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PubMed2006

A haptic face-inversion effect.

We examined whether a face-inversion effect occurs when participants explore faces by touch. We used a haptic version of the inversion paradigm with 3-D clay facemasks and non-face control objects (teapots) moulded from real objects. Young, neurologically intact, blindfolded participants performed a temporally unconstrained haptic same/different task in each of four stimulus conditions: upright facemasks, inverted facemasks, upright teapots, and inverted teapots. There was a significant inversion effect for faces in terms of accuracy, but none for teapots. The results are considered in terms of the consequences of sequential manual exploration for haptic face processing.

Adult↗
PubMed2006

Discrete Radon transform has an exact, fast inverse and generalizes to operations other than sums along lines.

Götz, Druckmüller, and, independently, Brady have defined a discrete Radon transform (DRT) that sums an image's pixel values along a set of aptly chosen discrete lines, complete in slope and intercept. The transform is fast, O(N2log N) for an N x N image; it uses only addition, not multiplication or interpolation, and it admits a fast, exact algorithm for the adjoint operation, namely backprojection. This paper shows that the transform additionally has a fast, exact (although iterative) inverse. The inverse reproduces to machine accuracy the pixel-by-pixel values of the original image from its DRT, without artifacts or a finite point-spread function. Fourier or fast Fourier transform methods are not used. The inverse can also be calculated from sampled sinograms and is well conditioned in the presence of noise. Also introduced are generalizations of the DRT that combine pixel values along lines by operations other than addition. For example, there is a fast transform that calculates median values along all discrete lines and is able to detect linear features at low signal-to-noise ratios in the presence of pointlike clutter features of arbitrarily large amplitude.

Journal Article↗
PubMed2003

Beta-arrestin-mediated activation of MAPK by inverse agonists reveals distinct active conformations for G protein-coupled receptors.

It is becoming increasingly clear that signaling via G protein-coupled receptors is a diverse phenomenon involving receptor interaction with a variety of signaling partners. Despite this diversity, receptor ligands are commonly classified only according to their ability to modify G protein-dependent signaling. Here we show that beta2AR ligands like ICI118551 and propranolol, which are inverse agonists for Gs-stimulated adenylyl cyclase, induce partial agonist responses for the mitogen-activated protein kinases extracellular signal-regulated kinase (ERK) 1/2 thus behaving as dual efficacy ligands. ERK1/2 activation by dual efficacy ligands was not affected by ADP-ribosylation of Galphai and could be observed in S49-cyc- cells lacking Galphas indicating that, unlike the conventional agonist isoproterenol, these drugs induce ERK1/2 activation in a Gs/i-independent manner. In contrast, this activation was inhibited by a dominant negative mutant of beta-arrestin and was abolished in mouse embryonic fibroblasts lacking beta-arrestin 1 and 2. The role of beta-arrestin was further confirmed by showing that transfection of beta-arrestin 2 in these knockout cells restored ICI118551 promoted ERK1/2 activation. ICI118551 and propranolol also promoted beta-arrestin recruitment to the receptor. Taken together, these observations suggest that beta-arrestin recruitment is not an exclusive property of agonists, and that ligands classically classified as inverse agonists rely exclusively on beta-arrestin for their positive signaling activity. This phenomenon is not unique to beta2-adrenergic ligands because SR121463B, an inverse agonist on the V2 vasopressin receptor-stimulated adenylyl cyclase, recruited beta-arrestin and stimulated ERK1/2. These results point to a multistate model of receptor activation in which ligand-specific conformations are capable of differentially activating distinct signaling partners.

Adrenergic beta-Agonists↗
PubMed1978

Autosomal locus regulates inverse relationship between sialic acid content and capacity of mouse erythrocytes to activate human alternative complement pathway.

