. The iMLS-B strains (n = 12) were highly resistant to the 14- and 15-membered macrolides, susceptible to the 16-membered macrolides (but highly resistant to josamycin after induction), and susceptible to HMR3004 (but intermediate or resistant after induction). The iMLS-C strains (n = 24) had lower levels of resistance to the 14- and 15-membered macrolides (with erythromycin MICs increasing two to four times after induction), were susceptible to the 16-membered macrolides (but resistant to josamycin after induction), and remained susceptible to HMR3004, also after induction. The erythromycin resistance genes in 100 isolates of the different groups were investigated by PCR. All cMLS and iMLS-A isolates tested had the ermAM (ermB) gene, whereas all iMLS-B and iMLS-C isolates had the ermTR gene (neither methylase gene was found in isolates of other groups). The M isolates had only the macrolide efflux (mefA) gene, which was also found in variable proportions of cMLS, iMLS-A, iMLS-B, and iMLS-C isolates. The three iMLS subtypes were easily differentiated by a triple-disk test set up by adding a josamycin disk to the erythromycin and clindamycin disks of the conventional double-disk test. Tetracycline resistance was not detected in any isolate of the iMLS-A subtype, whereas it was observed in over 90% of both iMLS-B and iMLS-C isolates.

Anti-Bacterial Agents↗
PubMed2000

A novel human immunodeficiency virus type 1 reverse transcriptase mutational pattern confers phenotypic lamivudine resistance in the absence of mutation 184V.

We describe a new human immunodeficiency virus type 1 (HIV-1) mutational pattern associated with phenotypic resistance to lamivudine (3TC) in the absence of the characteristic replacement of methionine by valine at position 184 (M184V) of reverse transcriptase. Combined genotypic and phenotypic analyses of clinical isolates revealed the presence of moderate levels of phenotypic resistance (between 4- and 50-fold) to 3TC in a subset of isolates that did not harbor the M184V mutation. Mutational cluster analysis and comparison with the phenotypic data revealed a significant correlation between moderate phenotypic 3TC resistance and an increased incidence of replacement of glutamic acid by aspartic acid or alanine and of valine by isoleucine at residues 44 and 118 of reverse transcriptase, respectively. This occurred predominantly in those isolates harboring zidovudine resistance-associated mutations (41L, 215Y). The requirement of the combination of mutations 41L and 215Y with mutations 44D and 44A and/or 118I for phenotypic 3TC resistance was confirmed by site-directed mutagenesis experiments. These data support the assumption that HIV-1 may have access to several different genetic pathways to escape drug pressure or that the increase in the frequency of particular mutations may affect susceptibility to drugs that have never been part of a particular regimen.

Anti-HIV Agents↗
PubMed2003

Heterogeneity of macrolide-lincosamide-streptogramin B resistance phenotypes in enterococci.

We determined the macrolide resistance phenotypes of 241 clinical isolates of erythromycin-resistant enterococci (MICs, > or = 1 microg/ml), including 147 Enterococcus faecalis strains and 94 Enterococcus faecium strains, collected from a hospital in Seoul, Korea, between 1999 and 2000. By the erythromycin (40 micro g)-josamycin (100 microg) double-disk test, 93 strains were assigned to the constitutive macrolide, lincosamide, and streptogramin B (MLS(B)) resistance (cMLS(B)) phenotype, and the remaining 148 strains were assigned to the inducible MLS(B) resistance (iMLS(B)) phenotype. Of the strains with the iMLS(B) phenotype, 36 exhibited a reversibly inducible MLS(B) (riMLS(B)) phenotype, i.e., blunting of the erythromycin zone of inhibition, which indicates that the 16-membered-ring macrolide josamycin is a more effective inducer than the 14-membered-ring macrolide erythromycin. Sequence analysis of the regulatory regions of the erm(B) genes from all of the strains exhibiting the riMLS(B) phenotype revealed not only erm(Bv) [where v represents variant; previously erm(AMR)] (n = 13), as reported previously, but also three kinds of erm(B) variants, which were designated erm(Bv1) (n = 17), erm(Bv2) (n = 3), and erm(Bv3) (n = 3), respectively. In lacZ reporter gene assays of these variants, the 16-membered-ring macrolide tylosin had stronger inducibility than erythromycin at > or = 0.1 microg/ml. These findings highlight the versatility of erm(B) in induction specificity.

Anti-Bacterial Agents↗
PubMed2006

Identifying functionally important mutations from phenotypically diverse sequence data.

