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PubMed1994

Primate T-lymphotropic virus type I LTR sequence variation and its phylogenetic analysis: compatibility with an African origin of PTLV-I.

Due to the low evolutionary rate and the limited horizontal transmission of human T-lymphotrophic virus type I (HTLV-I), its phylogenetic analysis reveals the movements and contacts of ancient populations. Since simian strains cannot be distinguished from human strains by phylogenetic criteria, this virus has appropriately been called primate T-lymphotropic virus type I (PTLV-I). We sequenced the LTR of six PTLV-I strains: three HTLV-I strains from African patients with tropical spastic paraparesis (TSP) (Equateur, Zaire), two laboratory HTLV-I strains of Japanese origin, MT-2 and MT-4, and one STLV-I from a baboon of the primate center in Sukhumi, Georgia. We applied four phylogenetic inference methods: neighbor-joining (NJ), unweighted pair group method using arithmetic averages (UPGMA), Fitch and Wagner parsimony (pars), and maximum likelihood (ML), to these 6 LTR sequences and 18 published LTR sequences (cosmopolitan, African, and Melanesian HTLV-I strains and African and Asian STLV-I strains). Three major HTLV-I subtypes can be identified with all four methods: the cosmopolitan HTLV-Ia, the central African HTLV-Ib, clearly descendant from a STLV-I CH-like African ancestral simian strain, and the Melanesian HTLV-Ic, probably descendant from an Asian STLV-I strain. We observe a segregation of PTLV-I sequences according to their geographical origin and not according to host species. The Zairean strains form a cluster closely related to an STLV-I strain isolated from a chimpanzee (STLV-I CH) and distinct from western African strains, which belong to the cosmopolitan subtype of HTLV-I. The Sukhumi STLV-I strain found in a captive-born baboon was of Asian descent. We experienced rooting problems with UPGMA when using HTLV-II as an outgroup. Concordant results with all four methods were obtained by eliminating HTLV-II LTR sequence fragments with bad alignment to HTLV-I. This resulted in a HTLV-II root node on the African STLV-I TAN90 terminal branch (with bootstrap values above 92% for the NJ and pars methods) and not on the Asian STLV-I PtM3 branch, as has been derived by others based on their use of UPGMA. The results of the analyses also support a higher evolutionary rate of PTLV-I in Asia, implying that the trees obtained with the NJ and ML methods have a higher reliability. These results are more compatible with an ancient African origin of PTLV-I than with an Asian origin.

Africa↗

PubMed1997

Initiation of SV40 DNA replication in vitro: analysis of the role played by sequences flanking the core origin on initial synthesis events.

Replication initiation events are suppressed over the SV40 core origin in vitro; they are also greatly reduced over sequences flanking the origin which contain binding sites for several transcription factors. To address the biochemical basis for the gap in initiation events over the flanking sequences, initial synthesis events have been characterized on templates lacking these sequences. Herein, it is demonstrated that previously functional initiation sites are nearly inactive when moved to positions that are proximal to the core origin. Thus, the gap in initiation events depends, in part, on the proximity of the initiation sites to the SV40 core origin. Additional experiments demonstrate that removal of the flanking sequences had little or no effect on DNA unwinding or on the efficiency of initiation of DNA synthesis in vitro. These results indicate that, under our in vitro conditions, initiation of SV40 DNA synthesis is not enhanced by binding of transcription factors to the flanking sequences.

Antigens, Viral, Tumor↗

PubMed1997

Two domains of the AL1 protein mediate geminivirus origin recognition.

The geminiviruses tomato golden mosaic virus (TGMV) and bean golden mosaic virus (BGMV) have bipartite genomes. Their A and B DNA components contain cis-acting sequences that function as origins of replication, while their A components encode the trans-acting replication proteins--AL1 and AL3. Earlier experiments demonstrated that virus-specific interactions between the cis- and trans-acting functions are required for TGMV and BGMV replication and that the AL1 proteins of the two viruses specifically bind their respective origins. In the current study, characterization of AL1 and AL3 proteins produced from plant expression cassettes in transient replication assays revealed that interaction between AL1 and the origin is responsible for virus-specific replication. The AL3 protein does not contribute to specificity but can be preferred by its cognate AL1 protein when replication is impaired. Analysis of chimeric proteins showed that two regions of AL1 act as specificity determinants during replication. The first domain is located between amino acids 1 and 116 and recognizes the AL1 origin binding site. The second region, which is between amino acids 121 and 209, is not dependent on the known AL1 DNA binding site. Analysis of wild type and chimeric proteins in transient transcription assays showed that AL1 also represses its own promoter in a virus-specific manner. Transcriptional specificity is conferred primarily by AL1 amino acids 1-93 with amino acids 121-209 making a smaller contribution. Together, these results demonstrated that the virus-specific interactions of AL1 during replication and transcription are complex, involving at least two discreet domains of the protein.

