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PubMed1980

Diversity among B6 strains of Agrobacterium tumefaciens.

A total of 20 laboratory substrains of Agrobacterium tumefaciens strain B6 were compared with respect to six characteristics, including 3-ketolactose production, lysogeny, octopine catabolism, tumorigenic host range, and plasmid content. Within this group of strains diversity was found for all characteristics except 3-ketolactose production. Six substrains were lysogenized with an omega-type phage, whereas one substrain appeared neither sensitive to nor lysogenized with this bacteriophage. All but two substrains catabolized octopine and induced tumors on carrot disks. These 18 substrains harbor deoxyribonucleic acid sequences homologous to pTiB6-806. The two substrains unable to catabolize octopine were nontumorigenic and lacked detectable Ti plasmid sequences. Of the 20 substrains, 13 also contained sequences homologous to the cryptic plasmid pAtB6-806; 2 of the 18 substrains tumorigenic on carrots failed to induce tumors on Kalanchoe leaves. Their inability to induced tumors on this host, could not be correlated with lysogeny, with the presence or absence of pAtB6-806, or with the very large cryptic plasmid recently described. The Ti plasmids from these two strains were indistinguishable from pTiB6-806 by restriction enzyme analysis and could genetically convert a cured A. tumefaciens strain to tumorigenicity on both plant species. The results with these two strains suggest that parameters of tumorigenicity, such as host range, may be controlled by the bacterial chromosome.

Arginine↗
PubMed1999

Divergence paresis: a nonlocalizing cause of diplopia.

OBJECTIVES: To determine the causes, clinical characteristics, and localizing value of divergence paresis, which is characterized by acquired and uncrossed diplopia when viewing distant targets, fusion when viewing near targets, and no limitation of ocular ductions. Controversy persists regarding the diseases underlying divergence paresis and the existence of a divergence "center." MATERIALS AND METHODS: The charts of 15 patients with divergence paresis examined between 1983 and 1998 were reviewed. All patients underwent neuroimaging and detailed ocular motility testing, with measurement of esotropia in prism diopters in 14 patients. RESULTS: Divergence paresis in 15 patients was idiopathic in three patients, was associated with central nervous system microangiopathy or infarct in seven patients, and clivus lymphoma, chronic lymphocytic leukemia with sinusitis, Wernicke ophthalmoplegia, Parkinson disease, myasthenia gravis, cryptic cerebellar vascular malformation, and childhood esotropia in one patient each (two patients had two diagnoses). The mean maximum esotropia was 10.4 prism diopters, and there was no significant correlation (Fisher exact test) between the magnitude of esotropia and vasculopathic etiology or posterior fossa lesion site. Although six patients had posterior fossa disease, neuroimaging showed no common circumscribed lesion site or evidence of increased intracranial pressure. CONCLUSIONS: Divergence paresis is an uncommon cause of acquired diplopia. Divergence paresis is associated with diverse central nervous system diseases and can be mimicked by myasthenia. The absence of a single consistent lesion in our study, which is the largest reported series, suggests that divergence paresis is a nonlocalizing cause of horizontal diplopia and that multiple or diffusely distributed neural structures may govern divergence. Alternatively, elusive divergence "centers" may not exist, and divergence paresis may arise from impaired inhibition or from defective passive antagonism of orbital structures to convergence.

Adolescent↗
PubMed1997

From genetic research into clinical practice.

The present genome era is characterized by speedy progress and prompt transfer of results into clinical practice. This creates the need for rapid disclosure of results and renewal of laboratory's protocols. Molecular cytogenetics has provided and increased ability to identify chromosomes, correlate chromosome structure with gene location, find out cryptic aberrations, and detect specific DNA sequences. These advances have allowed the confident discovery of a number of contiguous gene syndromes. The positional cloning and positional candidate strategies have greatly expedited the search process of disease genes, and become relevant methods for genes' discovery. Understanding the molecular basis of diseases has shown an unpredicted wide genetic heterogeneity, which has splitted single disorders into many clinically similar conditions, and added complexity to the nosology of human diseases. The opposite process, allelism, where clinical diversity results from allelic mutations, has lumped together many distinct disorders, by showing that different clinical entities are not necessarily due to mutations in different genes. Dynamic mutations have provided the molecular understanding of interindividual and intrafamilial variability including anticipation, in a number of diseases. The discovery of distinct correlations between the molecular pattern and disease severity is providing a unique opportunity for using molecular results to assess the clinical outcome. Diagnostic, presymptomatic and predictive molecular testing are becoming widely used and provide enormous opportunities for improving the lot of our patients.

