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PubMed2006

Flexible architecture of inducible morphological plasticity.

1. Predator-induced morphological defences are produced in response to an emergent predator regime. In natural systems, prey organisms usually experience temporal shifting of the composition of the predator assemblage and of the intensity of predation risk from each predator species. Although, a repetitive morphological change in response to a sequential shift of the predator regime such as alteration of the predator species or diminution of the predation risk may be adaptive, such flexible inducible morphological defences are not ubiquitous. 2. We experimentally addressed whether a flexible inducible morphological defence is accomplished in response to serial changes in the predation regime, using a model prey species which adopt different defensive morphological phenotypes in response to different predator species. Rana pirica (Matsui) tadpoles increased body depth and tail depth against the predatory larval salamander Hynobius retardatus (Dunn); on the other hand, they only increased tail depth against the predatory larval dragonfly Aeshna nigroflava (Martin). 3. Rana pirica tadpoles with the predator-specific phenotypes were subjected to removal or exchange of the predator species. After removal of the predator species, tadpoles with each predator-specific phenotype changed their phenotype to the nondefensive basic one, suggesting that both predator-specific phenotypes are costly to maintain. After an exchange of the predator species, tadpoles with each predator-specific phenotype reciprocally, flexibly shifted their phenotype to the now more suitable predator-specific one only by modifying their body part. The partial modification can effectively reduce time and energy expenditures involved in repetitive morphological changes, and therefore suggest that the costs of the flexible morphological changes are reduced.

Adaptation, Physiological↗
PubMed1999

Phase variable switching of in vivo and environmental phenotypes of Salmonella typhimurium.

Previously it was shown that S. typhimurium strain 798, which is known to cause persistent asymptomatic infections in pigs, exists in two phenotypes. One phenotype, which is called adhesive, was shown to produce pili, is adhesive to porcine enterocytes, is readily phagocytized, and then survives intracellularly in phagocytes. The other phenotype, termed non-adhesive, does not produce pili, does not attach to enterocytes, is phagocytized less efficiently, and does not survive within the phagocyte. Cells in each phenotype can freely switch to the other phenotype at a fairly high frequency and thus the shift between each phenotype is phase variation. Further analysis of these phenotypes identified 4 additional characteristics that were co-regulated by phase variation. The first is the enterocyte-specific adhesin, which was shown to be type 1 fimbriae. Mutations in fimA, the major pilin molecule, led to a decreased ability to colonize the gut of pigs and mice. The second characteristic is O-antigen production. Adhesive cells produce a long O-antigen (up to 18 subunits) while non-adhesive cells do not (only 1-2 subunits). The long O-antigen produced by the adhesive cells leads to resistance to serum and appears to be the result of phase variable expression of rfaL. A third locus, ebu, has been identified based on differential color production of colonies growing on Evans blue-Uranine plates. The relationship of this trait to in vivo survival or virulence is not known but ebu is genetically related to a family of transcriptional activators. The fourth locus, prv is located on the virulence plasmid and a mutation in prv results in delayed time to death in mice. It is hypothesized that the adhesive phenotype is the in vivo, virulent form, while the non-adhesive phenotype is the environmental, avirulent form. By modulating the fraction of cells in each phase, persistent asymptomatic infections can be promoted.

Animals↗
PubMed2004

Bioenergetic remodeling during cellular differentiation: changes in cytochrome c oxidase regulation do not affect the metabolic phenotype.

Myogenesis induces mitochondrial proliferation, a decrease in reactive oxygen species (ROS) production, and an increased reliance upon oxidative phosphorylation. While muscles typically possess 20%-40% excess capacity of cytochrome c oxidase (COX), undifferentiated myoblasts have only 5%-20% of the mitochondrial content of myotubes and muscles. We used two muscle lines (C2C12, Sol8) and 3T3-L1 pre-adipocytes to examine if changes in COX regulation or activity with differentiation cause a shift in metabolic phenotype (i.e., more oxidative, less glycolytic, less ROS). COX activity in vivo can be suppressed by its inhibitor, nitric oxide, or sub-optimal substrate (cytochrome c) concentrations. Inhibition of nitric oxide synthase via L-NAME had no effect on the respiration of adherent undifferentiated cells, although it did stimulate respiration of myoblasts in suspension. While cytochrome c content increased during differentiation, there was no correlation with respiratory rate or reliance on oxidative metabolism. There was no correlation between COX specific activity and oxidative metabolism between cell type or in relation to differentiation. These studies show that, despite the very low activities of COX, undifferentiated myoblasts and pre-adipocytes possess a reserve of COX capacity and changes in COX with differentiation do not trigger the shift in metabolic phenotype.

