SEARCH · Search PubMed

Results for “third generation sequencing”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources

PubMed2002

In addition to the SH3 binding region, multiple regions within the N-terminal noncatalytic portion of the cAMP-specific phosphodiesterase, PDE4A5, contribute to its intracellular targeting.

The long cyclic AMP (cAMP)-specific phosphodiesterase isoform, PDE4A5 (PDE4A subfamily isoform variant 5), when transiently expressed in COS-7 cells, was shown in subcellular fractionation studies to be associated with both membrane and cytosol fractions, with immunofluorescence analyses identifying PDE4A5 as associated both with ruffles at the cell margin and also at a distinct perinuclear localisation. Deletion of the first nine amino acids of PDE4A5 (1) ablated its ability to interact with the SH3 domain of the tyrosyl kinase, LYN; (2) reduced, but did not ablate, membrane association; and (3) disrupted the focus of PDE4A5 localisation within ruffles at the cell margin. This deleted region contained a Class I SH3 binding motif of similar sequence to those identified by screening a phage display library with the LYN-SH3 domain. Truncation to remove the PDE4A5 isoform-specific N-terminal region caused a further reduction in membrane association and ablated localisation at the cell margin. Progressive truncation to delete the PDE4A long isoform common region and then the long isoform-specific UCR1 did not cause any further change in membrane association or intracellular distribution. However, deletion up to the super-short form splice junction generated an entirely soluble 'core' PDE4A species. We propose that multiple sites in the N-terminal noncatalytic portion of PDE4A5 have the potential to associate with intracellular structures and thus define its intracellular localisation. At least two such sites lie within the PDE4A5 isoform-specific N-terminal region and these appear to be primarily responsible for targeting PDE4A5 to, and organising it within, the cell margin; one is an SH3 binding motif able to interact with LYN kinase and the other lies within the C-terminal portion of the PDE4A5 unique region. A third membrane association region is located within the N-terminal portion of UCR2 and appears to be primarily responsible for targeting to the perinuclear region. Progressive N-terminal truncation, to delete defined regions of PDE4A5, identified activity changes occurring upon deletion of the SH3 binding site region and then upon deletion of the membrane association site region located within UCR2. This suggests that certain of these anchor sites may not only determine intracellular targeting but may also transduce regulatory effects on PDE4A5 activity.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2006

Covalent connection of individualized, neutral, dendronized polymers on a solid substrate using a scanning force microscope.

The synthesis of a neutral, high-molar-mass, acrylamide-based, third-generation dendronized polymer (denpol) with a defined number of azide groups at its periphery is reported. An attach-to route is used in which a first-generation denpol is reacted with second-generation (G2) dendrons. The degree of structure perfection of the resulting denpol is quantified as 99.8 %. This value was obtained after the introduction of a fluorescence label at the sites that remained unaffected by the dendronization. The high coverage was independently confirmed for the dendronization of another first-generation polymer and a closely related G2 dendron. The third-generation denpol resulting from the first dendronization experiment was spin-coated as a sub-monolayer onto highly oriented graphite precoated with an ultrathin layer of C12H25NH2, which was introduced to provide a well-defined substrate for denpol adsorption and manipulation. Scanning force microscopy revealed single denpols, which could be moved across the surface and "welded" by covalent cross-linking induced by photochemical decomposition of the azides into highly reactive nitrenes. The successful formation of covalent bonds between two denpols was confirmed by mechanically challenging the link with the scanning force microscope (SFM) tip. This is the second reported case of a move-connect-prove sequence using polymers and the SFM, which for the first time employs noncharged denpols, thus widening the applicability of this method significantly.

Journal Article↗

PubMed2004

Whipple's disease.

Whipple's disease is a rare multisystemic infectious disorder affecting predominantly middle-aged men. Clinical manifestations are very variable with a very long, insidious, prediagnostic course. Weight loss, chronic diarrhea, arthralgias, and low-grade fever are characteristic features in most patients. Although gastrointestinal compromise is very common, atypical clinical forms are being increasingly recognized. Although a bacterial cause was strongly suggested for many years, the infectious agent was elusive until recently. The bacillus that was classified as an actinomycete was named Tropheryma whipplei and has singular characteristics. It presents affinity for the periodic acid-Schiff stain, but it is negative for Ziehl-Neelsen staining and has a characteristic trilamellar cell wall. Its genetic material has been recently sequenced, and culture was finally performed on a human fibroblast cell line. Pathological specimens show macrophage infiltration with mostly intracellular invasion of live bacteria. Immunologic factors, such as a subtle defect of cellular immunity possibly specific for the Whipple's bacterium, are believed to play a role in pathogenesis. The diagnosis requires the histologic assessment of diseased tissue, showing the characteristic infiltration, as a first approach, and confirmatory tests such as electron microscopy and/or polymerase chain reaction. Antibiotic treatment is mandatory and leads to a rapid clinical improvement and remission in most patients. Although the rationale for treatment is largely empiric, current recommendations include a 2-week parenteral therapy (third generation cephalosporin) followed by a long-term therapy with trimethoprim-sulphamethoxazole. This approach has been shown to reduce the number of relapses and was effective for prevention and/or treatment of the neurologic compromise.

