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PubMed2005

Correction of left hepatic vein redundancy in paediatric liver transplantation.

Redundancy of hepatic vein in the venous outflow reconstruction of partial graft in paediatric liver transplantation may occur when the graft hepatic vein is longer than anticipated. We describe two cases with outflow obstruction due to hepatic vein redundancy. The correction of the redundancy was made by pulling the graft caudally and to the left or right side of the abdominal cavity as determined by Doppler ultrasonography.

Female↗

PubMed2006

Redundancy and recombination in the Echinococcus AgB multigene family: is there any similarity with protozoan contingency genes?

Numerous genetic variants of the Echinococcus antigen B (AgB) are encountered within a single metacestode. This could be a reflection of gene redundancy or the result of a somatic hypermutation process. We evaluate the complexity of the AgB multigene family by characterizing the upstream promoter regions of the 4 already known genes (EgAgB1-EgAgB4) and evaluating their redundancy in the genome of 3 Echinococcus species (E. granulosus, E. ortleppi and E. multilocularis) using PCR-based approaches. We have ascertained that the number of AgB gene copies is quite variable, both within and between species. The most repetitive gene seems to be AgB3, of which there are more than 110 copies in E. ortleppi. For E. granulosus, we have cloned and characterized 10 distinct upstream promoter regions of AgB3 from a single metacestode. Our sequences suggest that AgB1 and AgB3 are involved in gene conversion. These results are discussed in light of the role of gene redundancy and recombination in parasite evasion mechanisms of host immunity, which at present are known for protozoan organisms, but virtually unknown for multicellular parasites.

Alleles↗

PubMed1995

Fate of neglected targets: a chronometric analysis of redundant target effects in the bisected brain.

The authors examined some of the sensorimotor effects of the split-brain operation to understand how a "dual mind" can produce unified behavior. They report psychophysical evidence of extinction to bilateral simultaneous stimulation in callosotomy patient J.W.: Although he could verbally report the occurrence of a unilateral left or right visual field target, left field report accuracy dropped by 34% when targets occurred bilaterally. Paradoxically, the same stimulus conditions produced abnormally robust redundant signal effects on simple manual and vocal reaction times, which exceeded predictions that were based on probability summation. Neural summation is often inferred from redundancy gain of this magnitude. Because this seems less likely after callosotomy, the authors suggest a model that is based on response competition between the disconnected hemispheres to account for J.W.'s redundant target effects. The dissociation between explicit report and motor performance is discussed.

Adult↗

PubMed1978

The role of spatial redundancy in grapheme recognition: perception or inference?

The question under investigation is whether spatial redundancy operates by restricting the number of valid alternatives at each serial position or whether it serves a perceptual function by keeping visually confusable graphemes from appearing in the same array and/or maximizing the distance between such graphemes when they do occur in the same array. The first experiment used the same-different task to establish a confusion matrix for 12 non-linguistic symbols. The spatial relation between the members of two pairs of confusable symbols was manipulated in a second experiment, which had subjects look for the presence or absence of a predetermined target symbol in single six-symbol linear arrays. Facilitation was found to be dependent upon the perceptual consequences of serial position constraint rather than upon the constraint per se. The constraint was most effective when it served to prevent members of visually confusable pairs from occurring in the same array. Since spatial redundancy may operate at the feature extraction stage by minimizing competition for the same sets of feature detectors and since words are likely to be high in spatial redundancy, the possibility is raised that part of the word superiority effect may be due to visual factors rather than to linguistic context.

Form Perception↗

PubMed2002

Redundancy gains and costs in cognitive processing: effects of short stimulus onset asynchronies.

In 7 experiments, the influence of varying stimulus onset asynchronies (SOAs) on the processing of redundant information about words and pseudowords was investigated. All stimuli were visually presented once or twice with 2 copies of the same item flashed either simultaneously or with short SOAs between presentations. The experiments revealed a redundancy gain for words that was absent for pseudowords. Furthermore, the redundancy gain disappeared at an SOA of 50 ms, and there was a gradual performance decline at longer SOAs. However, probing SOAs of 150 and 300 ms revealed that, compared with presentation of 1 target stimulus alone, words were processed significantly faster when target and redundantcopy appeared with a 150-ms lag. The results are tentatively explained in a neurocognitive framework.