Amino Acid Sequence↗

PubMed1992

Evolutionary origin of the class A and class C beta-lactamases.

The protein sequences of 18 class A beta-lactamases and 2 class C beta-lactamases were analyzed to produce a rooted phylogenetic tree using the DD peptidase of Streptomyces R61 as an outgroup. This tree supports the penicillin-binding proteins as the most likely candidate for the ancestoral origin of the class A and class C beta-lactamases, these proteins diverging from a common evolutionary origin close to the DD peptidase. The actinomycetes are clearly shown as the origin of the class A beta-lactamases found in other non-actinomycete species. The tree also divides the beta-lactamases from the Streptomyces into two subgroups. One subgroup is closer to the DD peptidase root. The other Streptomyces subgroup shares a common branch point with the rest of the class A beta-lactamases, showing this subgroup as the origin of the non-actinomycete class A beta-lactamases. The non-actinomycete class A beta-lactamase phylogenetic tree suggests a spread of these beta-lactamases by horizontal transfer from the Streptomyces into the non-actinomycete gram-positive bacteria and thence into the gram-negative bacteria. The phylogenetic tree of the Streptomyces class A beta-lactamases supports the possibility that horizontal transfer of class A beta-lactamases occurred within the Streptomyces.

Amino Acid Sequence↗

PubMed1995

Maternal origin of nucleated erythrocytes in peripheral venous blood of pregnant women.

We studied the origin of nucleated red blood cells (NRBC) in peripheral venous blood samples from 40 pregnant women carrying a male fetus, using a technique that allows direct chromosomal analysis by in situ hybridisation on immunologically and morphologically classified cells. Samples from ten nulligravid women were studied as controls. NRBC were enriched by negative magnetic activated cell sorting (miniMACS) using anti-CD45 monoclonal antibody. NRBC were detected by alkaline phosphatase anti-alkaline phosphatase immunostaining using a monoclonal anti-glycophorin A antibody. The origin of the NRBC was determined by fluorescence in situ hybridisation using X and Y specific probes. NRBC were found in 37 of the 40 pregnant women at a range of 1 to 230 per 20 ml of venous blood and in 6 of the 10 controls at a range of 1 to 3 per 20 ml of venous blood. All NRBC detected in the pregnant women were evidently of maternal origin, and in the pregnant women the number of NRBC was significantly higher (P < 0.05) than in the controls. Pregnancy per se seems to induce the appearance of maternal NRBC in the circulation, and it cannot therefore be assumed that NRBC isolated from the maternal blood are of fetal origin on the basis of morphology alone. Discrimination of fetal NRBC must occur for prenatal diagnosis of fetal genetic disorders.

Cell Nucleus↗

PubMed1993

The origin of cytologically unidentifiable chromosome abnormalities: six cases ascertained by targeted chromosome-band painting.

De novo chromosome structural abnormalities cannot always be diagnosed by the use of standard cytogenetic techniques. We applied a previously developed chromosome-band-specific painting method to the diagnosis of such rearrangements. The diagnostic procedures consisted of microdissection of an aberrant chromosomal region of a given patient, polymerase chain reaction (PCR) amplification of the dissected chromosomal DNA, and subsequent competitive fluorescence in situ hybridization (FISH) using the PCR products as a probe pool on metaphase chromosomes from the patient and/or a karyotypically normal person. With this strategy, we studied 6 de novo rearrangements (6p+, 6q+, 9p+, 17p+, +mar, and +mar) in 6 patients. These rearrangements had been seen by conventional banding but their origin could not be identified. In all 6 patients, we successfully ascertained the origin. Using an aberrant region-specific probe pool, FISH signals appeared on both the aberrant region and a region of another specific chromosome pair. A reverse probe pool that was generated through the microdissection of normal chromosomes at a candidate region for the origin of the aberration hybridized with both the aberrant and the candidate regions. We thus diagnosed one patient with 17p+ as having trisomy for 14q32-qter, one with 9p+ as having trisomy for 12pter-p12, one with 6q+ as having a tandem duplication (trisomy) of a 6q23-q25 segment, one with 6p+ as having a tandem duplication (trisomy) of a 6p23-q21.3 segment, one with a supernumerary metacentric marker chromosome as having tetrasomy for 18pter-cen, and the last with an additional small marker chromosome as having trisomy for 18p11.1 (or p11.2)-q11.2. The present targeted chromosome-band-painting method provides the simple and rapid preparation of a probe pool for region-specific FISH, and is useful for the diagnosis of chromosome abnormalities of unknown origin.