Anti-Bacterial Agents↗

PubMed2006

Encoding of motion targets by waves in turtle visual cortex.

Visual stimuli evoke wave activity in the visual cortex of freshwater turtles. Earlier work from our laboratory showed that information about the positions of stationary visual stimuli is encoded in the spatiotemporal dynamics of the waves and that the waves can be decoded using Bayesian detection theory. This paper extends these results in three ways. First, it shows that flashes of light separated in space and time and stimuli moving with three speeds can be discriminated statistically using the waves generated in a large-scale model of the cortex. Second, it compares the coding capabilities of spike rate and spike time codes. Spike rate codes were obtained by low-pass filtering the activities of individual neurons in the model with filters of different band widths. For the moving targets used in the study, detectability using spike rate codes is immune to the choice of a specific bandwidth, indicating that a coarse filter is able to adequately discriminate targets. Spike timing codes are binary sequences indicating the precise timing of spike activity of individual neurons across the cortex. Spike time codes generally perform better than do spike rate codes. Third, the encoding process is examined in terms of the underlying cellular mechanisms that result in the initiation, propagation and cessation of the wave. The period of peak detectability corresponds to the period in which waves are propagating across the cortex.

Action Potentials↗

PubMed2006

Mariner mutagenesis of Brucella melitensis reveals genes with previously uncharacterized roles in virulence and survival.

BACKGROUND: Random gene inactivation used to identify cellular functions associated with virulence and survival of Brucella spp has relied heavily upon the use of the transposon Tn5 that integrates at G/C base pairs. Transposons of the mariner family do not require species-specific host factors for efficient transposition, integrate nonspecifically at T/A base pairs, and, at a minimum, provide an alternative approach for gene discovery. In this study, plasmid vector pSC189, containing both the hyperactive transposase C9 and transposon terminal inverted repeats flanking a kanamycin resistance gene, were used to deliver Himar1 transposable element into the B. melitensis genome. Conjugation was performed efficiently and rapidly in less than one generation in order to minimize the formation of siblings while assuring the highest level of genome coverage. RESULTS: Although previously identified groups or classes of genes required for virulence and survival were represented in the screen, additional novel identifications were revealed and may be attributable to the difference in insertion sequence biases of the two transposons. Mutants identified using a fluorescence-based macrophage screen were further evaluated using gentamicin-based protection assay in macrophages, survival in the mouse splenic clearance model and growth in vitro to identify mutants with reduced growth rates. CONCLUSION: The identification of novel genes within previously described groups was expected, and nearly two-thirds of the 95 genes had not been previously reported as contributing to survival and virulence using random Tn5-based mutagenesis. The results of this work provide added insight with regard to the regulatory elements, nutritional demands and mechanisms required for efficient intracellular growth and survival of the organism.

Animals↗

PubMed1993

Characterization of the ovine LH beta-subunit gene: the promoter directs gonadotrope-specific expression in transgenic mice.

The alpha- and beta-subunits of the gonadotropin hormones are expressed in the gonadotrope cells of the anterior pituitary. There are no adequate in vitro systems for the analysis of beta-subunit gene expression. In this study, therefore, transgenic mice have been used to investigate the regulation of expression of the ovine luteinizing hormone beta-gene (oLH beta) in vivo. oLH beta was isolated, characterized, and 1.9 kb of the promoter fused to the bacterial reporter chloramphenicol acetyl-transferase (CAT). Three lines of transgenic mice were generated. CAT enzyme was detected in the pituitary of two lines, whereas the third line did not express. Measurement of endogenous luteinizing hormone and follicle stimulating hormone levels in both expressing lines revealed small differences when compared to controls, but these did not affect the fertility of the animals. Immunostaining of the anterior pituitary revealed that the oLH beta CAT transgene was expressed specifically in gonadotrope cells.

