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PubMed2003

The complete nucleotide sequence of two distinct geminiviruses infecting cucurbits in Vietnam.

We have characterised two distinct geminiviruses that infect cucurbit cultivars in Vietnam. The genomes of both viruses consisted of two circular ssDNA components (DNA-A and DNA-B), with a genome arrangement and coding sequence typical of viruses in the Begomovirus genus in the family Geminiviridae. The sequence of DNA-A of one of the viruses was approximately 97% similar to Squash leaf curl virus-China (SLCV-Ch), for which a DNA-B has yet to be identified. We have named this virus Squash leaf curl virus-Vietnam (SLCV-Vn). The intergenic region of the SLCV-Vn DNA-B contained a 40 nt deletion between the putative AC1 TATA box and the stem loop. A second virus isolated from loofa in southern Vietnam was only 80% similar to SLCV-Vn over the complete DNA-A sequence, however the nucleotide sequence in the coat protein coding regions was 95% similar. We have named this virus Loofa yellow mosaic virus-Vietnam (LYMV-Vn). Other regions of the SLCV-Vn and LYMV-Vn genomes differed markedly, suggesting the coat protein coding region was recombinant. The DNA-B of both viruses were only 60% similar over the complete nucleotide sequence, although the encoded amino acid sequence of the BC1 gene was 90% identical.

Base Sequence↗
PubMed2003

Age-stratified QTL genome scan analyses for anthropometric measures.

With the availability of longitudinal data, age-specific (stratified) or age-adjusted genetic analyses have the potential to localize different putative trait influencing loci. If age does not influence the locus-specific penetrance function within the range examined, age-stratified analyses will tend to yield comparable results for an individual trait. However, age-stratified results should vary across age strata when the locus-specific penetrance function is age dependent. In this paper, age-stratified and age-adjusted quantitative trait loci (QTL) linkage analyses were contrasted for height, weight, body mass index (BMI), and systolic blood pressure on a subset of the Framingham Heart Study. The strata comprised individuals with data present in each of three age groups: 31-49, 50-60, 61-79. Genome-wide QTL analyses were performed using SOLAR. Over all ages, a linkage signal for height was detected on chromosome 14q11.2 near marker GATA74E02A (LOD for ages 31-49 = 2.38, LOD for ages 50-60 = 1.84, LOD for ages 61-79 = 2.45). Evidence of linkage to BMI in the 31-49 age group was found on chromosome 3q22 (GATA3C02, LOD = 2.89, p = 0.0003) at the same location as the signal for weight (LOD = 3.10, p = 0.0002). Linkage was also supported on chromosome 1p22.1 for BMI (LOD = 2.21, p = 0.0014) and weight (LOD = 2.47, p = 0.0007) in the 31-49 age group. Our age-stratified results suggest that QTL that are expressed over long periods of time and affecting multiple, correlated traits may be identified using genome scan and variance-component methodology to help detect early and/or late gene expression.

Adult↗
PubMed1999

Genome-wide scan for autism susceptibility genes. Paris Autism Research International Sibpair Study.

Family and twin studies have suggested a genetic component in autism. We performed a genome-wide screen with 264 microsatellites markers in 51 multiplex families, using non-parametric linkage methods. Families were recruited by a collaborative group including clinicians from Sweden, France, Norway, the USA, Italy, Austria and Belgium. Using two-point and multipoint affected sib-pair analyses, 11 regions gave nominal P -values of 0.05 or lower. Four of these regions overlapped with regions on chromosomes 2q, 7q, 16p and 19p identified by the first genome-wide scan of autism performed by the International Molecular Genetic Study of Autism Consortium. Another of our potential susceptibility regions overlapped with the 15q11-q13 region identified in previous candidate gene studies. Our study revealed six additional regions on chromosomes 4q, 5p, 6q, 10q, 18q and Xp. We found that the most significant multipoint linkage was close to marker D6S283 (maximum lod score = 2.23, P = 0.0013).

Adolescent↗
PubMed1995

Interspecies gene exchange in bacteria: the role of SOS and mismatch repair systems in evolution of species.