The observation that mouse erythrocytes (E(m)) from 21 inbred strains had variable capabilities to activate the human alternative complement pathway permitted the demonstration that membrane sialic acid content was inversely related to activating capacity and was regulated by codominant alleles of a single autosomal locus. Linear regression analysis also demonstrated a significant inverse correlation between the sialic acid content of E(m) from four inbred strains and the concentration of beta1H required for decay-dissociation of the properdin-stabilized amplification convertase on the E(m). E(m) from F(1) hybrids derived from strains with high and low alternative pathway activating capacities and from their backcrosses exhibited the alternative pathway activating capacities expected if the activity were regulated by alleles of a single autosomal locus. That this same locus predominantly regulated the sialic acid content of E(m) was established by the significant inverse correlation between the sialic acid content and the alternative pathway activating capacity of E(m) from mice of the F(1) and backcross generations. Although the fluid phase interaction of C3, B, and [unk]D continuously generates C3b in a reaction augmented by properdin, it is the covalent attachment of C3b to bystander surfaces deficient in sialic acid that activates the alternative complement pathway at that site because of impaired binding of beta1H to C3b on such surfaces. Thus, discrimination between activating and nonactivating surfaces occurs after C3b deposition, and sialic acid deficiency represents the molecular basis for our earlier finding that activating particles circumvent the regulatory actions of the control proteins of the alternative pathway.

Animals↗
PubMed1981

Inversions between ribosomal RNA genes of Escherichia coli.

It might be anticipated that the presence of redundant but oppositely oriented sequences in a chromosome could allow inversion of the intervening material through homologous recombination. For example, the ribosomal RNA gene rrnD of Escherichia coli has the opposite orientation fro rrnB and rrnE and is separated from these genes by roughly 20% of the chromosome. Starting with a derivative of Cavalli Hfr, we have constructed mutants that have an inversion of the segment between rrnD and either rrnB or rrnE. These mutants are generally quite viable but do exhibit a slight reduction in growth rate relative to the parental strain. A major line of laboratory E. coli, W3110 and its derivatives, also has an inversion between rrnD and rrnE, probably created directly by a recombinational event between these highly homologous genes.

Crosses, Genetic↗
PubMed1985

Site-specific DNA inversion is enhanced by a DNA sequence element in cis.

A segment of the bacteriophage P1 genome, called the C segment, can be inverted by site-specific recombination; the two different orientations of the invertible segment confer different host ranges to the phage. Inversion is catalyzed by the product of the cin gene which is adjacent to one of the crossover sites flanking the C segment. The Cin-catalyzed recombination can be measured in trans by using tester plasmids in which inversion switches on antibiotic-resistance genes. We show here that an additional sequence, distinct from the two crossover sites, is needed in cis for efficient inversion. This sequence is part of the cin structural gene and stimulates recombination more than 100-fold. We have localized the major enhancer sequence on a 72-base-pair fragment and found its activity to be largely independent of the orientation or position of the sequence with respect to the crossover sites.

Journal Article↗
PubMed1987

A chloroplast DNA inversion marks an ancient evolutionary split in the sunflower family (Asteraceae).

We determined the distribution of a chloroplast DNA inversion among 80 species representing 16 tribes of the Asteraceae and 10 putatively related families. Filter hybridizations using cloned chloroplast DNA restriction fragments of lettuce and petunia revealed that this 22-kilobase-pair inversion is shared by 57 genera, representing all tribes of the Asteraceae, but is absent from the subtribe Barnadesiinae of the tribe Mutisieae, as well as from all families allied to the Asteraceae. The inversion thus defines an ancient evolutionary split within the family and suggests that the Barnadesiinae represents the most primitive lineage in the Asteraceae. These results also indicate that the tribe Mutisieae is not monophyletic, since any common ancestor to its four subtribes is also shared by other tribes in the family. This is the most extensive survey of the systematic distribution of an organelle DNA rearrangement and demonstrates the potential of such mutations for resolving phylogenetic relationships at higher taxonomic levels.

Journal Article↗
PubMed1987

Integration host factor is required for the DNA inversion that controls phase variation in Escherichia coli.