Amino Acid Sequence↗

PubMed1993

Human Fc gamma RI triggering of the mononuclear phagocyte respiratory burst.

This study investigates the role played by Fc gamma RI and Fc gamma RII in triggering the respiratory burst induced in human monocyte-like U937 cells by monoclonal chimaeric anti-NIP antibodies expressing the human IgG subclass and mouse IgG2b heavy chains. Respiratory burst activity was measured as superoxide generation. Four separate lines of evidence indicate a predominant role for Fc gamma RI in triggering superoxide generation induced by erythrocytes sensitized with up to the maximum of 100,000 IgG molecules per cell. Firstly, erythrocytes sensitized with mouse IgG2b anti-NIP antibodies which are not recognized by human Fc gamma RI, did not induce a response but when residue Glu-235 was replaced by Leu to give the lower hinge sequence of mouse IgG2a which is recognized by Fc gamma RI, the mutant bound to Fc gamma RI and induced a response equal to 80% of that given by chimaeric human IgG3. Chimaeric human IgG3 antibodies with amino acid substitutions in the lower hinge showed reduced activity and the greatest reductions (< 32% of wild type antibody activity) were associated with changes at Leu-235 which is critical for recognition by Fc gamma RI. Secondly, chimaeric human IgG4 antibodies which are not recognized by Fc gamma RII, were able to induce superoxide generation. The rank order of abilities of chimaeric human IgG subclass antibodies to induce responses was IgG3 > IgG1 > IgG4 > > IgG2. Thirdly, responses induced by chimaeric human IgG were inhibited by concns of monomeric human IgG3 in the nM range. Finally, chimaeric human IgG3 induced responses were inhibited by anti-Fc gamma RI, but not anti-Fc gamma RII monoclonal antibodies. Consistent with a major role for Fc gamma RI in triggering the responses of U937 cells, erythrocytes sensitized with chimaeric human IgG3 did not induce superoxide generation by neutrophils which express Fc gamma RII and Fc gamma RIII, or eosinophils which express Fc gamma RII, but neither of which expresses Fc gamma RI.

Antibodies, Monoclonal↗

PubMed1994

HLA-DQB10305 and -DQB10304 alleles among Sardinians. Evolutionary and practical implications for oligotyping.

This study, performed in individuals of Sardinian descent, reports an epidemiologic and molecular analysis of the recently identified DQB1*0304 and DQB1*0305 alleles. These two alleles having a gene frequency of 0.017 and 0.005, respectively, are not uncommon in Sardinia and are distributed fairly uniformly on the island. The analysis of DQB1 second and third exons of the two alleles revealed that although they have always been found included within the same DRB1*0403-DQA1*03 haplotype, they had a different origin. The sequence pattern of DQB1*0305 confirmed that it originated from the DQB1*0302 "recipient" gene by the insertion of a DQB1*0402 nucleotide stretch, within its beta-sheet region, while that of DQB1*0304 suggested that it originated from the DQB1*0301 gene, either by a single point mutation at codon 57 (GCC instead of GAC) or, alternatively, by a segmental transfer of a DQB1*0302 motif, including codon 57, within its alpha-helic region. Independently from the mechanism of generation, the fact that DQB1*0304 originated from DQB1*0301 allele was intriguing considering that, in over 1500 HLA class II Sardinian haplotypes examined, neither the putative parental DRB1*0403-DQA1*03-DQB1*0301 haplotypes were found. Finally, since the assignment of DQB1*0305 may be inaccurate with the traditional panel of probes commonly used for DQB1 oligotyping, the use of an additional oligonucleotide probe is recommended.

Alleles↗

PubMed1992

Characterization of unintegrated retroviral DNA with long terminal repeat-associated cell-derived inserts.