Genetic Diseases, Inborn↗
PubMed2003

Current concepts of the immunobiology and immunotherapy of cutaneous T cell lymphoma: insights gained through cross-talk between the clinic and the bench.

An understanding of the immunologic features of cutaneous T cell lymphoma (CTCL) has led to insights into the life cycle of the malignancy. The identification of the T cell lineage of the neoplastic CTCL cells has allowed unification of diverse clinical presentations under a single entity. The CD4 inducer T cell phenotype of the malignant cells has provided an understanding of the patient's ability to resist infection with certain bacteria. The clonality of the tumor cells, beyond its diagnostic implications, has made them a valuable resource for studying both normal and neoplastic T cell biology. The recently identified immunosuppressive features of the malignant T cells and their dependency for survival on an interaction with immature dendritic cells have explained previously cryptic clinical observations and identified new targets for immunotherapy. Future insights gained both from the bedside and the bench will provide not only an understanding of the immunobiology of the malignancy but also open new avenues for therapeutic intervention.

Cancer Vaccines↗
PubMed1992

Molecular population genetics of Escherichia coli: DNA sequence diversity at the celC, crr, and gutB loci of natural isolates.

The DNA sequences of three genes--celC, crr, and gutB--have been determined for each of 11 or 12 natural isolates of Escherichia coli from the ECOR collection. These genes encode the phosphoenolpyruvate-dependent phosphotransferase-system enzyme III proteins specific for beta-glucoside sugars (celC), glucose (crr), and glucitol (gutB), respectively. There is little evidence of recombination at or among these loci; among these strains, relationships inferred from each gene are largely consistent with each other and with the relationship inferred from multilocus enzyme electrophoresis. DNA sequence diversity is similar for all three genes, particularly when silent (synonymous) sites only are considered. This is surprising because there is much stronger codon usage bias at crr than at celC or gutB. The extent of divergence in the protein sequences encoded by these three genes varies considerably. The constitutively expressed glucose-specific enzyme is completely conserved. It is surprising that the inducible glucitol-specific enzyme, which is functional, is more variable than the cellobiose-specific enzyme, which is cryptic; the latter might be expected to be under less (if any) purifying selection.

Amino Acid Sequence↗
PubMed1989

Diversity of plasmids in Staphylococcus saprophyticus isolated from urinary tract infections in women.

A group of 150 Staphylococcus saprophyticus strains isolated from urinary tract infections in women were included in this study. Antimicrobial susceptibility tests showed that these isolates were sensitive to most antimicrobial agents. All strains were sensitive to penicillin, cephalothin, gentamicin, kanamycin, trimethoprim and nitrofurantoin. Resistance to tetracycline was present in 10.6% of the strains, to chloramphenicol in 4%, to erythromycin in 1.3% and to streptomycin in 1.3%. All strains were resistant to cadmium chloride as well as to novobiocin and nalidixic acid. Plasmid analysis showed that 82% of the strains harboured plasmids, some of them with complex plasmid profiles. Most plasmids were considered to be cryptic, although antibiotic resistance plasmids were identified in 18 isolates. Tetracycline resistance was encoded by a plasmid of c. 2.8 MDa, chloramphenicol resistance by a plasmid of c. 2.9 MDa and erythromycin resistance by a plasmid of c. 1.6 MDa. Streptomycin resistance could not be linked to the presence of any specific plasmid. Plasmid profiling seemed to be a good method for differentiating among S. saprophyticus strains.

Drug Resistance, Microbial↗
PubMed2002

Aberrant transposition of a Tc1-mariner element, impala, in the fungus Fusarium oxysporum.