Base Sequence↗

PubMed1977

The origin of the vasopressinergic and oxytocinergic fibres of the external region of the median eminence of the rat hypophysis.

The origin of the vasopressinergic and oxytocinergic nerve fibres of the external region of the rat median eminence was investigated by means of hypothalamic lesions, adrenalectomy and immunocytochemistry. The results obtained in bilaterally adrenalectomized animals with complete, or incomplete, destruction of the suprachiasmatic nuclei showed that, at least, the great majority of the vasopressinergic and oxytocinergic nerve fibres of the external region of the rat median eminence do not originate from the suprachiasmatic nuclei. From the observations obtained in bilaterally adrenalectomized animals with total or subtotal destruction of both paraventricular hypothalamic nuclei, it appears that the paraventricular nuclei must be the origin of (nearly) all the vasopressinergic and oxytocinergic nerve fibres of the external region of the rat median eminence. The results strongly suggest that both types of fibres originate from all parts of the paraventricular nuclei.

Adrenalectomy↗

PubMed1994

Laminar origin of striatal and thalamic projections of the prefrontal cortex in rhesus monkeys.

Prefrontostriatal and prefrontothalamic connections in rhesus monkeys have been shown to be organized in a topographic manner. These projections originate largely from infragranular layers V and VI. To examine whether the striatal and thalamic connections from the prefrontal cortex arise from separate neuronal populations or are collateralized, two different fluorescent retrograde tracers (diamidino yellow and fast blue) were injected into topographically similar regions of the head of the caudate nucleus and the mediodorsal nucleus in the same animal. The results show that although prefrontostriatal and prefrontothalamic projections arise from similar topographic regions, their laminar origins are distinctive. The connections to the head of the caudate nucleus originate mainly from layer Va, to a lesser extent from layer Vb, with a minor contribution from layers III and VI. In contrast, the projections to the mediodorsal nucleus emanate largely from layer VI, and also from layer Vb. Only occasional double-labeled neurons were observed, indicating that prefrontostriatal and prefrontothalamic connections originate from separate neuronal populations. The differential laminar distributions of neurons projecting to the head of the caudate nucleus and the mediodorsal nucleus suggest that these structures may receive independent types of information from the prefrontal cortex.

Amidines↗

PubMed1978

Mini-chromosomes: plasmids which carry the E. coli replication origin.

We have isolated plasmids by linking the 5.9 MD EcoRI fragment of E. coli that carries the origin of replication to an EcoRI fragment that carries an amplicillin resistance determinant, but lacks an origin of replication. 3 plasmids of this type, pOC1, pOC2, and pOC3, are described in detail in this report. Although the plasmids have some adverse effect on the growth properties of the host strain, their existence shows that two functioning chromosomal origins can coexist in one cell. Deletions generated from this type of plasmids allow an allocation of the origin of replication of E. coli within a DNA segment less than 0.4 MD in size.

Ampicillin↗

PubMed1975

Strains of Escherichia coli diploid for the chromosomal origin of DNA replication.

F' strains of E. coli have been isolated which are merodiploid for various chromosomal segments between 66 and 78 minutes. Strains diploid for the chromosomal DNA between the genes bgl and mtl grow slowly, have a reduced DNA/mass and an increased cell size. These properties could result if the chromosomal replication origin and a second, extrachromosomal, copy of the origin (located in this case on the F') were to compete for a substance required to initiate replication. We therefore suggest that these strains are diploid for the chromosomal origin of replication and that, therefore, the origin is located between bgl and mtl, that is between 71 and 73 minutes on the E. coli chromosome.

Bacterial Proteins↗

PubMed1980

Site-specific deletion at the replication origin of the antibiotic resistance factor R1.

