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GénoPlante-Info (GPI): a collection of databases and bioinformatics resources for plant genomics.

Génoplante is a partnership program between public French institutes (INRA, CIRAD, IRD and CNRS) and private companies (Biogemma, Bayer CropScience and Bioplante) that aims at developing genome analysis programs for crop species (corn, wheat, rapeseed, sunflower and pea) and model plants (Arabidopsis and rice). The outputs of these programs form a wealth of information (genomic sequence, transcriptome, proteome, allelic variability, mapping and synteny, and mutation data) and tools (databases, interfaces, analysis software), that are being integrated and made public at the public bioinformatics resource centre of Génoplante: GénoPlante-Info (GPI). This continuous flood of data and tools is regularly updated and will grow continuously during the coming two years. Access to the GPI databases and tools is available at http://genoplante-info.infobiogen.fr/.

Alleles↗

Genetic diversity of wild-type measles viruses: implications for global measles elimination programs.

Wild-type measles viruses have been divided into distinct genetic groups according to the nucleotide sequences of their hemagglutinin and nucleoprotein genes. Most genetic groups have worldwide distribution; however, at least two of the groups appear to have a more limited circulation. To monitor the transmission pathways of measles virus, we observed the geographic distribution of genetic groups, as well as changes in them in a particular region over time. We found evidence of interruption of indigenous transmission of measles in the United States after 1993 and identified the sources of imported virus associated with cases and outbreaks after 1993. The pattern of measles genetic groups provided a means to describe measles outbreaks and assess the extent of virus circulation in a given area. We expect that molecular epidemiologic studies will become a powerful tool for evaluating strategies to control, eliminate, and eventually eradicate measles.

Genetic Variation↗

Racial and ethnic variations in the prevalence of orofacial clefts in California, 1983-1992.

To investigate variations in the prevalence of oral cleft anomalies according to parental race and ethnicity and maternal country of birth, the authors analyzed a cohort of 2,221,755 live births and fetal deaths delivered between 1983 and 1992 to residents of California. A total of 2,329 cleft lip with or without cleft palate (CL +/- P) cases and 1,475 cleft palate alone (CP) cases were identified by the California Birth Defects Monitoring Program, a population-based registry. Compared to Whites, the prevalence of CL +/- P was lower among African Americans (prevalence ratio (PR) = 0.56, 95% confidence interval (CI) = 0.45-0.69), higher among Native Americans (PR = 1.81, CI = 1.20-2.69), and the same among the Japanese (PR = 1.07, CI = 0.62-1.82) and Chinese (PR = 0.96, CI = 0.71-1.29). The risk of CL +/- P was slightly lower among the offspring of foreign-born Chinese women relative to U.S.-born Chinese women (PR = 0.71, CI = 0.33-1.57), and slightly higher among foreign-born Filipinos relative to their U.S.-born counterparts (PR = 1.37, CI = 0.57-3.53), although confidence intervals around these risk estimates were wide owing to sparse data. For CP, lower prevalences were observed among African Americans (PR = 0.72, CI = 0.58-0.91) and Hispanics (PR = 0.77, CI = 0.67-0.87) than among Whites. The risk of CP was higher among foreign-born Filipinos compared to U.S.-born Filipinos (PR = 1.52, CI = 0.58-4.33), although the confidence interval around this estimate included unity. These prevalence variations may reflect differences in both environmental and genetic factors affecting clefting risk.

California↗

Lack of T cell dysfunction and programmed cell death in human immunodeficiency virus type 1-infected chimpanzees correlates with absence of monocytotropic variants.