Adipocytes↗
PubMed1983

Immortalization of rodent embryo fibroblasts by SV40 is maintained by the A gene.

SV40 can induce proliferation of primary cells from various origins and by making them escape from senescence confer a potential of unlimited division characteristic of established cell lines. We have studied this effect called immortalization with various mutants of the SV40 early genes. The results establish that the immortalized phenotype is controlled by the A gene in a reversible fashion. Cells immortalized at 33 degrees by a tsA mutant, revert to a "mortal" or senescent-like phenotype after temperature shift up to 39 degrees. The nature of these striking phenotypic changes is discussed.

Animals↗
PubMed2006

Endurance exercise differentially stimulates heart and axial muscle development in zebrafish (Danio rerio).

Mechanical load is an important factor in the differentiation of cells and tissues. To investigate the effects of increased mechanical load on development of muscle and bone, zebrafish were subjected to endurance swim training for 6 h/day for 10 wk starting at 14 days after fertilization. During the first 3 wk of training, trained fish showed transiently increased growth compared with untrained (control) fish. Increased expression of proliferating cell nuclear antigen suggests that this growth is realized in part through increased cell proliferation. Red and white axial muscle fiber diameter was not affected. Total cross-sectional area of red fibers, however, was increased. An improvement in aerobic muscle performance was supported by an increase in myoglobin expression. At the end of 10 wk of training, heart and axial muscle showed increased expression of the muscle growth factor myogenin and proliferating cell nuclear antigen, but there were major differences between cardiac and axial muscle. In axial muscle, expression of the "slow" types of myosin and troponin C was increased, together with expression of erythropoietin and myoglobin, which enhance oxygen transport, indicating a shift toward a slow aerobic phenotype. In contrast, the heart muscle shifts to a faster phenotype but does not become more aerobic. This suggests that endurance training differentially affects heart and axial muscle.

Animals↗
PubMed2006

Germ-line epigenetic modification of the murine A vy allele by nutritional supplementation.

Environmental effects on phenotype can be mediated by epigenetic modifications. The epigenetic state of the murine A vy allele is highly variable, and determines phenotypic effects that vary in a mosaic spectrum that can be shifted by in utero exposure to methyl donor supplementation. We have asked if methyl donor supplementation affects the germ-line epigenetic state of the A vy allele. We find that the somatic epigenetic state of A vy is affected by in utero methyl donor supplementation only when the allele is paternally contributed. Exposure to methyl donor supplementation during midgestation shifts A vy phenotypes not only in the mice exposed as fetuses, but in their offspring. This finding indicates that methyl donors can change the epigenetic state of the A vy allele in the germ line, and that the altered state is retained through the epigenetic resetting that takes place in gametogenesis and embryogenesis. Thus a mother's diet may have an enduring influence on succeeding generations, independent of later changes in diet. Although other reports have suggested such heritable epigenetic changes, this study demonstrates that a specific mammalian gene can be subjected to germ-line epigenetic change.

Alleles↗
PubMed2006

Covariance of phenotypically plastic traits induces an adaptive shift in host selection behaviour.

Flexibility in adult body size allows generalist parasitoids to use many host species at a cost of producing a range of adult sizes. Consequently, host selection behaviour must also maintain a level of flexibility as adult size is related to capture efficiency. In the present study, we investigated covariance of two plastic traits--size at pupation and host size selection behaviour-using Aphidius ervi reared on either Acyrthosiphon pisum or Aulacorthum solani, generating females of disparate sizes. Natal host was shown to change the ranking of perceived host quality with relation to host size. Parasitoids preferentially attacked hosts that corresponded to the size of the second instar of their natal host species. This resulted in optimal host selection behaviour when parasitoids were exposed to the same host species from which they emerged. Parasitoid size was positively correlated with host size preference, indicating that females use relative measurements when selecting suitable hosts. These coadapted gene complexes allow generalist parasitoids to effectively use multiple host species over several generations. However, the fixed nature of the behavioural response, within a parasitoid's lifetime, suggests that these traits may have evolved in a patchy host species environment.