Analysis of interspecies matings between S. typhimurium and E. coli indicates that the genetic barrier that separates these (and perhaps many other) related species is primarily recombinational. The structural component of this barrier is genomic sequence divergence. The mismatch repair enzymes act as potent inhibitors of interspecies recombination, whereas the SOS system acts as an inducible positive regulator. Interspecies mating triggers a RecBC-dependent SOS response in female bacteria that increases recombination mainly through overproduction of the RecA protein. Mismatch repair acts to reduce the mutation rate and recombination between similar sequences, whereas SOS acts to increase both. These opposing activities allow mismatch repair and SOS systems to determine both the rate of accumulation of sequence divergence and the extent of genetic isolation, which are the key components of the speciation process.

Biological Evolution↗
PubMed1997

Impact of changes in GC content on the silent molecular clock in murids.

Murid nuclear genomes are more homogeneous in GC content than those of most mammals, which leads to the question of how such important compositional changes have accumulated. This paper reports on relationships between frequencies of synonymous differences and GC change, in the lineages leading to human and murids. For this, we used the four-species approach: GC changes between human and murids were compared to the frequencies of synonymous differences, measured between two independent species without GC change (bovine and pig), by using orthologous genes common to all four species. We report three conclusions: (1) Among genes with little GC change, 60% of the variability of synonymous substitution frequencies is explained by the gene-specific rate component. (2) GC changes in murid genomes are independent of the gene-specific rate component. Slowly evolving genes in pig bovine comparison can show strong GC change in murids. (3) By using a GC-independent estimate of the substitution rate, we show that GC changes in murid genomes increase synonymous substitution frequencies. The GC homogenization considerably weakens the gene-specific conservation of substitution rates in murids, and could explain part of the increase of evolutionary rates observed in this group. We present a mechanism that can account for the evolution of the GC homogenization in murids.

Animals↗
PubMed2005

Mining time-dependent gene features.

This paper presents an application of the Independent Component Analysis (ICA) method to genomic data. In particular, experimentally produced perturbation effects over the E.coli bacterium are monitored through the changes of gene expression values observed at regular times, and until steady state has been reached. The aim is to control the response of the SOS system to DNA damage. We might assume that only part of the genetic regulatory network is affected directly by the perturbation conditions, as indirect cascade effects might also be present, and some genes may change just because of randomness. ICA decomposes the gene matrix and identifies groups of genes belonging to a certain estimated component by virtue of co-expression; it is of course of interest to establish co-regulation dynamics, which might underlie the captured correlation. Stronger forms of dependence, like Mutual Information, are thus computed and compared with linear correlation in order to validate the results and establish the role of the identified components in determining the network dynamics.

Algorithms↗
PubMed1982

Site-specific cleavage/packaging of herpes simplex virus DNA and the selective maturation of nucleocapsids containing full-length viral DNA.

Defective genomes present in serially passaged herpes simplex virus (HSV) stocks have been shown to consist of tandemly arranged repeat units containing limited sets of the standard virus DNA sequences. Invariably, the HSV defective genomes terminate with the right (S component) terminus of HSV DNA. Because the oligomeric forms can arise from a single repeat unit, it has been concluded that the defective genomes arise by a rolling circle mechanism of replication. We now report on our studies of defective genomes packaged in viral capsids accumulating in the nuclei and in mature virions (enveloped capsids) translocated into the cytoplasm of cells infected with serially passaged virus. These studies have revealed that, upon electrophoresis in agarose gels, the defective genomes prepared from cytoplasmic virions comigrated with nondefective standard virus DNA (M(r) 100 x 10(6)). In contrast, DNA prepared from capsids accumulating in nuclei consisted of both full-length defective virus DNA molecules and smaller DNA molecules of discrete sizes, ranging in M(r) from 5.5 to 100 x 10(6). These smaller DNA species were shown to consist of different integral numbers (from 1 to approximately 18) of defective genome repeat units and to terminate with sequences corresponding to the right terminal sequences of HSV DNA. We conclude on the basis of these studies that (i) sequences from the right end of standard virus DNA contain a recognition signal for the cleavage and packaging of concatemeric viral DNA, (ii) the sequence-specific cleavage is either a prerequisite for or occurs during the entry of viral DNA into capsid structures, and (iii) DNA molecules significantly shorter than full-length standard viral DNA can become encapsidated within nuclear capsids provided they contain the cleavage/packaging signal. However, capsids containing DNA molecules significantly shorter than standard virus DNA are not translocated into the cytoplasm.

Capsid↗
PubMed2005

Toward a biopsychosocial model for 21st-century genetics.