We previously determined that the impalaD transposable element of Fusarium oxysporum was able to mobilize a non autonomous copy of impala ( niaD::imp::hph), inserted in the niaD gene encoding nitrate reductase. Generally, mobilization results in the recovery of Nia(+) revertants at low frequency. In the course of this study, we recovered a transformant that gave rise to Nia(+) revertants at a high rate. These revertants displayed atypical phenotypes and showed a niaD hybridization pattern different from that in more typical revertants. Molecular analysis of the structure of the transformant and atypical revertants indicated that (i) in the transformant, two copies of impala, one defective and one active, were inserted at the same genomic locus in a head-to-head orientation; and (ii) all the revertants analyzed presented the same chromosomal rearrangement, an inversion resulting in the replacement of the niaD promoter by a new sequence containing a cryptic promoter. We also frequently observed additional DNA rearrangements (deletion or inversion) in these revertants. The sequences at the rearrangement junctions indicated the occurrence of a transposition event that used the ITRs (Inverted Terminal Repeats) of separate transposons arranged in direct orientation. These features can be interpreted as the consequences of an aberrant transposition process. Such a process may account for the rearrangements observed in some genomic regions containing multiple transposon ends, and could serve as a mechanism for the generation of genetic diversity.

Base Sequence↗
PubMed1992

Distinct genetic groups of Giardia intestinalis distinguished by restriction fragment length polymorphisms.

The taxonomic status of the parasitic protozoal species Giardia intestinalis depends on the morphological similarity of all Giardia isolated from humans and the presumption that Giardia are host-specific. On the basis of electrophoretic data derived from examination of 26 enzyme loci in Australian isolates, it has been proposed that G. intestinalis is a species complex comprising three or four genetically distinct (but morphologically cryptic) species. These received the tentative designations of genetic groups I-IV (R. H. Andrews, M. Adams, P. F. L. Boreham, G. Mayrhofer & B. P. Meloni. International Journal for Parasitology 19, 183-190, 1989). In the present study, two unrelated DNA probes (one specific for a gene encoding a trophozoite surface protein, the other detecting a non-coding repetitive sequence within the G. intestinalis genome) were used in Southern hybridization analyses to examine 10 axenic isolates of G. intestinalis, established from diverse geographical regions in Australia, together with the Portland-1 isolate from the USA. Both probes identified every isolate unambiguously as belonging to one or other of two genetic clusters. Electrophoretic analysis of the same samples indicated that these clusters correspond to the previously defined genetic groups I and II. No heterogeneity was apparent within the seven group I isolates using either probe. However, when probed with the repetitive sequence, the four isolates belonging to group II exhibited small differences in banding patterns, suggesting that this group may be less homogeneous than group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Exclusion of glucosyl-hydroxymethylcytosine DNA containing bacteriophages is overcome by the injected protein inhibitor IPI*.

The Escherichia coli isolate CT596 excludes infection by the Myoviridae T4 ip1(-) phage that lacks the encapsidated IPI* protein normally injected into the host with the phage DNA. Screening of a CT596 genomic library identified adjacent genes responsible for this exclusion, gmrS (942 bp) and gmrD (708 bp) that are encoded by a cryptic prophage DNA. The two genes are necessary and sufficient to confer upon a host the ability to exclude infection by T4 ip1(-) phage and other glucosyl-hydroxymethylcytosine (glc-HMC) Tevens lacking the ip1 gene, yet allow infection by phages with non-glucoslyated cytosine (C) DNA that lack the ip1 gene. A plasmid expressing the ip1 gene product, IPI*, allows growth of Tevens lacking ip1 on E. coli strains carrying the cloned gmrS/gmrD genes. Members of the Teven family carry a diverse and, in some cases, expanded set of ip1 locus genes. In vivo analysis suggests a family of gmr genes that specifically target sugar-HMC modified DNA have evolved to exclude Teven phages, and these exclusion genes have in turn been countered by a family of injected exclusion inhibitors that likely help determine the host range of different glc-HMC phages.

5-Methylcytosine↗
PubMed2005

Oncogene amplification in transforming myelodysplasia.

The MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both lymphoid and myeloid leukemia and has also been shown to undergo submicroscopic self-fusion/partial duplication. We report 29 patients with cytogenetic evidence of 11q23 alteration, all of which demonstrate molecular cytogenetic evidence of amplification of the MLL gene by fluorescence in situ hybridization (FISH). In all MLL cases, the patients were clinically classified as having transforming myelodysplasia (RAEB/RAEBT) or AML. An additional patient with AML was found by 24-color and gene-specific FISH to have AML1 oncogene amplification. Four patients had been previously diagnosed with cancer and had received topoisomerase II targeted drug therapy which is known to be associated with fusion transcripts involving the MLL and AML1 genes. MLL amplification appeared in various forms: an atypical banded region that bridges from 11q23 into a dicentric chromosome, expanded regions emanating from band 11q23, chromosome 11 paint-positive rings with "spoke-like" MLL amplification, and expansion at sites other than chromosome 11 (including extra markers) in the absence of one of the 11 homologues. The fluorescence pattern in most cases suggests palindromic duplication with neighboring sequences in the long arm of chromosome 11. As opposed to MYCN amplification in hsrs (homogeneously staining regions) and double minutes in neuroblastoma, amplification of MLL in most cases occurred at the site of the gene. All of our patients rapidly developed refractory AML. The frequency and clinical correlations of MLL gene amplification in leukemia will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies. The reported MLL cases represented about 1% of the total abnormal MDS/AML cases over 8 years. A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-, and a missing or abnormal chromosome 11, may help direct appropriate follow-up studies. The MLL and the AML1 oncogenes appear to be the only oncogenes amplified at the natural site of the gene. Both genes also show a high degree of diversity of pathogenic mechanisms of leukemia evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.

Adult↗
PubMed1991

Proto-splice site model of intron origin.

It is proposed that nuclear pre-mRNA introns (classical introns) were first generated as by-products during the evolution of alternative splicing. They were formed whenever two splice sites within the coding sequence of ancestral genes were used at a frequency that removed the coding constraint from the intervening sequence. Once introns had evolved, it is suggested that they were spread by the splicing machinery which inserted them into proto or cryptic-splice sites of other genes by reverse splicing, so giving rise to genes that have introns yet are not alternatively spliced. It is argued that 5' and 3' splice sites evolved from common ancestral splice sites, referred to as proto-splice sites, that were bidirectional and had a core consensus sequence of C or A, A, G, R, which remains today as the immediate flanking sequence of most introns. The ancestral splicing machinery, although inefficient, would have been capable of generating vast mRNA diversity by splicing between proto-splice sites. Natural selection would be expected to have preserved mutations that increased the amounts of advantageously spliced mRNA. It is argued that this process drove the evolution of present 5' and 3' splice sites from a subset of proto-splice sites and also drove the evolution of a more efficient splicing machinery. The positions of most introns that evolved directly from the coding sequence would be expected to correlate with protein structure.

Animals↗
PubMedDate not supplied

Trophic controls on stage transformations of a toxic ambush-predator dinoflagellate.

The toxic dinoflagellate, Pfiesteria piscicida, was recently implicated as the causative agent for about 50% of the major fish kills occurring over a three-year period in the Albemarle-Pamlico Estuarine System of the southeastern USA. Transformations between life-history stages of this dinoflagellate are controlled by the availability of fresh fish secretions or fish tissues, and secondarily influenced by the availability of alternate prey including bacteria, algae, microtauna, and mammalian tissues. Toxic zoospores of P. piscicida subdue fish by excreting lethal neurotoxins that narcotize the prey, disrupt its osmoregulatory system, and attack its nervous system. While prey are dying, the zoospores feed upon bits of fish tissue and complete the sexual phase of the dinoflagellate life cycle. Other stages in the complex life cycle of P. piscicida include cryptic forms of filose, rhizopodial, and lobose amoebae that can form within minutes from toxic zoospores, gametes, or planozygotes. These cryptic amoebae feed upon fish carcasses and other prey and, thus far, have proven less vulnerable to microbial predators than flagellated life-history stages. Lobose amoebae that develop from toxic zoospores and planozygotes during colder periods have also shown ambush behavior toward live fish. In the presence of abundant flagellated algal prey, amoeboid stages produce nontoxic zoospores that can become toxic and form gametes when they detect what is presumed to be a threshold level of a stimulatory substance(s) derived from live fish. The diverse amoeboid stages of this fish "ambush-predator" and at least one other Pfiesteria-like species are ubiquitous and abundant in brackish waters along the western Atlantic and Gulf Coasts, indicating a need to re-evaluate the role of dinoflagellates in the microbial food webs of turbid nutrient-enriched estuaries.