The recombinant plasmid pRK101 carrying the complete replication origin of the antibiotic resistance factor R1 suffers frequently a deletion of 218 base pairs, removing parts or all of the origin sequence. This deletion seems to occur always when the Pst-E fragment carrying the replication origin is inserted into the cloning vector pBR322 in an orientation where the direction of R1 replication is the same as that of the vector plasmid and frequently when it is inserted in the opposite direction. DNA sequence analysis around the junction site generated by the deletion in three independently isolated deletion mutants reveals that the deletion occurs at a specific site, namely the end of a 22 bp sequence which is repeated almost identically at the other end of a segment of 197 bp. During the deletion one repeat unit is removed whereas the other is retained. The DNA sequence included by the two repeats contains high symmetric structures, i.e. inverted repeats, direct repeats and palindromes which may represent regulatory sites of the origin.

Anti-Bacterial Agents↗

PubMed1988

Origin of the extra chromosome in trisomy 18. A study on five patients using a restriction fragment length polymorphism.

The parental origin of an extra chromosome in five patients with trisomy 18 was traced using a restriction fragment length polymorphism (RFLP) of the human prealbumin (PA) gene, localized to 18p11.1-q12.1, as a genetic marker. MspI digests of the genomic DNAs of the five patients, their parents and normal controls were hybridized with the PA-cDNA. Densitometric analysis on the gene dose of the polymorphic fragments of these patients revealed that three had originated from a maternal meiotic error. The other two patients were uninformative for the parental origin of trisomy 18. Our results indicate that nondisjunctional errors leading to trisomy 18 may occur predominantly at the maternal meiosis, consistent with the results of previous studies on the parental origin of trisomies 21 and 13.

Chromosomes, Human, Pair 18↗

PubMed1984

Sequence of centromere separation another mechanism for the origin of nondisjunction.

The most commonly accepted view about the origin of aneuploidy is that it is due to errors in meiotic division. However, its rare occurrence makes it difficult to explain recurrent births of trisomic children to some parents. This problem causes more serious concern when one accepts that an abnormal (n + 1 or n - 1) sperm would enter fertilization by overriding thousands, or even millions, of normal haploid sperms. Also, the failure of aneuploidy to be induced in the offspring of mammals treated with mutagens raises questions about the effectiveness of the accepted mode of origin of errors. Current concepts also do not explain why one observes more errors of meiotic I, than of meiotic II, origin. It is known that most chromosomes separating at meta-anaphase junction in mitosis follow a nonrandom, genetically controlled sequence of separation. The present proposal makes use of out-of-phase separation of a rare chromosome, like premature separation in mitosis of the X in elderly humans or of an 18 in parents of trisomy 18 children. The suggestion is made that such out-of-phase separation results in aneuploid cell lines by total failure of the centromere to separate or by it separating too early, before the spindle is formed. The prematurely separating centromeres, it appears, do not attach to spindle fibers and hence cause nondisjunction. Such nondisjunction in embryonic stages will produce apparently normal individuals with mosaicism in somatic and/or gametic tissue. An individual carrying mosaicism in gonadal tissue will produce a large number of abnormal gametes, one of which may have a reasonable chance of entering fertilization. This mode of origin of aneuploidy takes care of all questions raised above and finds support in the data available in the literature. Several of the suggestions made in the hypothesis are easily testable.

Adult↗

PubMed1982

Trisomy 21: origin of non-disjunction.

The Q-band heteromorphisms of chromosome 21 were used in a sample of 48 families with a Down's syndrome child to evaluate the origin of non-disjunction. The parental origin and the meiotic error were determined in 27 families, and in eight families only partial information was obtained. Paternal and maternal origin of non-disjunction was in a 1:3 ratio. Failures were five times more frequent in first than in second meiotic division in both sexes. The mean parental age and environmental factors in relation to the origin of the anomaly are discussed. Our results are compared with those obtained previously in similar studies by other authors.

Chromosomes, Human, 21-22 and Y↗

PubMed1977

Experimental analysis of the origin of the wing musculature in avian embryos.