Adaptation, Physiological↗
PubMed2000

CC chemokine receptor (CCR)2 is required for langerhans cell migration and localization of T helper cell type 1 (Th1)-inducing dendritic cells. Absence of CCR2 shifts the Leishmania major-resistant phenotype to a susceptible state dominated by Th2 cytokines, b cell outgrowth, and sustained neutrophilic inflammation.

There is growing evidence that chemokines and their receptors regulate the movement and interaction of antigen-presenting cells such as dendritic cells (DCs) and T cells. We tested the hypothesis that the CC chemokine receptor (CCR)2 and CCR5 and the chemokine macrophage inflammatory protein (MIP)-1alpha, a ligand for CCR5, influence DC migration and localization. We found that deficiency of CCR2 but not CCR5 or MIP-1alpha led to distinct defects in DC biology. Langerhans cell (skin DC) density in CCR2-null mice was normal, and their ability to migrate into the dermis was intact; however, their migration to the draining lymph nodes was markedly impaired. CCR2-null mice had lower numbers of DCs in the spleen, and this was primarily due to a reduction in the CD8alpha(1) T helper cell type 1 (Th1)-inducing subset of DCs. Additionally, there was a block in the Leishmania major infection-induced relocalization of splenic DCs from the marginal zone to the T cell areas. We propose that these DC defects, in conjunction with increased expression of B lymphocyte chemoattractant, a B cell-specific chemokine, may collectively contribute to the striking B cell outgrowth and Th2 cytokine-biased nonhealing phenotype that we observed in CCR2-deficient mice infected with L. major. This disease phenotype in mice with an L. major-resistant genetic background but lacking CCR2 is strikingly reminiscent of that observed typically in mice with an L. major-susceptible genetic background. Thus, CCR2 is an important determinant of not only DC migration and localization but also the development of protective cell-mediated immune responses to L. major.

Animals↗
PubMed2002

Increased number of CCR5+ CD4 T cells among south Indian adults probably associated with the low frequency of X4 phenotype of HIV-1 in India.

BACKGROUND & OBJECTIVE: The shift of the human immunodeficiency virus (HIV) from nonsyncytium inducing strains (NSI/R5) to syncytium inducing strains (SI/X4) seen in subtype B infections during progression to acquired immunodeficiency syndrome (AIDS) is less frequently reported in subtype C. NSI and SI strains differ in the co-receptor they utilize to infect a T-cell. We postulated that a larger pool of CD4 T cells expressing CCR5 would be present among individuals in the Indian population. To validate this hypothesis, we estimated the percentage of CD4 cells expressing CCR5 or CXCR4 molecules among healthy south Indian adults and HIV infected individuals. METHODS: HIV-1 infected and uninfected adult volunteers, belonging to the four southern states of India with Tamil/Malayalam/Kannada or Telugu as their spoken language were prospectively recruited. A two colour flowcytometry examination of the blood sample was done using the following monoclonals; anti-CD45 (FITC)/CD14 (PE), anti IgG1 (FITC)/IgG2a (PE), anti-CD3 (FITC)/CD4 (PE), anti-CD3 (FITC)/CD8 (PE), anti-CD4 (FITC) and anti CCR5 (PE) or anti CXCR4 (PE). RESULTS: In the healthy population (n = 30) studied, 24.6 per cent of CD4 T cells expressed CCR5 and the percentage of CD4 T cells expressing CXCR4 was 80.4. Among the HIV infected individuals (n = 51) the percentage of CD4 T cells expressing CCR5 and CXCR4 was 26.8 and 78.7 per cent respectively. INTERPRETATION & CONCLUSION: The percentage of CD4 cells expressing CCR5 and CXCR4 in both the HIV uninfected and infected adults was significantly higher in the south Indian population than in the West. The larger pool of CCR5 positive CD4 cells probably allows for the R5 HIV strain to have a replication advantage over X4 HIV strains. This may explain the lack of shift in the viral phenotype during disease progression and also the perceived rapid progression of the disease in India compared to the West.