Animals↗
PubMedDate not supplied

Localization of clathrin light-chain sequences mediating heavy-chain binding and coated vesicle diversity.

At least four distinct forms of clathrin light chains are found in mammalian cells. This molecular variability derives from tissue-specific patterns of expression of LCa and LCb genes. Sequence analysis shows an overall homology of 60% between LCa and LCb and the presence of brain-specific insertion sequences. These findings suggest that the different light chains have both shared and specialized functions. To address this question we have used a panel of monoclonal antibodies to identify two structurally and functionally distinct regions in the clathrin light-chain sequences. One region (residues 158-208) is exposed in native clathrin structures (triskelions and coated vesicles) and includes the brain-specific insertion sequences. The second region (residues 93-157), which is cryptic in native clathrin structures, is involved in binding the clathrin heavy chain and contains the region of strongest homology with intermediate filament proteins.

Adrenal Glands↗
PubMed1999

Sequences flanking the centromere of human chromosome 10 are a complex patchwork of arm-specific sequences, stable duplications and unstable sequences with homologies to telomeric and other centromeric locations.

Little is known about sequence organization close to human centromeres, despite empirical and theoretical data which suggest that it may be unusual. Here we present maps which physically define large sequence duplications flanking the centromeric satellites of human chromosome 10, together with a fluorescence in situ hybridization (FISH) analysis of pericentromeric sequence stability. Our results indicate that the duplications on each chromosome arm are organized into two blocks of approximately 250 and 150 kb separated by approximately 300 kb of non-duplicated DNA. The larger proximal blocks, containing ZNF11A, ZNF33A and ZNF37A (10p11) and ZNF11B, ZNF33B and ZNF37B (10q11), are inverted. However, the smaller distal blocks, containing D10S141A (10p11) and D10S141B (10q11), are not. A primate FISH analysis indicates that these loci were duplicated before the divergence of orang-utans from other Great Apes, that a cytogenetically cryptic pericentric inversion may have been involved in the formation of the flanking duplications and that they have undergone further rearrangement in other primate species. More surprising is the fact that sequences across the entire pericentromeric region appear to have undergone unprecedented levels of duplication, transposition, inversion and either deletion or sequence divergence in all primate species analysed. Extrapolating our data to the whole genome suggests that a minimum of 50 Mb of DNA in centromere-proximal regions is subject to an elevated level of mechanistically diverse sequence rearrangements compared with the bulk of genomic DNA.

Animals↗
PubMed2000

Sequence variation in the ribosomal DNA internal transcribed spacer of Tridacna crocea.

DNA-based genetic markers are needed to augment existing allozyme markers in the assessment of genetic diversity of wild giant clam populations. The dearth of polymorphic mitochondrial DNA regions amplified from known universal polymerase chain reaction (PCR) primers has led us to search other regions of the genome for viable sources of DNA polymorphism. We have designed tridacnid-specific PCR primers for the amplification of internal transcribed spacer regions. Sequences of the first internal transcribed spacer segment (ITS-1) revealed very high polymorphism, showing 29% variation arising from base substitutions alone. Preliminary restriction analysis of the ITS regions using 8 restriction enzymes revealed cryptic changes in the DNA sequence. These mutations are promising as marker tools for differentiating geographically separated populations. Such variation in the ITS region can possibly be used for population genetic analysis.

Journal Article↗
PubMed2000

A critical reappraisal of the fossil record of the bilaterian phyla.