Adult↗

PubMed2005

Redundant cell death mechanisms as relics and backups.

Here we review recent observations indicating the existence of redundant cell death mechanisms. We speculate that this redundancy reflects a particular evolutionary history for cellular demise. Autophagic or apoptotic elements might have been added to a primordial death mechanism, initially improving cell dismantling and later acquiring the ability to act themselves as death effectors. The resulting redundancy of cell death mechanisms has pathophysiological implications.

Animals↗

PubMed1999

Information and redundancy: key concepts in understanding the genetic control of health and intelligence.

A model is proposed in which information from the environment is analysed by complex biological decision-making systems which are highly redundant. A correct response is intelligent behaviour which preserves health; incorrect responses lead to disease. Mutations in genes which code for the redundant systems will accumulate in the genome and impair decision-making. The number of mutant genes will depend upon a balance between the new mutation rate per generation and systems of elimination based on synergistic interaction in redundant systems. This leads to a polygenic pattern of inheritance for intelligence and the common diseases. The model also gives a simple explanation for some of the hitherto puzzling aspects of work on the genetic basis of intelligence including the recorded rise in IQ this century. There is a prediction that health, intelligence and socio-economic position will be correlated generating a health differential in the social hierarchy. Furthermore, highly competitive societies will place those least able to cope in the harshest environment and this will impair health overall. The model points to a need for population monitoring of somatic mutation in order to preserve the health and intelligence of future generations.

Genetic Predisposition to Disease↗

PubMed2004

RHAMM, a receptor for hyaluronan-mediated motility, compensates for CD44 in inflamed CD44-knockout mice: a different interpretation of redundancy.

We report here that joint inflammation in collagen-induced arthritis is more aggravated in CD44-knockout mice than in WT mice, and we provide evidence for molecular redundancy as a causal factor. Furthermore, we show that under the inflammatory cascade, RHAMM (receptor for hyaluronan-mediated motility), a hyaluronan receptor distinct from CD44, compensates for the loss of CD44 in binding hyaluronic acid, supporting cell migration, up-regulating genes involved with inflammation (as assessed by microarrays containing 13,000 cDNA clones), and exacerbating collagen-induced arthritis. Interestingly, we further found that the compensation for loss of the CD44 gene does not occur because of enhanced expression of the redundant gene (RHAMM), but rather because the loss of CD44 allows increased accumulation of the hyaluronic acid substrate, with which both CD44 and RHAMM engage, thus enabling augmented signaling through RHAMM. This model enlightens several aspects of molecular redundancy, which is widely discussed in many scientific circles, but the processes are still ill defined.

Animals↗

PubMed1972

A unique form of terminal redundancy in adenovirus DNA molecules.

A unique form of terminal redundancy has been observed in DNA molecules extracted from several human adenovirus serotypes. Electron microscopic studies reveal that single-stranded circular molecules are formed when native DNA is denatured and then annealed. Temperatures approaching the T(m) of native DNA are required to convert circles to linear molecules, indicating a high degree of self-complementarity between terminal base sequences of DNA strands. Single-stranded circles are not generated if a limited number of nucleotides (2-4%) are removed from the 3' ends of native DNA by digestion with Escherichia coli exonuclease III before denaturation and annealing. The lenght of the redundant segment appears to differ among major serotypic groups, and a possible association between increased length of the redundant segment and increased oncogenic capability of virus serotype is suggested. Evidence for the configuration of the duplex closure region of circular molecules is also presented.

Adenoviridae↗

PubMed1996

Cell-type and promoter-context dependent retinoic acid receptor (RAR) redundancies for RAR beta 2 and Hoxa-1 activation in F9 and P19 cells can be artefactually generated by gene knockouts.