In asymptomatic human immunodeficiency virus (HIV) infection in humans, disturbed T cell functions such as anergy and programmed cell death, thought to result from inappropriate signaling by antigen-presenting cells due to HIV infection, precede increase in virus load, decline in CD4+ T cell numbers, and subsequent disease progression. Here, in 3 long-term HIV-1-infected asymptomatic chimpanzees, antigen-presenting cell function was intact and T cells had normal proliferative capacity with no evidence of HIV-1-associated programmed cell death. Polymerase chain reaction analysis demonstrated low frequencies of cells harboring proviral DNA. Primary virus isolation from the infected animals demonstrated the absence of monocytotropic HIV-1 variants, in concordance with complete insusceptibility of chimpanzee monocytes for HIV-1 infection. Possibly, because of the incapacity of HIV-1 to infect monocytes, systemic immune dysfunction will not occur, contributing to controlled viral replication and maintenance of the asymptomatic state in HIV-infected chimpanzees.

Amino Acid Sequence↗

Genetic diversity among varieties and wild species accessions of pea (Pisum sativum L.) based on molecular markers, and morphological and physiological characters.

Random amplified polymorphic DNA, simple sequence repeat, and inter-simple sequence repeat markers were used to estimate the genetic relations among 65 pea varieties (Pisum sativum L.) and 21 accessions from wild Pisum subspecies (subsp.) abyssinicum, asiaticum, elatius, transcaucasicum, and var. arvense. Fifty-one of these varieties are currently available for growers in western Canada. Nei and Li's genetic similarity (GS) estimates calculated using the marker data showed that pair-wise comparison values among the 65 varieties ranged from 0.34 to 1.00. GS analysis on varieties grouped according to their originating breeding programs demonstrated that different levels of diversity were maintained at different breeding programs. Unweighted pair-group method arithmetic average cluster analysis and principal coordinate analysis on the marker-based GS grouped the cultivated varieties separately from the wild accessions. The majority of the food and feed varieties were grouped separately from the silage and specialty varieties, regardless of the originating breeding programs. The analysis also revealed some genetically distinct varieties such as Croma, CDC Handel, 1096M-8, and CDC Acer. The relations among the cultivated varieties, as revealed by molecular-marker-based GS, were not significantly correlated with those based on the agronomic characters, suggesting that the 2 systems give different estimates of genetic relations among the varieties. However, on a smaller scale, a consistent subcluster of genotypes was identified on the basis of agronomic characters and their marker-based GS. Furthermore, a number of variety-specific markers were identified in the current study, which could be useful for variety identification. Breeding strategies to maintain or enhance the genetic diversity of future varieties are proposed.

Genetic Markers↗

The abundance of short proteins in the mammalian proteome.

Short proteins play key roles in cell signalling and other processes, but their abundance in the mammalian proteome is unknown. Current catalogues of mammalian proteins exhibit an artefactual discontinuity at a length of 100 aa, so that protein abundance peaks just above this length and falls off sharply below it. To clarify the abundance of short proteins, we identify proteins in the FANTOM collection of mouse cDNAs by analysing synonymous and non-synonymous substitutions with the computer program CRITICA. This analysis confirms that there is no real discontinuity at length 100. Roughly 10% of mouse proteins are shorter than 100 aa, although the majority of these are variants of proteins longer than 100 aa. We identify many novel short proteins, including a "dark matter" subset containing ones that lack detectable homology to other known proteins. Translation assays confirm that some of these novel proteins can be translated and localised to the secretory pathway.

Amino Acid Sequence↗

Indel mutation in transcription factor PabHLH2 regulates amygdalin accumulation and kernel bitterness in apricot.