Interspecific grafts of somites, as well as parts of the somatic plate mesoderm, have been made between quail and chick embryos (stages 12--14 H. H.) at the level of the prospective wing bud in order to examine the relationship between somites and wing bud myogenesis. The stability of the natural quail nuclear labelling makes it possible to follow the developmental fate of grafted mesodermal cells in the host embryo. Embryos examined after subsequent incubation periods of 3--7 days show the following distribution of somatic and somitic cells within the wing bud: as soon as the three zones of different cell density within the mesoderm can be distinguished, cells of somitic origin are limited to the prospective myogenic area which is made up of mixed population of somatic and somitic cells, whereas the prospective chondrogenic area as well as the subectodermal zone only consists of cells originated from the somatic plate mesoderm. After further incubation, single muscle blastema are present which were also seen to be a mixture of somatic and somitic cells. The cells of muscular bundles are of somitic origin, while the muscle connective tissue cells are derived from the somatic plate mesoderm. After grafting into the coelomic cavity or on the chorio-allantoic membrane, fragments of the somatic plate mesoderm previously isolated from quail embryos (stage 14 H.H.) at the level of the prospective wing bud exhibit well developed skeletal elements, but fail to differentiate any musculature. These experimental investigations support previous evidence for a somitic origin of wing bud myogenic cells. Histological and scanning electron microscopic studies of the brachial somites and the adjacent somatic plate mesoderm of chick embryo (stages 13--15 H.H.) reveal that migration of still undifferentiated somitic cells into the brachial somatic plate mesoderm begins to take place in embryos at stage 14.

Animals↗

PubMed1988

AsnC, a multifunctional regulator of genes located around the replication origin of Escherichia coli, oriC.

The expression of the gidA gene which is located immediately counterclockwise of the replication origin of Escherichia coli, oriC, was found to be negatively regulated by the AsnC protein in an in vitro transcription-translation system. This effect is not due to simple repression of transcription originating at the gidA promoter, because the AsnC protein did not change the level of gidA promoter dependent transcription as analysed by promoter-galK fusions and by S1 mapping. From these data we conclude that the AsnC protein controls gidA gene expression at a post-transcriptional level. gidA is the third gene in the oriC region, besides asnA and asnC, whose expression is under AsnC control. However, the mechanisms involved are different: regulation of transcription in the case of asnA and asnC and post-transcriptional control of gidA. The gidA promoter was mapped by deletion analysis and by S1 mapping. We defined two regions that affect promoter activity negatively. Additional transcripts, regulated by AsnC, started more than 300 bp upstream of the gidA promoter and were found to enter the gidA region. These transcripts, originating either at the mioC and/or the ansC promoter traverse the replication origin.

Asparaginase↗

PubMed1983

A comparison of the origin of replication of pSa with R6K.

The plasmid pOri3 is a derivative of the origin of replication of pSa. Replication is defective as a result of a truncated repA gene, the product of which is required for plasmid replication. The defective replication is complemented by the presence of the intact repA gene of pSa, or by the presence of the plasmid R6K. The basis of this complementation has been examined by comparing the nucleotide sequence of the origin of pSa with that of R6K. A 13 base pair sequence present twice in the origin of pSa has homology with a 13 base pair sequence that is present fourteen times in the origin of R6K. These sequences may be the binding sites for the initiator proteins of these two plasmids. The location of these binding sites relative to the genes for the initiator proteins suggests that an autoregulatory control mechanism for the synthesis of the initiator proteins may also play a role in the control of plasmid copy number.

Base Sequence↗

PubMed1987

Chromosomal initiation in Bacillus subtilis may involve two closely linked origins.

When the dnaB37 initiation mutant of Bacillus subtilis is returned to a permissive temperature following a period at 45 degrees C, a synchronous round of DNA replication immediately ensues. Using this system we have been able to analyse the first fragments to be replicated while avoiding the use of thymine starvation or inhibitors of DNA replication. Such treatments are necessary to achieve even modest synchrony in germinating spores. Our results showed that the first fragment to be replicated was a 4 kb BamHI-SalI restriction fragment, BS6. In contrast, when the analysis was performed out in the presence of novobiocin, an inhibitor of DNA gyrase, replication from BS6 was inhibited and the first fragment to be replicated was BS5, a 5.6 kb fragment located 1.7 kb to the right of BS6. Replication from both putative origins was suppressed by rifamycin and was dependent upon dnaB. The results are discussed in relation to previous attempts to identify the first replicating fragment in germinating spores. We also discuss the possibility that B. subtilis contains two origins and suggest that either can act as the primary origin under certain conditions, or alternatively that both origins may act in concert in normal bidirectional replication, each site being required for the leading strand in each direction.

Bacillus subtilis↗