Here we present a simple statistical method to determine the phenotypic contribution of a single mutation from libraries of mutants with diverse phenotypes in which each mutant contains a multitude of mutations. The central premise of this method is that, given M phenotypic classes, mutations that do not affect the phenotype should partition among the M classes according to a multinomial distribution. Deviations from this distribution are indicative of a link between specific mutations and phenotypes. We suggest that this method will aid the engineering of functional nucleic acids, proteins, and other biomolecules by uncovering target sites for rational mutagenesis. As a proof of the principle, we show how the method can be used to deduce the individual effects of mutations in a set of 69 P(L)-lambda promoter variants. Each of these promoters was generated by error-prone PCR and incorporated numerous mutations. The activity of the promoters was assayed using flow cytometry to measure the fluorescence of a green fluorescent protein reporter gene. Our analysis of the sequences of these mutants revealed seven positions having a statistically significant correlation with promoter activity. Using site-directed mutagenesis, we constructed point mutations for several sites, both statistically significant and insignificant, and combinations of these sites. Our results show that the statistical method correctly elucidated the phenotypic manifestations of these mutations. We suggest that this method may be useful for expediting directed evolution experiments by allowing both desired and undesired mutations to be identified and incorporated between rounds of mutagenesis.

Base Sequence↗
PubMed2005

Phenotypic switching in Candida glabrata accompanied by changes in expression of genes with deduced functions in copper detoxification and stress.

Most strains of Candida glabrata switch spontaneously between a number of phenotypes distinguishable by graded brown coloration on agar containing 1 mM CuSO4, a phenomenon referred to as "core switching." C. glabrata also switches spontaneously and reversibly from core phenotypes to an irregular wrinkle (IWr) phenotype, a phenomenon referred to as "irregular wrinkle switching." To identify genes differentially expressed in the core phenotypes white (Wh) and dark brown (DB), a cDNA subtraction strategy was employed. Twenty-three genes were identified as up-regulated in DB, four in Wh, and six in IWr. Up-regulation was verified in two unrelated strains, one a and one alpha strain. The functions of these genes were deduced from the functions of their Saccharomyces cerevisiae orthologs. The majority of genes up-regulated in DB (78%) played deduced roles in copper assimilation, sulfur assimilation, and stress responses. These genes were differentially up-regulated in DB even though the conditions of growth for Wh and DB, including CuSO4 concentration, were identical. Hence, the regulation of these genes, normally regulated by environmental cues, has been usurped by switching, presumably as an adaptation to the challenging host environment. These results are consistent with the suggestion that switching provides colonizing populations with a minority of cells expressing a phenotype that allows them to enrich in response to an environmental challenge, a form of rapid adaptation. However, DB is the most commonly expressed phenotype at sites of host colonization, in the apparent absence of elevated copper levels. Hence, up-regulation of these genes by switching suggests that in some cases they may play roles in colonization and virulence not immediately obvious from the roles played by their orthologs in S. cerevisiae.

Candida glabrata↗
PubMed1987

Trichomonas vaginalis NYH286 phenotypic variation may be coordinated for a repertoire of trichomonad surface immunogens.

Trichomonas vaginalis isolate NYH286 was fractionated with immunoglobulin G of sera from patients with trichomoniasis. Subpopulations of trichomonads with phenotypes of either patient serum-immunoglobulin G reactive (PS+) or nonreactive (PS-) were obtained. Flow cytofluorometry of PS+ and PS- subpopulations with a monoclonal antibody called C20A3 which reacts with a high-molecular-weight immunogen of T. vaginalis gave corresponding fluorescent (positive) and nonfluorescent (negative) phenotypes. No relationship was seen between PS+ and PS- phenotypes and binding of soybean agglutinin, wheat germ agglutinin, and concanavalin A, showing that PS- organisms still possessed carbohydrate moieties on their surfaces based on lectin binding. Phenotypic variation among the PS+ and PS- trichomonads was observed during in vitro growth. A positive-to-negative phenotype shift was also recorded for parasites obtained from lesions of mice subcutaneously infected with PS+ trichomonads. The involvement of surface proteins in the differential PS+ and PS- reactions was supported by soluble antigen and whole cell radioimmunoprecipitation assays. Finally, enhanced parasitism and killing of HeLa cells in monolayer cultures were observed for PS- subpopulations as compared with PS+ counterparts. The data support the idea that phenotypic variation for T. vaginalis may be coordinated for a repertoire of trichomonad immunogens and that such membrane dynamics influence expression of virulence determinants for these sexually transmitted disease agents.

Antibodies, Monoclonal↗