Amygdalin, the phytochemical responsible for the characteristic bitterness of apricot (Prunus armeniaca L.) kernels, also exhibits significant bioactive properties and therapeutic potential. Genetic regulation of amygdalin content is therefore a key objective in apricot breeding programs aimed at quality improvement. In this study, we conducted quantitative trait loci (QTL) mapping to uncover the genetic basis of sweet-bitter differentiation in apricot kernels. We identified a 15-bp insertion/deletion (indel) polymorphism strongly related to kernel bitterness, with marker validation achieving 100% concordance across 601 apricot germplasm accessions. Notably, this polymorphic site is located within the helix-loop-helix (HLH) domain of the basic HLH (bHLH) transcription factor PabHLH2. Protein interaction analyses revealed that the 15-bp deletion variant impaired dimerization capacity, reducing transcriptional activation of downstream targets. Using yeast one-hybrid screening and dual-luciferase reporter assays, we identified PaCYP71AN24 and PaCYP79D16 as direct transcriptional targets of PabHLH2. Functional characterization further indicated that the PabHLH2a variant (harboring the 15-bp insertion) significantly enhanced the promoter activity of these cytochrome P450 genes compared with the deletion variant. Transient overexpression and silencing experiments in apricot kernels further confirmed that the 15-bp insertion positively regulates both PaCYP71AN24/PaCYP79D16 expression and prunasin accumulation, the immediate biosynthetic precursor of amygdalin. Overall, these findings provide mechanistic insights into the allelic variation underlying kernel bitterness and delineate the molecular cascade of amygdalin biosynthesis. The identified molecular markers and functional characterization establish a basis for marker-assisted breeding of low-amygdalin apricot cultivars, supporting the dual-purpose utilization of kernels in food and pharmaceutical industries.

Amygdalin↗

Use of linear type and production data to supplement early predicted transmitting abilities for productive life.

Genetic evaluations for the length of productive life based on actual DHIA culling data have been available in the US since January 1994. Although substantial genetic variation in productive life exists, the reliability of selection is often low, particularly for recently progeny-tested bulls having daughters that have not yet had an opportunity to be culled. Correlated production and conformation traits, which have higher heritability than productive life and are available earlier in life, may be used to enhance evaluations of productive life for young bulls that have little or no direct culling information available. Genetic correlations between productive life and milk, fat, dairy form, and udder traits ranged from +0.22 to +0.46. The maximum reliability of the indirect prediction of productive life from 16 correlated type and production traits was 0.56, and the maximum reliability from a subset of 10 traits was 0.51. Indirect information about productive life that was derived from type and production traits was combined with actual culling information to increase the total amount of available information for many recently progeny-tested bulls. The procedures described herein for enhancing direct evaluations for the productive life of dairy sires with indirect information about production and type were implemented by the USDA Animal Improvement Programs Laboratory and the Holstein Association USA in July 1994.

Animals↗

Gene expression patterns in human liver cancers.

Hepatocellular carcinoma (HCC) is a leading cause of death worldwide. Using cDNA microarrays to characterize patterns of gene expression in HCC, we found consistent differences between the expression patterns in HCC compared with those seen in nontumor liver tissues. The expression patterns in HCC were also readily distinguished from those associated with tumors metastatic to liver. The global gene expression patterns intrinsic to each tumor were sufficiently distinctive that multiple tumor nodules from the same patient could usually be recognized and distinguished from all the others in the large sample set on the basis of their gene expression patterns alone. The distinctive gene expression patterns are characteristic of the tumors and not the patient; the expression programs seen in clonally independent tumor nodules in the same patient were no more similar than those in tumors from different patients. Moreover, clonally related tumor masses that showed distinct expression profiles were also distinguished by genotypic differences. Some features of the gene expression patterns were associated with specific phenotypic and genotypic characteristics of the tumors, including growth rate, vascular invasion, and p53 overexpression.

Carcinoma, Hepatocellular↗

Methodologic European external quality assurance for DNA sequencing: the EQUALseq program.