Advances in genomic research are increasingly identifying genetic components in major health and mental health disorders. This article presents a Family System Genetic Illness model to address the psychosocial challenges of genomic conditions for patients and their families, and to help organize this complex biopsychosocial landscape for clinical practice and research. This model clusters genomic disorders based on key characteristics that define types of disorders with similar patterns of psychosocial demands over time. Key disease variables include the likelihood of developing a disorder based on specific genetic mutations, overall clinical severity, timing of clinical onset in the life cycle, and whether effective treatment interventions exist to alter disease onset and/or progression. For disorders in which carrier, predictive, or presymptomatic testing is available, core nonsymptomatic time phases with salient developmental challenges are described pre- and post-testing, including a long-term adaptation phase. The FSGI model builds on Rolland's Family System Illness model, which identifies psychosocial types and phases of chronic disorders after clinical onset. The FSGI model is designed to be flexible and responsive to future discoveries in genomic research. Its utility is discussed for research, preventive screening, family assessment, treatment planning, and service delivery in a wide range of healthcare settings.

Adaptation, Psychological↗
PubMed1996

Genomic organization of lactic acid bacteria.

Current knowledge of the genomes of the lactic acid bacteria, Lactococcus lactis and Streptococcus thermophilus, and members of the genera Lactobacillus, Leuconostoc, Pediococcus and Carnobacterium, is reviewed. The genomes contain a chromosome within the size range of 1.8 to 3.4 Mbp. Plasmids are common in Lactococcus lactis (most strains carry 4-7 different plasmids), some of the lactobacilli and pediococci, but they are not frequently present in S. thermophilus, Lactobacillus delbrueckii subsp. bulgaricus or the intestinal lactobacilli. Five IS elements have been found in L. lactis and most strains carry multiple copies of at least two of them; some strains also carry a 68-kbp conjugative transposon. IS elements have been found in the genera Lactobacillus and Leuconostoc, but not in S. thermophilus. Prophages are also a normal component of the L. lactis genome and lysogeny is common in the lactobacilli, however it appears to be rare in S. thermophilus. Physical and genetic maps for two L. lactis subsp. lactis strains, two L. lactis subsp. cremoris strains and S. thermophilus A054 have been constructed and each reveals the presence of six rrn operons clustered in less than 40% of the chromosome. The L. lactis subsp. cremoris MG1363 map contains 115 genetic loci and the S. thermophilus map has 35. The maps indicate significant plasticity in the L. lactis subsp. cremoris chromosome in the form of a number of inversions and translocations. The cause(s) of these rearrangements is (are) not known. A number of potentially powerful genetic tools designed to analyse the L. lactis genome have been constructed in recent years. These tools enable gene inactivation, gene replacement and gene recovery experiments to be readily carried out with this organism, and potentially with other lactic acid bacteria and Gram-positive bacteria. Integration vectors based on temperate phage attB sites and the random insertion of IS elements have also been developed for L. lactis and the intestinal lactobacilli. In addition, a L. lactis sex factor that mobilizes the chromosome in a manner reminiscent to that seen with Escherichia coli Hfr strains has been discovered and characterized. With the availability of this new technology, research into the genome of the lactic acid bacteria is poised to undertake a period of extremely rapid information accrual.

Bacteriophages↗
PubMed1984

Looking for epilepsy genes.

The complexity of the human genome creates special problems in understanding the genetic component of disease processes. An estimated 50,000 genes exist in the human genome and it is reasonable to assume that mutation in any one of these genes may result in an inherited disorder. Because of the complex pattern of gene expression controlling the development and organization of the central nervous system, insights into the genetic component, if any, of diseases such as epilepsy are most accessible to analysis by genetic linkage studies. Advances in the manipulation of DNA have made possible more effective acquisition of genotypic information in humans by studying the inheritance of restriction fragment length polymorphisms using cloned DNA probes. Two approaches exist to utilize this technology in studying inherited disorders. The first approach consists of genotypic determinations in affected families with cloned genes in which a mutation might result in the phenotype observed. Analysis of these data will show whether the inheritance of an allele of the candidate gene is linked to the disease. The second approach relies upon the construction with these probes of a linkage map for the human genome such that disease families can be screened in order to determine with which of these markers the phenotype is linked, indicating the map position of a gene associated with the inherited disorder. The use of these new approaches enables investigators to screen either specific biochemical defects in disease families or to identify the underlying genetic mechanisms in inherited disorders whose phenotype is expressed only in the intact human.