It has long been assumed that the extant bilaterian phyla generally have their origin in the Cambrian explosion, when they appear in an essentially modern form. Both these assumptions are questionable. A strict application of stem- and crown-group concepts to phyla shows that although the branching points of many clades may have occurred in the Early Cambrian or before, the appearance of the modern body plans was in most cases later: very few bilaterian phyla sensu stricto have demonstrable representatives in the earliest Cambrian. Given that the early branching points of major clades is an inevitable result of the geometry of clade diversification, the alleged phenomenon of phyla appearing early and remaining morphologically static is seen not to require particular explanation. Confusion in the definition of a phylum has thus led to attempts to explain (especially from a developmental perspective) a feature that is partly inevitable, partly illusory. We critically discuss models for Proterozoic diversification based on small body size, limited developmental capacity and poor preservation and cryptic habits, and show that the prospect of lineage diversification occurring early in the Proterozoic can be seen to be unlikely on grounds of both parsimony and functional morphology. Indeed, the combination of the body and trace fossil record demonstrates a progressive diversification through the end of the Proterozoic well into the Cambrian and beyond, a picture consistent with body plans being assembled during this time. Body-plan characters are likely to have been acquired monophyletically in the history of the bilaterians, and a model explaining the diversity in just one of them, the coelom, is presented. This analysis points to the requirement for a careful application of systematic methodology before explanations are sought for alleged patterns of constraint and flexibility.

Animals↗
PubMed2006

Use of real-time quantitative PCR targeting the msp2 protein gene to identify cryptic Anaplasma phagocytophilum infections in wildlife and domestic animals.

Anaplasma phagocytophilum is an emerging pathogen throughout much of the Holarctic, where Ixodes spp. tick vectors occur. This organism was expected to be present at study sites in Humboldt County, north-western California, based on the presence of appropriate tick vectors, seropositivity in sentinel hosts, and previously reported human infections. However, despite high seroprevalence suggesting circulating A. phagocytophilum, active infections in dogs and wildlife (including suspected reservoir species) were rare using published polymerase chain reaction (PCR) protocols. This finding was possible if the published PCR protocol lacked sensitivity for strains in the study areas. We report a new TaqMan-PCR (TM-PCR) assay targeting the msp2 gene that has greater sensitivity and specificity for diverse A. phagocytophilum strains from this region. The new assay detected as few as one plasmid copy and a range of genetically diverse strains of A. phagocytophilum. Specificity was confirmed by failure to amplify targets of closely related bacteria. Application of the TM-PCR to samples from northern California confirmed PCR-positivity in 94 woodrats (71%; n=134), three (4%; n=80) bears, and seven (7%; n=97) domestic dogs. The msp2 TM-PCR protocol appears to be more sensitive for use in assays of samples from parts of western North America and possibly in other regions where populations are genetically diverse or divergent from eastern United States strains of A. phagocytophilum.

Anaplasma phagocytophilum↗
PubMed2005

Rangewide population genetic structure of the African malaria vector Anopheles funestus.

Anopheles funestus is a primary vector of malaria in Africa south of the Sahara. We assessed its rangewide population genetic structure based on samples from 11 countries, using 10 physically mapped microsatellite loci, two per autosome arm and the X (N = 548), and 834 bp of the mitochondrial ND5 gene (N = 470). On the basis of microsatellite allele frequencies, we found three subdivisions: eastern (coastal Tanzania, Malawi, Mozambique and Madagascar), western (Burkina Faso, Mali, Nigeria and western Kenya), and central (Gabon, coastal Angola). A. funestus from the southwest of Uganda had affinities to all three subdivisions. Mitochondrial DNA (mtDNA) corroborated this structure, although mtDNA gene trees showed less resolution. The eastern subdivision had significantly lower diversity, similar to the pattern found in the codistributed malaria vector Anopheles gambiae. This suggests that both species have responded to common geographic and/or climatic constraints. The western division showed signatures of population expansion encompassing Kenya west of the Rift Valley through Burkina Faso and Mali. This pattern also bears similarity to A. gambiae, and may reflect a common response to expanding human populations following the development of agriculture. Due to the presumed recent population expansion, the correlation between genetic and geographic distance was weak. Mitochondrial DNA revealed further cryptic subdivision in A. funestus, not detected in the nuclear genome. Mozambique and Madagascar samples contained two mtDNA lineages, designated clade I and clade II, that were separated by two fixed differences and an average of 2% divergence, which implies that they have evolved independently for approximately 1 million years. Clade I was found in all 11 locations, whereas clade II was sampled only on Madagascar and Mozambique. We suggest that the latter clade may represent mtDNA capture by A. funestus, resulting from historical gene flow either among previously isolated and divergent populations or with a related species.

Africa South of the Sahara↗