BACKGROUND: DNA sequencing is a key technique in molecular diagnostics, but to date no comprehensive methodologic external quality assessment (EQA) programs have been instituted. Between 2003 and 2005, the European Union funded, as specific support actions, the EQUAL initiative to develop methodologic EQA schemes for genotyping (EQUALqual), quantitative PCR (EQUALquant), and sequencing (EQUALseq). Here we report on the results of the EQUALseq program. METHODS: The participating laboratories received a 4-sample set comprising 2 DNA plasmids, a PCR product, and a finished sequencing reaction to be analyzed. Data and information from detailed questionnaires were uploaded online and evaluated by use of a scoring system for technical skills and proficiency of data interpretation. RESULTS: Sixty laboratories from 21 European countries registered, and 43 participants (72%) returned data and samples. Capillary electrophoresis was the predominant platform (n = 39; 91%). The median contiguous correct sequence stretch was 527 nucleotides with considerable variation in quality of both primary data and data evaluation. The association between laboratory performance and the number of sequencing assays/year was statistically significant (P <0.05). Interestingly, more than 30% of participants neither added comments to their data nor made efforts to identify the gene sequences or mutational positions. CONCLUSIONS: Considerable variations exist even in a highly standardized methodology such as DNA sequencing. Methodologic EQAs are appropriate tools to uncover strengths and weaknesses in both technique and proficiency, and our results emphasize the need for mandatory EQAs. The results of EQUALseq should help improve the overall quality of molecular genetics findings obtained by DNA sequencing.

European Union↗

Tissue transglutaminase and apoptosis: sense and antisense transfection studies with human neuroblastoma cells.

In this report, we show that the overexpression of tissue transglutaminase (tTG) in the human neuroblastoma cell line SK-N-BE(2) renders these neural crest-derived cells highly susceptible to death by apoptosis. Cells transfected with a full-length tTG cDNA, under the control of a constitutive promoter, show a drastic reduction in proliferative capacity paralleled by a large increase in cell death rate. The dying tTG-transfected cells exhibit both cytoplasmic and nuclear changes characteristic of cells undergoing apoptosis. The tTG-transfected cells express high Bcl-2 protein levels as well as phenotypic neural cell adhesion molecule markers (NCAM and neurofilaments) of cells differentiating along the neuronal pathway. In keeping with these findings, transfection of neuroblastoma cells with an expression vector containing segments of the human tTG cDNA in antisense orientation resulted in a pronounced decrease of both spontaneous and retinoic acid (RA)-induced apoptosis. We also present evidence that (i) the apoptotic program of these neuroectodermal cells is strictly regulated by RA and (ii) cell death by apoptosis in the human neuroblastoma SK-N-BE(2) cells preferentially occurs in the substrate-adherent phenotype. For the first time, we report here a direct effect of tTG in the phenotypic maturation toward apoptosis. These results indicate that the tTG-dependent irreversible cross-linking of intracellular protein represents an important biochemical event in the induction of the structural changes featuring cells dying by apoptosis.

Apoptosis↗

Adaptive changes to training in adipose tissue lipolysis are genotype dependent.

In order to study the effects of heredity and of physical training on adipose tissue morphology and metabolism, 15 pairs of monozygotic twins (MZ) (six males and nine females), aged from 16 to 24 years, weighing 56.2 +/- 9.1 kg and with 13.9 +/- 8.2 percent body fat, were submitted to a biopsy of adipose tissue in the suprailiac region. In addition, eight pairs of twins (four male and four female) took part in a 20-week ergocycle training program, five days a week, 40 min a day, at 80 percent of their maximal heart rate. Adipocyte diameter (AD) was assessed on collagenase isolated fat cells. Basal (BL), epinephrine submaximal (10(-5) M) (ESML) and epinephrine maximal stimulated lipolysis (10(-4) M) (EML) were determined on isolated fat cells. Intraclass correlation coefficients indicated significant intrapair resemblance before training for all fat morphological and metabolic indicators (0.78 less than or equal to ri less than or equal to 0.93). Training significantly increased VO2 max (pre: 44.7 +/- 7.6 (ml/kg) vs post: 50.8 +/- 5.0; P less than or equal to 0.001). No training effect was found in percent body fat and AD. Training significantly increased BL, ESML, and EML (P less than or equal to 0.01). Moreover, twins of the same MZ pair yielded identical responses in ESML and EML with training. Intraclass coefficients for the magnitude of change in activity over pretraining values reached 0.84 and 0.90 respectively. Apparently a genetically determined response to training could not be found for BL. These results show that training per se has an effect on adipose tissue lipolysis beyond variation in fatness. Furthermore, sensitivity of stimulated lipolysis to training appears to have a genetic basis.