Chromosome Mapping↗
PubMed1986

Looking for epilepsy genes: clinical and molecular genetic studies.

The complexity of the human genome creates special problems in understanding the genetic component of disease processes. An estimated 50,000 genes exist in the human genome, and it is reasonable to assume that mutation in any one of these genes may result in an inherited disorder. Because of the complex pattern of gene expression controlling the development and organization of the central nervous system (CNS), insights into the genetic component, if any, of diseases such as epilepsy are most accessible to analysis by genetic linkage studies. Advances in the manipulation of DNA have made possible more effective acquisition of genotypic information in humans by studying the inheritance of restriction fragment length polymorphisms (RFLPs) using cloned DNA probes. Two approaches exist to utilize this technology in studying inherited disorders. The first approach consists of genotypic determinations in affected families with cloned genes in which a mutation might result in the phenotype observed. Analysis of these data will show whether the inheritance of an allele of the candidate gene is linked to the disease. The second approach relies upon the construction with these probes of a linkage map for the human genome such that disease families can be screened in order to determine with which of these markers the phenotype is linked, indicating the map position of a gene associated with the inherited disorder. The use of these new approaches enables investigators to screen either specific biochemical defects in disease families or to identify the underlying genetic mechanisms in inherited disorders whose phenotype is expressed only in the intact human (84). The first step in localizing the chromosomal site of specific epilepsies is to define their pattern of inheritance. This determination is now being carried out for benign juvenile myoclonic epilepsy; 50 multigenerational families are being studied in three separate epilepsy programs in Los Angeles, Winston-Salem, North Carolina, and Berlin. Concurrent with these studies, investigators are combining the principles of classic linkage analysis, using 30 protein markers, with the use of RFLPs to determine the chromosomal location of juvenile myoclonic epilepsy. Two problems appear formidable, however. First, since the chromosomal location of specific epilepsies is unknown, the entire human genome must be screened.(ABSTRACT TRUNCATED AT 400 WORDS)

Chromosome Mapping↗
PubMed2006

Mouse genomic representational oligonucleotide microarray analysis: detection of copy number variations in normal and tumor specimens.

Genomic amplifications and deletions, the consequence of somatic variation, are a hallmark of human cancer. Such variation has also been observed between "normal" individuals, as well as in individuals with congenital disorders. Thus, copy number measurement is likely to be an important tool for the analysis of genetic variation, genetic disease, and cancer. We developed representational oligonucleotide microarray analysis, a high-resolution comparative genomic hybridization methodology, with this aim in mind, and reported its use in the study of humans. Here we report the development of a representational oligonucleotide microarray analysis microarray for the genomic analysis of the mouse, an important model system for many genetic diseases and cancer. This microarray was designed based on the sequence assembly MM3, and contains approximately 84,000 probes randomly distributed throughout the mouse genome. We demonstrate the use of this array to identify copy number changes in mouse cancers, as well to determine copy number variation between inbred strains of mice. Because restriction endonuclease digestion of genomic DNA is an integral component of our method, differences due to polymorphisms at the restriction enzyme cleavage sites are also observed between strains, and these can be useful to follow the inheritance of loci between crosses of different strains.

Animals↗
PubMed2001

Genome-wide ENU mutagenesis to reveal immune regulators.

A complete list of molecular components for immune system function is now available with the completion of the human and mouse genome sequences. However, identification and functional annotation of genes involved in immunological processes require a discovery methodology that can efficiently and broadly analyze the complex interplay of these components in vivo. Our recent experience indicates that genome-wide chemical mutagenesis in the mouse is an extremely powerful methodology for the identification of genes required for complex immunological processes.

Animals↗
PubMed1994

Geminivirus replication origins have a modular organization.