We have used a replication-competent shuttle vector based on the genome of Rous sarcoma virus to characterize genomic rearrangements that occur during retrovirus replication. The strategy involved cloning circular DNA that was generated during an acute infection. While analyzing a class of retroviral DNA clones that are greater than full length, we found several clones which had acquired nonviral inserts in positions adjacent to the long terminal repeats (LTRs). There appear to be two distinct mechanisms leading to the incorporation of cellular sequences into these clones. Three of the molecules contain a cell-derived insert at the circle junction site between two LTR units. Two of these molecules appear to be the results of abortive integration attempts, because of which, in each case, one of the LTRs is missing 2 bases at its junction with the cell-derived insert. In the third clone, pNO220, the cellular sequences are flanked by an inappropriately placed copy of the tRNA primer-binding site on one side and a partial copy of the U3 sequence as part of the LTR on the other side. A fourth molecule we characterized, pMD96, has a single LTR with a U5-bounded deletion of viral sequences spanning gag and pol, with cell-derived sequences inserted at the site of the deletion; its origin may be related mechanistically to pNO220. Sequence analysis indicates that all of the cellular inserts were derived from the cell line used for the acute infection rather than from sequences carried into the cell as part of the virus particle. Northern (RNA) analysis of cellular RNA demonstrated that the cell-derived sequences of two clones, pNO220 and pMD96, were expressed as polyadenylated RNA in uninfected cells. One mechanism for the joining of viral and cellular sequences suggested by the structures of pNO220 and pMD96 is recombination occurring during viral DNA synthesis, with cellular RNA serving as the template for the acquisition of cellular sequences.

Animals↗

PubMed1989

Clinical consequences of a human non-fluorescent Y chromosome (Ynf).

A new case of ambiguous genitalia and immature tissue in the left gonad is presented. Cytogenetic findings with various techniques demonstrated that the distal two-thirds of the long arm of the Y chromosome is deleted. Q-banding showed a non-fluorescent Y; three positive bands were however noted when the DA/DAPI technique was applied. After a review of the literature, it was concluded that the non-fluorescent Y chromosome (Ynf) when inherited from generation to generation is a heteromorphism in normal males. However, in our case, where the proband's Y is lacking the fluorescent segment, a simple deletion does not appear to adequately explain the DA/DAPI positive bands. Possibly, a deletion followed by a structural rearrangement of the non-fluorescent segment had occurred de novo. The highly Y-specific DNA sequences present in the fluorescent segment are absent in these patients. The abnormal development in these cases is due to the presence of the 45,X cell line. The gene responsible for spermatogenesis has been localized to the non-fluorescent region in the long arm of the Y chromosome. Furthermore, it is concluded that two types of non-fluorescent Y chromosomes can be found in the population; one is a normal inherent heteromorphic variant, while the other appears to be an abnormality, especially in cases with azoospermia. Such distinctions should clearly be established prior to genetic counseling for patients with so called Ynf or del (Yd).

Chromosome Banding↗

PubMed2006

A molecular phylogeny of the Dactylogyridae sensu Kritsky & Boeger (1989) (Monogenea) based on the D1-D3 domains of large subunit rDNA.

Phylogenetic analyses based on the partial large subunit rDNA (LSU) sequences of polyonchoinean monogeneans belonging to the Dactylogyridea and Monocotylidea were generated to investigate relationships among various subfamilies of the Dactylogyridae sensu Kritsky & Boeger, 1989. Monophyly of the Dactylogyridae was supported by all analyses performed. Status of the Ancyrocephalidae sensu Bychowsky & Nagibina, 1978 and Ancyrocephalinae sensu Kritsky & Boeger, 1989 was revised based on the present data. All phylogenetic analyses indicated polyphyletic origins of the Ancyrocephalidae and Ancyrocephalinae. Freshwater species of Ancyrocephalinae (Actinocleidus, Ancyrocephalus, Cleidodiscus and Urocleidus) and Ancylodiscoidinae (Thaparocleidus) collected from the fish in European waters were positioned at the base of the Dactylogyridae. The Dactylogyrinae formed a monophyletic group, sister to a clade including the Pseudodactylogyrinae and the tropical and subtropical Ancyrocephalinae. Analyses including only data set on Dactylogyridea were focused on relationships between representatives of the Asian and European Dactylogyrus species. Dactylogyrus species formed a monophyletic group, and the parasite colonization appeared to follow the dispersal history of the Cyprinidae from Asia to Europe. Three lineages of Dactylogyrus species were recognized: the first including species specific to hosts of Asian origin, the second by Dactylogyrus species from Chinese fish hosts, and the third included Dactylogyrus species from European cyprinids and one species from a percid host. The position of D. cryptomeres from Gobio gobio seems to be unresolved.

Animals↗

PubMed2000

Mutation in the PAX6 gene in twenty patients with aniridia.