By using RAR type (alpha, beta, or gamma)-specific synthetic retinoids and a pan-retinoic X receptor (RXR)-specific ligand, we have investigated the contribution of RARs and RXRs in the activation of RA target genes and the differentiation of embryonal carcinoma cells. We demonstrate cell-type- and promoter context-dependent functional redundancies that differ between the three RAR types for mediating the induction of RARbeta2 and Hoxa-1 in wild-type, RARgamma-/- and RARalpha-/- F9 cells and in P19 cells. The extent of redundancy between RARs is further modulated by the synergistic activation of RXRs with a pan-RXR agonist. We also demonstrate that the expression of RARbeta2 is auto-inducible in RARgamma-/- but not in wild-type F9 cells, indicating that the functional redundancies observed between RARs in gene disruption studies can be artefactually generated. Thus, even though all three RARs can functionally substitute each other for inducing the expression of RA target genes and cell differentiation, one RAR can cell-specifically override the activity of the other RARs. Interestingly, only RARgamma can mediate the retinoic acid-induced differentiation of wild-type F9 cells, whereas the differentiation of P19 cells can be mediated by either RARalpha or RARgamma.

Cell Differentiation↗

PubMed2003

Non-redundant role of Shc in Erk activation by cytoskeletal reorganization.

We have shown previously that cytoskeletal reorganization (CSR) induced by pharmacological reagents such as colchicine or cytochalasins can up-regulate the urokinase-type plasminogen activator (uPA) gene via the Ras/Erk signaling pathway. In this present study using the small interfering RNA technique, we have found that ShcA adapter proteins play a rather active role in CSR-induced Erk activation, contrary to their mostly redundant role in other signaling pathways, e.g. growth factor-induced Erk activation, where Grb2 can bind directly to the receptor tyrosine kinase and activate Erk in the absence of ShcA. ShcA knockdown abolished CSR-induced activation of both Erk and the uPA promoter. Expression of small interfering RNA-escaping silent mutants of p52 or p46 but not p66 ShcA isoform efficiently rescued CSR-induced Erk activation. Moreover, we have shown that phosphorylation of either Tyr-239/Tyr-240 or Tyr-313 in p52(ShcA) can mediate CSR-induced Erk activation equally well. In a quest for molecules upstream of ShcA in this signaling, we found that CSR-induced ShcA tyrosine phosphorylation, its association with Grb2, Erk activation, and uPA gene expression were all dependent on Rho kinase, p38 mitogen-activated protein kinase, and Src. In summary, we have found a novel, non-redundant role for ShcA in contrast to its redundant role in many other signaling pathways.

Adaptor Proteins, Signal Transducing↗

PubMed2004

Limited redundancy of the proprotein convertase furin in mouse liver.

Furin is an endoprotease of the family of mammalian proprotein convertases and is involved in the activation of a large variety of regulatory proteins by cleavage at basic motifs. A large number of substrates have been attributed to furin on the basis of in vitro and ex vivo data. However, no physiological substrates have been confirmed directly in a mammalian model system, and early embryonic lethality of a furin knock-out mouse model has precluded in vivo verification of most candidate substrates. Here, we report the generation and characterization of an interferon inducible Mx-Cre/loxP furin knock-out mouse model. Induction resulted in near-complete ablation of the floxed fur exon in liver. In sharp contrast with the general furin knock-out mouse model, no obvious adverse effects were observed in the transgenic mice after induction. Histological analysis of the liver did not reveal any overt deviations from normal morphology. Analysis of candidate substrates in liver revealed complete redundancy for the processing of the insulin receptor. Variable degrees of redundancy were observed for the processing of albumin, alpha(5) integrin, lipoprotein receptor-related protein, vitronectin and alpha(1)-microglobulin/bikunin. None of the tested substrates displayed a complete block of processing. The absence of a severe phenotype raises the possibility of using furin as a local therapeutic target in the treatment of pathologies like cancer and viral infections, although the observed redundancy may require combination therapy or the development of a more broad spectrum convertase inhibitor.