Adult↗
PubMed2005

Sugars inhibit expression of the rugose phenotype of Vibrio cholerae.

Vibrio cholerae can shift to a rugose colony phenotype, reflecting expression of an exopolysaccharide that provides protection against a variety of environmental stresses. Our data indicate that expression of the rugose phenotype is inhibited by a variety of sugars, including sucrose, dextrose, arabinose, fructose, and maltose. Inhibition by sucrose may be one factor in explaining the failure of rugose strains to grow on thiosulfate citrate bile salts sucrose agar, the primary selective medium for V. cholerae.

Carbohydrates↗
PubMed1996

Haptoglobin polymorphism and chronic hepatitis C.

BACKGROUND/AIMS: Haptoglobin (Hp) is a hemoglobin-binding acute phase protein characterized by a genetic polymorphism due to the existence of two different alleles encoding for the alpha chain of the protein. Three phenotypes have been described: Hp 1-1, Hp 2-1 and Hp 2-2. The latter two forms are known to possess immunoglobulin-like properties and play a role in the immune response. Recently, it has been shown that in subjects suffering from hepatitis C, serum Hp concentrations were lower than in the reference population. In the present study we examined whether the haptoglobin phenotype distribution in chronic HCV patients was different from the reference population. We also looked for possible relationships between Hp phenotypes and hepatitis C virus types and response to interferon alpha therapy. Moreover, Hp concentrations were determined. METHODS: The study population consisted of 239 Caucasian patients with proven hepatitis C. Hp phenotypes were determined using starch gel electrophoresis of hemoglobin-supplemented serum, followed by peroxidase staining. Serum Hp concentrations were assayed with an immunonephelometric method. Hepatitis C virus was genotyped and classified according to an internationally accepted system. Two hundred and twenty healthy Caucasian blood-donors served as the reference population. RESULTS: In the reference population, 35 individuals (15.9%) had Hp 1-1, 106 persons (48.2%) had Hp 2-1 and 79 had Hp 2-2 (35.9%), resulting in an Hp 1 allele frequency of 0.400, which is in agreement with the Hardy-Weinberg equilibrium. Hp phenotype distributions and Hp allele frequencies in the chronic hepatitis C virus patient group differed significantly from those obtained in the reference population. In the patient population, 59 individuals (24.7%) had Hp 1-1, 112 persons (46.9%) had Hp 2-1 and 68 had Hp 2-2 (28.5%). This resulted in an Hp 1 allele frequency of 0.481, which is in agreement with the Hardy-Weinberg equilibrium. No statistically significant differences were found between Hp phenotype distribution and hepatitis C virus types or response to interferon alpha therapy. CONCLUSIONS: The observed shift in Hp phenotype distribution in chronic hepatitis C may point to a role of Hp in the natural evolution of hepatitis C.

Adult↗
PubMed2005

Effects of T3 treatment on HSP72 and calcineurin content of functionally overloaded rat plantaris muscle.

The content of both heat shock protein 72 (HSP72) and calcineurin (CaN) in skeletal muscle fibers have been reported to be associated with the slow phenotype. The purpose of the present study was to determine the adaptations/contributions of HSP72 and CaN to experimental conditions producing dramatic shifts in fiber phenotype. Two weeks of functional overload (FO) of the rat plantaris by cutting the tendons of its major synergists resulted in a shift towards a slower MHC profile. Two weeks of thyroid hormone (T3) administration (150 microg/kg/day, i.p.) resulted in a shift towards a faster MHC profile in control rats and an attenuation of the shift towards a slower profile in FO rats. HSP72 and CaN-A content were 63% and 47% higher, respectively, in the plantaris of FO than age-matched control rats. These increases were significantly attenuated by T3 treatment in FO rats. CaN-B levels were approximately 50% higher in FO and FO plus T3-treated than control rats. T3 treatment alone had no effect on the levels of HSP72, CaN-A or -B in control rats. Therefore, chronic overload of a muscle results in an increase in the percentage of slow fibers/MHC and enhances the levels of HSP72 and CaN. In turn, these FO-induced adaptations are attenuated by T3 treatment. Combined, these results indicate that muscle HSP72 and CaN protein levels are modulated by mechanical stress and that their levels appear to be related to changes in fiber type/MHC composition, at least in chronically overloaded muscles.