Adipose Tissue↗

[Genetic factors in myocardial infarction--Results from a candidate gene and a genome-wide approach between beta blockers].

BACKGROUND: Coronary artery disease and myocardial infarction are the most frequent causes of death in the Western societies. Even nowadays, every second myocardial infarction is lethal and hits the patients unexpectedly without previous signs or symptoms. In order to install preventive measures most efficiently, it is necessary to have a detailed knowledge on the pathophysiology of the disease. The identification of patients who are at high risk for suffering from myocardial infarction can be done with epidemiological methods, such as the determination of "traditional" risk factors, like arterial hypertension, hypercholesterolemia, diabetes mellitus or smoking), or eventually in the future using molecular genetic testing. This is of great importance especially for asymptomatic siblings and children from myocardial infarction patients. POLYMORPHISMS: Although traditional risk factors occur frequently in families, they explain only in part the familial accumulation of coronary artery disease. Furthermore, stron genetic effects on the development of coronary artery disease and myocardial infarction have been demonstrated in several studies. These genetic effects can be examined by 1. a candidate gene approach, or 2. a systematic screening of the whole genome. In the first step, several polymorphisms (sequence variations) wee examined in several candidate genes in which a significant influence on a cardiovascular risk factor or intermediate phenotype (such as atherogeneic lipid profile or arterial hypertension) has been shown in the literature. We thus examined in a large population of patients with myocardial infarction and a sample of the general population the effects of the HindIII polymorphism in the lipoproteinlipase gene, of the -344T/C promoter polymorphism in the aldosterone synthase gene and of the 825C/T polymorphism in the gene of the beta3 subunit of the G protein gene (GNB3). In the general population, we could show an association with unfavorable lipid levels in men and in postmenopausal (but not premenopausal) women for the H2H2 genotype of the HindIII lipoproteinlipase polymorphism. However, the theoretical increase in risk for this genotype is not large enough to demonstrate a significant association with myocardial infarction in the population examined. With the promoter polymorphism in the aldosterone synthase gene, anthropometrical and echocardiographical data did not suggest that the polymorphism is a risk factor for myocardial infarction nor for left ventricular remodeling after myocardial infarction, which was observed in earlier studies. Furthermore, we could show an association with arterial hypertension in our general population sample with the polymorphism in the GNB3 gene. However, no association could be demonstrated for this polymorphism with myocardial infarction. AFFECTED SIB-PAIR APPROACH: In a systematic screening of the genome for genes that are relevant in the pathogenesis of coronary artery disease or myocardial infarction, an affected sib-pair approach was followed. 1,261 families were identified in which at least two brothers or sisters were affected with myocardial infarction or severe coronary artery disease, such as percutaneous coronary intervention or coronary after bypass grafting. In a subpopulation of 513 families and 1,407 individuals, we performed a total genome screening. The analyses using the variance component method and the SOLAR program revealed a susceptibility locus for myocardial infarction of chromosome 14q32 with a lod score of 3.89 (genome-wide p < 0.05). This locus comprises a region of about seven centi-Morgan and contains approximately 150 genes. Furthermore, a comprehensive analysis including the cardiovascular risk factors showed that 1. this myocardial infarction locus is unique and does not overlap with chromosomal loci for well-established risk factors, 2. cardiovascular risk factors, such as Lp(a), diabetes mellitus, serum lipids, or arterial hypertension have strong genetic components. CONCLUSION: These findings do not exclude a role of cardiovascular s do not exclude a role of cardiovascular risk factors or candidate genes in the pathogenesis of myocardial infarction, but rather demonstrate that risk factors may act as surrogates of specific underlying disease mechanisms. It is thus necessary to perform a comprehensive analysis of complex polygenic diseases, such as myocardial infarction, including both, established cardiovascular risk factors and genomic data.