The on-and-off expression (phase variation) of type 1 fimbriae, encoded by fimA, in Escherichia coli is controlled by the inversion of a promoter-containing 314-base-pair DNA element. This element is flanked on each side by a 9-base-pair inverted, repeat sequence and requires closely linked genes for inversion. Homology analysis of the products of these genes, fimB and fimE, reveals a strong similarity with the proposed DNA binding domain of lambda integrase, which mediates site-specific recombination in the presence of integration host factor. Integration host factor, encoded by himA and hip/himD, binds to the sequence 5' TNYAANNNRTTGAT 3', where Y = pyrimidine and R = purine, in mediating integration-excision. In analyzing the DNA flanking the fim 314-base-pair inversion sequence, we found the adjacent sequence 5' TTTAACTTATTGAT 3', which corresponds perfectly with the consensus integration host factor binding site. To characterize the role of himA in phase variation, we transduced either a deletion of himA or an insertionally inactivated hip/himD gene into an E. coli strain with a fimA-lacZ operon fusion. We found the rate of phase variation decreases sharply from 10(-3) to less than 10(-5) per cell per generation. Southern hybridization analysis demonstrates that the himA mutation results in a failure of the switch-generated genetic rearrangement. When the transductant was transformed with a himA+ plasmid, normal switching returned. Thus integration host factor is required for normal type 1 fimbriae phase variation in E. coli.

Bacterial Adhesion↗
PubMed1987

Unusual structure of geranium chloroplast DNA: A triple-sized inverted repeat, extensive gene duplications, multiple inversions, and two repeat families.

Physical and gene mapping studies reveal that chloroplast DNA from geranium (Pelargonium hortorum) has sustained a number of extensive duplications and inversions, resulting in a genome arrangement radically unlike that of other plants. At 217 kilobases in size, the circular chromosome is about 50% larger than the typical land plant chloroplast genome and is by far the largest described to date, to our knowledge. Most of this extra size can be accounted for by a 76-kilobase inverted duplication, three times larger than the normal chloroplast DNA inverted repeat. This tripling has occurred primarily by spreading of the inverted repeat into regions that are single copy in all other chloroplast genomes. Consequently, 10 protein genes that are present only once in all other land plants are duplicated in geranium. At least six inversions, occurring in both the inverted repeat and large single-copy region, must be postulated to account for all of the gene order differences that distinguish the geranium genome from other chloroplast genomes. We report the existence in geranium of two families of short dispersed repeats and hypothesize that recombination between repeats may be the major cause of inversions in geranium chloroplast DNA.

Journal Article↗
PubMed1988

Gin-mediated DNA inversion: product structure and the mechanism of strand exchange.

Inversion of the G loop of bacteriophage Mu requires the phage-encoded Gin protein and a host factor. The topological changes in a supercoiled DNA substrate generated by the two purified proteins were analyzed. More than 99% of the inversion products were unknotted rings. This result excludes synapsis by way of a random collision of recombination sites, because the resulting entrapped supercoils would be converted into knots by recombination. Instead, the recombination sites must come together in the synaptic complex in an ordered fashion with a fixed number of supercoils between the sites. The linking number of the substrate DNA increases by four during recombination. Thus, in three successive rounds of inversion, the change in linking number was +4, +8, and +12, respectively. These results lead to a quantitative model for the mechanism of Gin recombination that includes the distribution of supercoils in the synaptic complex, their alteration by strand exchange, and specific roles for the two proteins needed for recombination.

Bacteriophage lambda↗
PubMed1992

Magnetic resonance imaging of perfusion using spin inversion of arterial water.

A technique has been developed for proton magnetic resonance imaging (MRI) of perfusion, using water as a freely diffusable tracer, and its application to the measurement of cerebral blood flow (CBF) in the rat is demonstrated. The method involves labeling the inflowing water proton spins in the arterial blood by inverting them continuously at the neck region and observing the effects of inversion on the intensity of brain MRI. Solution to the Bloch equations, modified to include the effects of flow, allows regional perfusion rates to be measured from an image with spin inversion, a control image, and a T1 image. Continuous spin inversion labeling the arterial blood water was accomplished, using principles of adiabatic fast passage by applying continuous-wave radiofrequency power in the presence of a magnetic field gradient in the direction of arterial flow. In the detection slice used to measure perfusion, whole brain CBF averaged 1.39 +/- 0.19 ml.g-1.min-1 (mean +/- SEM, n = 5). The technique's sensitivity to changes in CBF was measured by using graded hypercarbia, a condition that is known to increase brain perfusion. CBF vs. pCO2 data yield a best-fit straight line described by CBF (ml.g-1.min-1) = 0.052pCO2 (mm Hg) - 0.173, in excellent agreement with values in the literature. Finally, perfusion images of a freeze-injured rat brain have been obtained, demonstrating the technique's ability to detect regional abnormalities in perfusion.