Animals↗
PubMed2006

Redirection of allergen-specific TH2 responses by a modified adenine through Toll-like receptor 7 interaction and IL-12/IFN release.

BACKGROUND: Natural or synthetic ligands of Toll-like receptors (TLRs), such as CpG-containing oligodeoxynucleotides and imidazoquinolines, affect the functional phenotype of antigen-specific human T lymphocytes by inducing cytokine release by cells of the innate immunity. OBJECTIVE: In vitro investigation of the ability of substitute adenines (SAs) to affect antigen-presenting cells and shift the functional phenotype of specific human T(H)2 cells was performed. METHODS: The functional profile of hapten- and allergen-specific T-cell lines obtained in the absence or presence of modified adenines was assessed by means of quantitative real-time PCR, flow cytometry, and ELISAs. Activation of TLRs was evaluated by means of nucleofection of HEK293 cells. RESULTS: The synthetic heterocycle, chemically related to adenine with substitution in positions 2-, 8-, and 9- (SA-2), but not its related derivative lacking 2- and 8- substitutions, stimulated the production of high amounts of IL-12, IL-10, TNF-alpha, and IL-6 by CD14(+) cells and IFN-alpha and CXCL10 by blood dendritic cell antigen (BDCA)-4(+) plasmacytoid dendritic cells. A nuclear factor kappaB-dependent signaling pathway mediated by SA-2 ligation of TLR7 was responsible for these effects. SA-2 also redirected the in vitro differentiation of either Dermatophagoides pteronyssinus group 1 or amoxicillin-specific T(H)2 cells toward the T(H)1/T(H)0 phenotype, with parallel downregulation of GATA-3 and upregulation of T-box expressed in T cells transcription factors. CONCLUSION: Critical substitutions of the adenine backbone confer the ability to activate TLR7, inducing the production of modulatory cytokines able to shift human allergen-specific T(H)2 cells to a T(H)1/T(H)0 phenotype. CLINICAL IMPLICATIONS: Appropriately modified adenines might be used as effective adjuvants for the development of novel immunotherapeutic strategies of allergic disorders.

Adenine↗
PubMed2003

Biliary tract malformations.

The biliary tree extends from the canals of Hering at the margin of the most peripheral portal tracts to the ampulla of Vater. Malformations occur at every level of this structure. Phenotypic features dominate present understanding of these malformations and of the disorders with which they are associated. Classifications of disease will likely shift from a phenotypic basis to a genotypic basis as genes implicated in biliary tree development and function are identified. Involvement of such genes in biliary tree disorders now considered inflammatory, such as extrahepatic biliary atresia, awaits study. The concept of "feeble cholangiocytes" postnatally susceptible to the effects of "toxic bile" is presented.

Biliary Tract↗
PubMed2006

Systemic administration of IGF-I enhances oxidative status and reduces contraction-induced injury in skeletal muscles of mdx dystrophic mice.

The absence of dystrophin and resultant disruption of the dystrophin glycoprotein complex renders skeletal muscles of dystrophic patients and dystrophic mdx mice susceptible to contraction-induced injury. Strategies to reduce contraction-induced injury are of critical importance, because this mode of damage contributes to the etiology of myofiber breakdown in the dystrophic pathology. Transgenic overexpression of insulin-like growth factor-I (IGF-I) causes myofiber hypertrophy, increases force production, and can improve the dystrophic pathology in mdx mice. In contrast, the predominant effect of continuous exogenous administration of IGF-I to mdx mice at a low dose (1.0-1.5 mg.kg(-1).day(-1)) is a shift in muscle phenotype from fast glycolytic toward a more oxidative, fatigue-resistant, slow muscle without alterations in myofiber cross-sectional area, muscle mass, or maximum force-producing capacity. We found that exogenous administration of IGF-I to mdx mice increased myofiber succinate dehydrogenase activity, shifted the overall myosin heavy chain isoform composition toward a slower phenotype, and, most importantly, reduced contraction-induced damage in tibialis anterior muscles. The deficit in force-producing capacity after two damaging lengthening contractions was reduced significantly in tibialis anterior muscles of IGF-I-treated (53 +/- 4%) compared with untreated mdx mice (70 +/- 5%, P < 0.05). The results provide further evidence that IGF-I administration can enhance the functional properties of dystrophic skeletal muscle and, compared with results in transgenic mice or virus-mediated overexpression, highlight the disparities in different models of endocrine factor delivery.