Tomato golden mosaic virus (TGMV) and bean golden mosaic virus (BGMV) are closely related geminiviruses with bipartite genomes. The A and B DNA components of each virus have cis-acting sequences necessary for replication, and their A components encode trans-acting factors are required for this process. We showed that virus-specific interactions between the cis- and trans-acting functions are required for TGMV and BGMV replication in tobacco protoplasts. We also demonstrated that, similar to the essential TGMV AL1 replication protein, BGMV AL1 binds specifically to its origin in vitro and that neither TGMV nor BGMV AL1 proteins bind to the heterologous origin. The in vitro AL1 binding specificities of the B components were exchanged by site-directed mutagenesis, but the resulting mutants were not replicated by either A component. These results showed that the high-affinity AL1 binding site is necessary but not sufficient for virus-specific origin activity in vivo. Geminivirus genomes also contain a stem-loop sequence that is required for origin function. A BGMV B mutant with the TGMV stem-loop sequence was replicated by BGMV A, indicating that BGMV AL1 does not discriminate between the two sequences. A BGMV B double mutant, with the TGMV AL1 binding site and stem-loop sequences, was not replicated by either A component, indicating that an additional element in the TGMV origin is required for productive interaction with TGMV AL1. These results suggested that geminivirus replication origins are composed of at least three functional modules: (1) a putative stem-loop structure that is required for replication but does not contribute to virus-specific recognition of the origin, (2) a specific high-affinity binding site for the AL1 protein, and (3) at least one additional element that contributes to specific origin recognition by viral trans-acting factors.

Base Sequence↗
PubMed2006

Fluorescent labels for proteomics and genomics.

Fluorescent labeling reagents are an essential component of a huge industry built on sensitive fluorescence detection. This technology has grown over 30 years and is in some ways mature. Excellent labeling reagents with close to maximum theoretical brightness are available in many different colors. Large fluorescent proteins like phycobiliproteins are also widely used that are exceedingly bright. Other fluorescent proteins like the GFP family can be obtained for creating genetically encoded protein labels in living cells. A new 'solid state' quantum dot technology is being exploited for large-scale multiparameter labeling. This technology provides the 'ultimate' photostable labeling reagent. Still, there are advances to be made. Not available is the ultimate tool kit of low molecular weight, strongly light absorbing, photostable labels with narrow emission bands ranging from the UV to the IR.

Electrophoresis, Gel, Two-Dimensional↗
PubMed2001

Taking a functional genomics approach in molecular medicine.

The elucidation of genetic components of human diseases at the molecular level provides crucial information for developing future causal therapeutic intervention. High-throughput genome sequencing and systematic experimental approaches are fuelling strategic programs designed to investigate gene function at the biochemical, cellular and organism levels. Bioinformatics is one important tool in functional genomics, although showing clear limitations in predicting ab initio gene structures, gene function and protein folds from raw sequence data. Systematic large-scale data-set generation, using the same type of experiments that are used to decipher the function of single genes, are being applied on entire genomes. Comparative genomics, establishment of gene catalogues, and investigation of cellular and tissue molecular profiles are providing essential tools for understanding gene function in complex biological networks.

Animals↗
PubMed2002

Molecular phylogenetics and mitochondrial genomic evolution in the chamaeleonidae (Reptilia, Squamata).

A phylogenetic hypothesis for the lizard family Chamaeleonidae is generated from 1503 aligned base positions (883 parsimony-informative) of mitochondrial DNA for specimens representing 59 species (57 ingroup and two outgroup). Sequences are reported for a genomic segment encoding eight transfer RNAs, NADH dehydrogenase component 2 (ND2), and portions of NADH dehydrogenase component 1 (ND1) and cytochrome c oxidase subunit 1 (COI). Newly reported genomic rearrangements and duplications support the hypothesis that mitochondrial gene order and content are destabilized by phylogenetic loss of a functional origin for light-strand replication between the genes encoding tRNA(Asn) and tRNA(Cys). A novel gene order characterizes all sampled Brookesia except B. nasus. Brookesia nasus, the apparent sister taxon of a clade formed by all other Brookesia, has the ancestral gene order but contains a large tandem duplication. An apparently noncoding 220 base pair insertion between the genes encoding ND2 and tRNA(Trp) is reported for Bradypodion tavetanum. Phylogenetic analysis identifies nine clades whose ancestral lineages diverged early in chamaeleonid evolutionary history: (1) Brookesia (possibly excluding B. nasus), (2) Chamaeleo subgenus Chamaeleo (excluding C. namaquensis), (3) Chamaeleo subgenus Trioceros, (4) viviparous Bradypodion, (5) oviparous Bradypodion, (6) genus Furcifer (except F. balteatus), and (7-9) three distinct clades of Calumma. Chamaeleo namaquensis, Brookesia nasus, Furcifer balteatus, Rhampholeon brevicaudatus, and R. spectrum represent ancient lineages dating to approximately the same time. Multiple independent losses and a possible secondary gain of horns are inferred for Trioceros. Viviparity has at least two separate origins in chameleons, one in Bradypodion and

Animals↗