Animals↗
PubMed1993

Free energies for refolding of the common beta turn into the inverse-common beta turn: simulation of the role of D/L chirality.

Quantitative estimates of the Gibbs free-energy change (delta G) for refolding of one beta-turn conformation into another would assist rational protein design. For beta-turn models, we studied a chirally representative set of nine peptides of the form CH3CO-L1-L2-NHCH3, where loop residues L1 (i + 1) and L2 (i + 2) are achiral Gly (G), L-Ala (A), or D-Ala (a). The stabilities of their common (type I) and inverse-common (type I') beta-turn conformers (GGI is the type-I GG conformer, etc.) were estimated by free-energy simulations using explicit water molecules. An alpha-hydrogen atom of a Gly residue at L1 or L2 was replaced by a methyl group by slow growth. The resulting conformers were less stable than GGI and GGI' by about 1-3 kcal/mol (delta G = 0.9 kcal/mol for AGI and aGI', 1.0 kcal/mol for GAI and GaI', 2.1 kcal/mol for aGI and AGI', and 2.8 kcal/mol for GaI and GAI'; 1 kcal = 4.18 kJ). The delta G value for simultaneous growth of one methyl group at L1 and another at L2 was the sum of the two component delta G values. The delta G values for I-->I' refolding of the common beta-turn conformer into the inverse-common beta-turn conformer ranged over 6 kcal/mol (-3.0 for aa, -1.8 for Ga, -1.1 for aG, -0.7 for Aa, 0 for GG, 0.7 for aA, 1.1 for AG, 1.8 for GA, and 3.0 for AA). Thus, replacing L-Ala by D-Ala at both L1 and L2 of a common beta turn may contribute as much as 6 kcal/mol toward its refolding as an inverse-common beta turn.

Amino Acid Sequence↗
PubMed1997

A selective inverse agonist for central cannabinoid receptor inhibits mitogen-activated protein kinase activation stimulated by insulin or insulin-like growth factor 1. Evidence for a new model of receptor/ligand interactions.

In the present study, we showed that Chinese hamster ovary (CHO) cells transfected with human central cannabinoid receptor (CB1) exhibit high constitutive activity at both levels of mitogen-activated protein kinase (MAPK) and adenylyl cyclase. These activities could be blocked by the CB1-selective ligand, SR 141716A, that functions as an inverse agonist. Moreover, binding studies showed that guanine nucleotides decreased the binding of the agonist CP-55,940, an effect usually observed with agonists, whereas it enhanced the binding of SR 141716A, a property of inverse agonists. Unexpectedly, we found that CB1-mediated effects of SR 141716A included inhibition of MAPK activation by pertussis toxin-sensitive receptor-tyrosine kinase such as insulin or insulin-like growth factor 1 receptors but not by pertussis toxin-insensitive receptor-tyrosine kinase such as the fibroblast growth factor receptor. We also observed similar results when cells were stimulated with Mas-7, a mastoparan analog, that directly activates the Gi protein. Furthermore, SR 141716A inhibited guanosine 5'-0-(thiotriphosphate) uptake induced by CP-55,940 or Mas-7 in CHO-CB1 cell membranes. This indicates that, in addition to the inhibition of autoactivated CB1, SR 141716A can deliver a biological signal that blocks the Gi protein and consequently abrogates most of the Gi-mediated responses. By contrast, SR 141716A had no effect on MAPK activation by insulin or IGF1 in CHO cells lacking CB1 receptors, ruling out the possibility of a direct interaction of SR 141716A with the Gi protein. This supports the notion that the Gi protein may act as a negative intracellular signaling cross-talk molecule. From these original results, which considerably enlarge the biological properties of the inverse agonist, we propose a novel model for receptor/ligand interactions.