Animals↗
PubMed2000

Inter- and intra-site genetic diversity of natural field populations of rice tungro bacilliform virus in the Philippines.

The genetic structure of rice tungro bacilliform virus (RTBV) populations within and between growing sites was analyzed in a collection of natural field isolates from different rice varieties grown in eight tungro-endemic sites of the Philippines. Total DNA extracts from 345 isolates were digested with EcoRV restriction enzyme and hybridized with a full-length probe of RTBV, a procedure shown in preliminary experiments capable of revealing high levels of polymorphism in RTBV field isolates. In the total population, 17 distinct EcoRV-based genome profiles (genotypes) were identified and used as indicators for virus diversity. Distinct sets of genotypes occurred in Isabela and North Cotabato provinces suggesting a geographic isolation of virus populations. However, among the sites in each province, there were few significant differences in the genotype compositions of virus populations. The number of genotypes detected at a site varied from two to nine with a few genotypes dominating. In general the isolates at a site persisted from season to season indicating a genetic stability for the local virus population. Over the sampling time, IRRI rice varieties, which have green leafhopper resistance genes, supported similar virus populations to those supported by other varieties, indicating that the variety of the host exerted no apparent selection pressures. Insect transmission experiments on selected RTBV field isolates showed that dramatic shifts in genotype and phenotype distributions can occur in response to host/environmental shifts.

Agriculture↗
PubMed1990

Genetic analysis of suppressors of the veA1 mutation in Aspergillus nidulans.

Light-dependent conidiation in the filamentous ascomycete, Aspergillus nidulans, is contingent on the allelic state of the velvet (veA) gene. Light dependence is abolished by a mutation in this gene (veA1), which allows conidiation to occur in the absence of light. We have isolated and characterized six extragenic suppressors of veA1 that restore the light-dependent conidiation phenotype. Alleles of four genes, defined by complementation tests, were subjected to extensive genetic and phenotypic analysis. The results of light-dark shifting experiments and the phenotypes of double mutant combinations are consistent with the possibility that the expression of the light-dependent phenotype is regulated by specific interactions of the suppressor gene products with the velvet gene product and with each other.

Alleles↗
PubMed1980

Comparison of virulence markers of peritoneal and fallopian tube isolates with endocervical Neisseria gonorrhoeae isolates from women with acute salpingitis.

Neisseria gonorrhoeae strains which cause acute salpingitis are presumed to ascend the genital tract from the cervix. Previous studies utilized isolates obtained from endocervical canal cultures, although it was not known if the isolates truly represented the organisms present in the fallopian tubes. In this study, we compared N. gonorrhoeae isolates from endocervical canal cultures with fallopian tube or peritoneal cul-de-sac isolates or isolates from both sites obtained at laparoscopy. Potential virulence markers were studied, including colony phenotype, auxotype, antimicrobial agent susceptibility, protein patterns on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and susceptibility to normal human serum. Six of seven cervical isolates had the same antibiograms and molecular weight for major outer membrane proteins as those of the corresponding peritoneal isolates. Auxotypes also were the same and included prototrophic, proline-requiring, and proline-and-arginine-requiring isolates. The isolates as a group appeared to be very susceptible to the bactericidal action of pooled serum from normal women. Colony phenotypes varied between sites; the fallopian tubecul-de-sac isolates were predominantly of transparent phenotype and piliated. The cervical isolates were either mixtures of equal quantities of opaque and transparent phenotypes or predominantly opaque phenotype. By these markers, patients' N. gonorrhoeae cervical isolates appeared to be the same as their isolates from fallopian tubes except for a difference or shift in colony phenotype.

Anti-Bacterial Agents↗