Albumins↗

PubMed2004

Translation of a yeast mitochondrial tRNA synthetase initiated at redundant non-AUG codons.

Although initiation of translation at non-AUG codons occurs occasionally in prokaryotes and higher eukaryotes, it has not been reported in yeast until very recently. Evidence presented here shows that redundant ACG codons are recognized as alternative translation start sites for ALA1, the only gene in Saccharomyces cerevisiae coding for alanyl-tRNA synthetase. ALA1 is shown to be a bifunctional gene that provides both cytoplasmic and mitochondrial activities. Unlike most bifunctional genes that contain alternative in-frame AUG initiators, there is only one AUG codon, designated AUG1, close to the 5'-end of the ALA1 open reading frame. Transcriptional mapping identified three overlapping transcripts, with 5'-ends at positions 54, 105, and 117 nucleotides upstream of AUG1, respectively. Site-specific mutagenesis demonstrated that the cytoplasmic and mitochondrial functions of ALA1 are provided by two protein isoforms with distinct amino termini; that is, a short cytoplasmic form initiated at AUG1 and a longer mitochondrial isoform initiated at two upstream in-frame ACG codons, i.e. ACG(-25) and ACG(-24). These two ACG codons function redundantly in initiation of translation. Either codon can function in the absence of the other. The short transcript appears to serve as the template for the cytoplasmic form, whereas the longer transcripts are likely to code for both isoforms via alternative initiation. Because yeast ribosomes in general cannot efficiently recognize a non-AUG initiator, this unique feature of redundancy of non-AUG initiators in a single mRNA may in itself represent a novel paradigm for translation initiation from poor initiators.

Amino Acyl-tRNA Synthetases↗

PubMed2006

Redundancy of non-AUG initiators. A clever mechanism to enhance the efficiency of translation in yeast.

It was recently shown that ALA1, the only alanyl-tRNA synthetase gene in Saccharomyces cerevisiae, uses two successive ACG triplets as the translation initiators for its mitochondrial form. Evidence presented here argues that the second ACG triplet not only acts as a remedial initiation site for scanning ribosomes that skip the first ACG, but also enhances the activity of the preceding initiator by providing a preferable "A" at its relative position +4. Therefore, ALA1 constructs with redundant ACG initiators exhibit stronger complementing activity and express a higher level of protein than do those with a single ACG initiator. A similar scenario is seen when a single or redundant ACG triplets are placed in the positions of the first and second AUG initiators of VAS1, which serve as the start sites of the mitochondrial and cytoplasmic forms of valyl-tRNA synthetase, respectively. Cumulatively, the results suggest that this feature of redundancy of non-AUG initiators in a single mRNA per se may represent a novel paradigm for improving the efficiency of a poor or otherwise nonproductive initiation event.

Alanine-tRNA Ligase↗

PubMed1998

Weighted ancestral area analysis and a solution of the redundant distribution problem.

A new cladistic method for the estimation of ancestral areas is based on reversible parsimony in combination with a weighting scheme that weights steps in positionally plesiomorphic branches more highly than steps in positionally apomorphic branches. By applying this method to cladograms of human mitochondrial DNA, the method is superior to previously proposed algorithms. The method is also an appropriate tool for the solution of the redundant distribution problem in area cladograms. Under the assumption of allopatric speciation, redundant distributions, i.e., sympatry of sister groups, show that dispersal has occurred; thus, the ancestral area of at least one sister group was smaller than the combined distribution of its descendants. With the weighted ancestral area analysis, the ancestral areas can be confined and at least some dispersal events can be distinguished from possible vicariance events. As applied to a cladogram of the Polypteridae, weighted ancestral area analysis is superior to Brooks parsimony analysis (assumption 0) and component analysis under assumptions 1 and 2 (Nelson and Platnick, 1981, Systematics and biogeography: Cladistics and vicariance. Columbia Univ. Press, New York.) in resolving redundancies. The results of the weighted ancestral area analysis may differ from the results of dispersal-vicariance analysis, because the rules of dispersal-vicariance analysis indirectly favor the questionable assumption that the ancestral species occupied only one unit area.