Adenylate Cyclase Toxin↗
PubMed1997

Agonist-independent activation of Gz by the 5-hydroxytryptamine1A receptor co-expressed in Spodoptera frugiperda cells. Distinguishing inverse agonists from neutral antagonists.

The human 5-hydroxytryptamine1A receptor, when expressed in Spodoptera frugiperda (Sf9) cells, facilitates the binding of [35S]GTPgammaS to a co-expressed GTP-binding regulatory protein, Gz, consistent with constitutive activity. The antagonists 4-(2'-methoxyphenyl)-1-[2'(n-2"-pyridinyl)-p-iodobenzamido]ethyl-p ipe razine (p-MPPI) and the related fluorobenzamido analogue p-MPPF had little (p-MPPI) or no (p-MPPF) effect on this activity. In contrast, a third antagonist, the neuroleptic spiperone, produced an almost complete suppression. Thus, using G protein activation as an index of receptor activity, p-MPPF was classified as a neutral antagonist, p-MPPI as a partial inverse agonist, and spiperone as essentially a full inverse agonist. As predicted, spiperone displayed properties consistent with a special form of noncompetitive antagonism when used to displace the agonist [125I]R-(+)-trans-8-hydroxy-2-[N-n-propyl-N-(3'-iodo-2'-propenyl)amin o]tetralin. Our data profile Sf9 cells as a unique vehicle for the characterization of inverse agonists, as these cells support a systematic pairing of mammalian receptors and G proteins, quantitative assays of G protein activation, and unambiguously labeled populations of coupled and uncoupled receptors.

Aminopyridines↗
PubMed1998

Intracellular translocation and stability of apolipoprotein B are inversely proportional to the length of the nascent polypeptide.

We have studied the relationship between the length of apolipoprotein B (apoB) and its intracellular translocation and stability using McArdle RH7777 (McA-RH7777) cells expressing recombinant human apoB variants, ranging in size from B15 to B100. The translocational status of apoB was assessed based on trypsin sensitivity of apoB using isolated microsomes as well as permeabilized cells. In isolated microsomes, shorter apoB variants (</=B48) were 75-100% resistant to exogenous trypsin digestion, whereas apoB variants larger than B48 were less than 40% trypsin-resistant. Experiments with hepatic microsomes isolated from rat or transgenic mice expressing human B48 and B100 also confirmed the high trypsin accessibility of B100 compared with B48. In permeabilized cells, apoB variants shorter than B48 were relatively resistant to exogenous trypsin (percentage of trypsin-resistant apoB greater than 70%) in contrast to recombinant human B72 and B100, which were only 55 and 42% trypsin-resistant, respectively. The trypsin sensitivity of human B100 was comparable with that of endogenous rat B100 in McA-RH7777 cells as well as endogenous B100 in HepG2 cells (percentages of trypsin-resistant cells were as follows: for human B100 construct, 42 +/- 7.5%; for endogenous McA-RH7777 B100, 52 +/- 2.9%; and for endogenous HepG2 B100, 46 +/- 6.3%). Overall, an inverse correlation between the length of apoB and its resistance to exogenous trypsin was evident irrespective of the model system examined. An inverse relationship was also observed between the size of apoB and its co-translational resistance to proteasomal degradation. Truncated apoB constructs were relatively insensitive to proteasome inhibition by MG132 co-translationally (during the pulse) compared with the full-length B100, which was highly sensitive (apoB recovered in the presence of MG132 as a percentage of control was as follows: B15, 127%; B29, 94%; B48, 110%; B72, 140%; B100, 282%). Post-translationally (over a 2-h chase), a similar inverse relationship was found, with B100 being the least stable in comparison with truncated apoB variants. In summary, as the size of the nascent apoB chain increases, there appears to be a greater cytosolic exposure of the polypeptide, leading to a higher sensitivity to proteasomal degradation.

Animals↗
PubMed1999

Regulation of peripheral cannabinoid receptor CB2 phosphorylation by the inverse agonist SR 144528. Implications for receptor biological responses.