This is a report on the nature of the mutations in the PAX6 gene in twenty patients with aniridia. Five of the twenty patients had sporadic aniridia with deletions in chromosome 11p13. Three of the five had WAGR syndrome (Wilms tumor, aniridia, genitourinary anomalies, mental retardation), and the other two had deletions whose breakpoints occurred between the PAX6 and the WT1 genes. Allelic losses at PAX6 were of paternal origin. The remaining fifteen patients with aniridia had intragenic mutations in the PAX6 gene, with mutations found from exon 5 to exon 12. Twelve cases of dysfunctional PAX6 were due to premature termination of the protein by nonsense mutations (five cases), splicing defect (one case), deletion (two cases), deletion-insertions (two cases), and tandem repeat insertions (two cases). One patient (P2) had a PAX6 protein with de novo in-frame deletion of alanine, arginine, and proline at codon positions 37, 38, and 39. These codons are in the paired box region, and codon 38 is in contact with the phosphate group of the sugar-phosphate backbone of the target DNA. Another patient (P8) had a single nucleotide transition at c.1182 (nucleotide number, Genbank accession #M93650, used as in Glaser et al. [1992]), which generated both a missense mutation (Q255H) and a splicing defect. A missense mutation was found at G387E in a third patient (P10). All observed mutations support the notion that haploinsufficiency in PAX6 results in aniridia and associated eye anomalies.

Aniridia↗

PubMed1990

Bacterial expression of human muscarinic receptor fusion proteins and generation of subtype-specific antisera.

A family of five muscarinic acetylcholine receptor genes (m1-m5) encode highly related proteins; however, for methodological reasons it has not been possible to detect the gene products individually. To develop antibody probes specific for the receptor subtypes, unique regions of m1-m5 cDNAs, corresponding to the third cytoplasmic (i3) loops, were subcloned into bacterial expression vectors and the fusion proteins expressed in E. coli were used to generate rabbit antisera. These antisera react specifically with the respective fusion proteins on immunoblots and selectively immunoprecipitate each of the native cloned receptors. Since the i3 loops are immunogenic and the epitopes in the cloned receptors are accessible to antibodies, this approach should be valuable for immunological studies of the native receptors.

Amino Acid Sequence↗

PubMed1993

The Rb97D gene encodes a potential RNA-binding protein required for spermatogenesis in Drosophila.

Many proteins that bind RNA contain a common RNA-binding domain, the RNP motif. We have been studying two Drosophila RNP motif proteins, Hrb98DE and Hrb87F, which are hnRNA-binding proteins. We report here the characterization of the Rb97D gene, which encodes a protein that is closely related to the Hrb proteins in the RNP motif domain, but has a distinctive proline-rich C-terminal domain. The gene is located at 97D on the right arm of the third chromosome, near the rough gene. Multiple transcripts from the Rb97D gene are present at varying levels throughout development. The transcripts are generated by alternative processing in the coding and 3' untranslated regions, and can encode two protein isoforms. Analysis of a mutant containing a P element inserted into the 5' untranslated region of the gene demonstrates that Rb97D is required for male fertility. Possible models for the function of Rb97D in testes are discussed.

Amino Acid Sequence↗

PubMed1992

Novel mutation in the human immunodeficiency virus type 1 reverse transcriptase gene that encodes cross-resistance to 2',3'-dideoxyinosine and 2',3'-dideoxycytidine.

We have used the technique of in vitro selection to generate variants of human immunodeficiency virus type 1 (HIV-1) that are resistant to 2',3'-dideoxyinosine (ddI) and cross-resistant to 2',3'-dideoxycytidine (ddC). The complete reverse transcriptase (RT)-coding regions, plus portions of flanking sequences, of viruses possessing a ddI-resistant phenotype were cloned and sequenced by polymerase chain reaction (PCR)-based methods. We observed that several of these viruses possessed mutations at amino acid sites 184 (Met-->Val; ATG-->GTG) and 294 (Pro-->Ser; CCA-->TCA). These mutations were introduced in the pol gene of infectious, cloned HXB2-D DNA by site-directed mutagenesis. Viral replication assays confirmed the importance of site 184 with regard to resistance to ddI. The recombinant viruses thus generated displayed more than fivefold-greater resistance to ddI than parental HXB2-D did. Moreover, more than fivefold-greater resistance to ddC was also documented; however, the recombinant viruses continued to be inhibited by zidovudine (AZT). No resistance to ddI, ddC, or AZT was introduced by inclusion of mutation site 294 in the pol gene of HXB2-D. PCR analysis performed on viral samples obtained from patients receiving long-term ddI therapy confirmed the presence of mutation site 184 in five of seven cases tested. In three of these five positive cases, the wild-type codon was also detected, indicating that mixtures of viral quasispecies were apparently present. Viruses possessing a ddI resistance phenotype were isolated from both subjects whose viruses contained only the mutated rather than wild-type codon at position 184 as well as from a third individual, whose viruses appeared to be mostly of the mutated variety.