Algorithms↗

PubMed2005

Binaural redundancy and inter-aural time difference cues for patients wearing a cochlear implant and a hearing aid in opposite ears.

We investigated speech perception advantages arising from the use of inter-aural time difference cues, and from the provision of redundant information by the use of a hearing aid contralateral to a cochlear implant (bimodal hearing devices). Thirty-eight subjects (14 normally hearing and 23 hearing-impaired) participated in this study. The effect of binaural redundancy was assessed by comparing the signal-to-noise ratio (SNR) required for 50% correct identification of sentences in noise when listening monaurally to that when listening binaurally. The use of inter-aural time difference cues was determined by comparing the binaural SNRs obtained with or without a noise delay of 700 micros between ears. Results indicated adults who used bimodal hearing devices benefited from binaural redundancy, but children did not. Whereas normally hearing subjects used inter-aural time difference cues to improve speech perception in noise, neither adults nor children who used bimodal hearing devices were able to do so.

Adolescent↗

PubMed1966

Redundant myelin sheaths and other ultrastructural features of the toad cerebellum.

Some of the myelin sheaths in the cerebellum of normal adult toads exhibit extensive evaginations of their full thickness. These redundant flaps of myelin are collapsed; i.e., they contain no axon and have no lumen. They extend away from the parent axonal myelin sheaths and tend to enfold other myelinated fibers or granule cell perikarya, producing bizarre configurations of myelin and what appear to be partially or completely myelinated cell bodies. In some instances, only the redundant flap of myelin appears in the plane of section, and its attachment to an axonal myelin sheath in another plane is only inferred. Single lamellae of myelin also tend to invest cerebellar granule cells and other processes, and these too appear to fold on themselves producing two- or four-layered segments. It is suggested that there are two phases of myelinogenesis: an initial "wrapping" phase, followed by a prolonged second phase during which internodes of myelin increase in both length and girth by a process other than wrapping, and that the occurrence of redundant myelin sheaths may reflect overgrowth of myelin during the second phase. Observations on the general organization of the toad cerebellum and on the ultrastructural cytology of its layers are also presented.

Animals↗

PubMed2006

Conditional dominant mutations in the Caenorhabditis elegans gene act-2 identify cytoplasmic and muscle roles for a redundant actin isoform.

Animal genomes each encode multiple highly conserved actin isoforms that polymerize to form the microfilament cytoskeleton. Previous studies of vertebrates and invertebrates have shown that many actin isoforms are restricted to either nonmuscle (cytoplasmic) functions, or to myofibril force generation in muscle cells. We have identified two temperature-sensitive and semidominant embryonic-lethal Caenorhabditis elegans mutants, each with a single mis-sense mutation in act-2, one of five C. elegans genes that encode actin isoforms. These mutations alter conserved and adjacent amino acids predicted to form part of the ATP binding pocket of actin. At the restrictive temperature, both mutations resulted in aberrant distributions of cortical microfilaments associated with abnormal and striking membrane ingressions and protrusions. In contrast to the defects caused by these dominant mis-sense mutations, an act-2 deletion did not result in early embryonic cell division defects, suggesting that additional and redundant actin isoforms are involved. Accordingly, we found that two additional actin isoforms, act-1 and act-3, were required redundantly with act-2 for cytoplasmic function in early embryonic cells. The act-1 and -3 genes also have been implicated previously in muscle function. We found that an ACT-2::GFP reporter was expressed cytoplasmically in embryonic cells and also was incorporated into contractile filaments in adult muscle cells. Furthermore, one of the dominant act-2 mutations resulted in uncoordinated adult movement. We conclude that redundant C. elegans actin isoforms function in both muscle and nonmuscle contractile processes.

Actin Cytoskeleton↗