We recently demonstrated that the selective cannabinoid receptor antagonist SR 144528 acts as an inverse agonist that blocks constitutive mitogen-activated protein kinase activity coupled to the spontaneous autoactivated peripheral cannabinoid receptor (CB2) in the Chinese hamster ovary cell line stably transfected with human CB2. In the present report, we studied the effect of SR 144528 on CB2 phosphorylation. The CB2 phosphorylation status was monitored by immunodetection using an antibody specific to the COOH-terminal CB2 which can discriminate between phosphorylated and non-phosphorylated CB2 isoforms at serine 352. We first showed that CB2 is constitutively active, phosphorylated, and internalized at the basal level. By blocking autoactivated receptors, inverse agonist SR 144528 treatment completely inhibited this phosphorylation state, leading to an up-regulated CB2 receptor level at the cell surface, and enhanced cannabinoid agonist sensitivity for mitogen-activated protein kinase activation of Chinese hamster ovary-CB2 cells. After acute agonist treatment, serine 352 was extensively phosphorylated and maintained in this phosphorylated state for more than 8 h after agonist treatment. The cellular responses to CP-55,940 were concomitantly abolished. Surprisingly, CP-55,940-induced CB2 phosphorylation was reversed by SR 144528, paradoxically leading to a non-phosphorylated CB2 which could then be fully activated by CP-55,940. The process of CP-55,940-induced receptor phosphorylation followed by SR 144528-induced receptor dephosphorylation kept recurring many times on the same cells, indicating that the agonist switches the system off but the inverse agonist switches the system back on. Finally, we showed that autophosphorylation and CP-55, 940-induced serine 352 CB2 phosphorylation involve an acidotropic GRK kinase, which does not use Gibetagamma. In contrast, SR 144528-induced CB2 dephosphorylation was found to involve an okadaic acid and calyculin A-sensitive type 2A phosphatase.

Amino Acid Sequence↗
PubMed2004

Insulin-like growth factor-1 (IGF-1) inversely regulates atrophy-induced genes via the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway.

Skeletal muscle size is regulated by anabolic (hypertrophic) and catabolic (atrophic) processes. We first characterized molecular markers of both hypertrophy and atrophy and identified a small subset of genes that are inversely regulated in these two settings (e.g. up-regulated by an inducer of hypertrophy, insulin-like growth factor-1 (IGF-1), and down-regulated by a mediator of atrophy, dexamethasone). The genes identified as being inversely regulated by atrophy, as opposed to hypertrophy, include the E3 ubiquitin ligase MAFbx (also known as atrogin-1). We next sought to investigate the mechanism by which IGF-1 inversely regulates these markers, and found that the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway, which we had previously characterized as being critical for hypertrophy, is also required to be active in order for IGF-1-mediated transcriptional changes to occur. We had recently demonstrated that the IGF1/PI3K/Akt pathway can block dexamethasone-induced up-regulation of the atrophy-induced ubiquitin ligases MuRF1 and MAFbx by blocking nuclear translocation of a FOXO transcription factor. In the current study we demonstrate that an additional step of IGF1 transcriptional regulation occurs downstream of mTOR, which is independent of FOXO. Thus both the Akt/FOXO and the Akt/mTOR pathways are required for the transcriptional changes induced by IGF-1.

Active Transport, Cell Nucleus↗
PubMed2001

Prenatal diagnosis of translocation and a single pericentric inversion 9: the value of fetal ultrasound.

A total of 2741 high-risk pregnant mothers underwent invasive prenatal procedures, and in 94 of them (3.4%), fetal chromosomal or genetic anomalies were detected. In this study, we report on single pericentric inversions of chromosome 9 as well as translocations, which constituted 32% (30 of 94) and 16% (15 of 94) of all identified chromosomal or genetic abnormalities, respectively. In six fetuses of the 30 with an inversion of chromosome 9, ultrasound findings were abnormal and consisted of hydramnios, anhydramnios, hydroureter, hydronephrosis, encephalocele and prune belly syndrome, occurring singly or in combination. Among the 15 fetuses with chromosomal translocations, five had sonographic abnormalities. In conclusion, we found detailed ultrasound survey of fetuses with either translocations or inversions of chromosome 9 to be an additional source of useful information concerning fetal status that could be of value in genetic counselling of affected parents.

Journal Article↗