Acquired Immunodeficiency Syndrome↗

PubMed1977

Alterations in differentiation and pyrimidine pathway enzymes in 5-azacytidine resistant variants of a myoblast line.

5-azacytidine at concentrations higher than 5 muM inhibited the differentiation of a rat myoblast line in vitro. It was also somewhat cytotoxic at this level. Variants resistant to the cytotoxic effect of 5-azacytidine were obtained which were simultaneously unable to differentiate into myotubes and exhibited altered morphology. These characteristics were retained by the variants when subcultured in the absence of the drug for over 700 generations. Several of the azacytidine resistant cells were more susceptible than the parental line to the lethal action of 5-bromodeoxyuridine and adenosine, but not that of cytosine arabinoside, ouabain or 8-azaguanine. The variants were capable of transporting uridine, thymidine and 5-azacytidine. The uridine kinase activity was one-half to one-third of than in the parental cells but it was not missing completely in any of the variants. Two independently isolated variants selected for detailed study showed a 2- to 3-fold increase in the activity of orotidylic acid decarboxylase. This enzyme in the variants in contrast to that of the parental cells was completely insensitive to the inhibitory effect of a nucleotide generated from ATP and 5-azacytidine in cell extracts (probably 5-azacytidine monophosphate). These observations point to the possibility the 5-azacytidine resistance arises in myoblasts due to an alteration of the components of two target pathways of this drug, viz., the de novo pyrimidine pathway and an undefined sequence leading to the synthesis of membrane components.

Adenosine↗

PubMed1999

Characterization of autoantibodies generated in mice by immunization with the C-terminal region of Trypanosoma cruzi ribosomal P1 and P2 proteins.

The R13 peptide sequence (EEEDDDMGFGLFD) that corresponds to the C-terminal region of Trypanosoma cruzi ribosomal P1 and P2 proteins differs from the eukariotic P consensus sequence EESDDDMGFGLFD (H13) only in a nonconservative amino acid substitution. Since the immunization with R13 peptide coupled to a carrier protein like OVA would break the tolerance to a self-sequence and generate autoantibodies, we characterized the antibodies induced in mice by R13 immunization, analyzing by ELISA their capacity to bind to R13 and the self-sequence H13. Besides, we studied the course of these reactivities a long time after immunization. It was found that all R13-immunized mice had antibodies against H13 and this reactivity was always lower than R13 reactivity. The anti-H13 reactivity evaluated by competitive ELISA demonstrated that the H13 peptide is able to inhibit the binding of immune sera to R13 at high doses. When the levels and the avidity of anti-R13 and anti-H13 were evaluated at 10 and 80 days post third immunization, it was observed that anti-R13 levels were higher than anti-H13 levels in all sera from 10 days after the third immunization. However, avidity of both antibodies was high. In sera from 80 days post third immunization, anti-R13 and anti-H13 levels and avidity either remained elevated or showed a rise, whereas anti-OVA levels declined. Moreover, when ECG traces were obtained from immunized mice, the heart functional alterations observed at 10 days continued at 80 days after the third immunization, showing an association with the levels of the antibodies. In addition, the isotype pattern that recognizes R13 and the self-sequence H13 is different. For anti-R13 response, IgG1 reactivity was higher than IgG2; meanwhile, for anti-H13 response IgG2 reactivity was higher than IgG1. These results indicate that sera from R13-immunized mice bind the H13 sequence and this autoreactivity may be self-perpetuating.

Amino Acid Sequence↗

PubMed1992

Relative rates of nucleotide substitution at the rbcL locus of monocotyledonous plants.

We subjected 35 rbcL nucleotide sequences from monocotyledonous taxa to maximum likelihood relative rate tests and estimated relative differences in rates of nucleotide substitution between groups of sequences without relying on knowledge of divergence times between taxa. Rate tests revealed that there is a hierarchy of substitution rate at the rbcL locus within the monocots. Among the taxa analyzed the grasses have the most rapid substitution rate; they are followed in rate by the Orchidales, the Liliales, the Bromeliales, and the Arecales. The overall substitution rate for the rbcL locus of grasses is over 5 times the substitution rate in the rbcL of the palms. The substitution rate at the third codon positions in the rbcL of the grasses is over 8 times the third position rate in the palms. The pattern of rate variation is consistent with the generation-time-effect hypothesis. Heterogenous rates of substitution have important implications for phylogenetic reconstruction.

Genes, Plant↗