Adrenergic beta-Antagonists↗

Conservation and diversity of HMW1 and HMW2 adhesin binding domains among invasive nontypeable Haemophilus influenzae isolates.

The pathogenesis of nontypeable Haemophilus influenzae (NTHi) begins with adhesion to the rhinopharyngeal mucosa. In almost 80% of NTHi clinical isolates, the HMW proteins are the major adhesins. The prototype HMW1 and HMW2 proteins, identified in NTHi strain 12, exhibit different binding specificities. The two binding domains have been localized in regions of maximal sequence dissimilarity (40% identity, 58% similarity). Two areas within these binding domains have been found essential for full level adhesive activity (designated the core-binding domains). To investigate the conservation and diversity of the HMW1 and HMW2 core-binding domains among isolates, PCR and DNA sequencing were used. First, we separately amplified the hmw1A-like and hmw2A-like structural genes in nine invasive NTHi isolates, discovering two new hmwA alleles, whose sequences are herein reported. Then, the hmw1A-like and hmw2A-like PCR products were used as the template in nested PCR to produce amplicons encompassing the encoding sequences of the two core-binding domains. In-depth sequence analysis was then performed among sequences of each group, with the support of specific computer programs. Overall, extensive sequence diversity among isolates was highlighted. However, similarity plots showed patterns consisting of peaks of relatively high similarity alternating with strongly divergent regions. The phylogenetic tree clearly indicated the HMW1-like and HMW2-like core-binding domain sequences as two clusters. Distinct sets of conserved amino acid motifs were identified within each group of sequences using the MEME/MOTIFSEARCH tool. Since HMW adhesins could represent candidates for future vaccines, identification of specific patterns of conserved motifs in otherwise highly variable regions is of great interest.

Adhesins, Bacterial↗

Programmed transcription of the var gene family, but not of stevor, in Plasmodium falciparum gametocytes.

The var genes encode Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) proteins, a set of highly diverse surface-expressed proteins that mediate adhesion of erythrocytes infected with asexual blood-stage parasites to host endothelium. Switching among expressed PfEMP1 variants in the course of a blood-stage infection is a key component of antigenic variation, and thus immune evasion, by the parasite. The majority of var loci are found in the subtelomeric regions of P. falciparum chromosomes associated with members of other multigene families, including stevor. Both PfEMP1 and STEVOR are expressed in gametocytes, the transmissible parasite stage, but the role of these proteins in the biology of sexual-stage parasites remains unknown. PfEMP1 may continue to mediate antigenic variation in gametocytes, which need to persist in the host for many days before reaching maturity. Using quantitative reverse transcription-PCR and Northern hybridization, we demonstrate that transcription of a defined subset of type C var loci occurs during gametocyte development in vitro. This transcriptional program occurs in gametocytes regardless of the var expression phenotype of their asexual progenitors and therefore is subject to regulatory processes distinct from those that manage antigenic variation in the asexual parasite. In contrast, the same stevor variants are transcribed in both gametocytes and their asexual progenitors. We also provide evidence that for both asexual parasites and gametocytes, var and stevor transcription patterns are not linked to each other.

Animals↗

[International Workshop on Molecular Epidemiology. Proposals of the Interdisciplinary Group on American Trypanosomiasis and Leishmaniasis].

Parasite diseases such as Leishmaniases and American Trypanosomiases have been increasingly important in Mexico and other countries of the American Region. In known areas, these diseases are highly endemic, and in recently opened developing areas became a new threat to public health. Some social groups working in natural resources exploitation, agriculture, animal stock and public labor are particularly affected. The molecular epidemiology approach to these diseases is linking valuable capabilities and resources within the academic and operational institutions actual working in genetic polymorphism, strain characterization and PRC identification of Trypanosoma and Leishmania parasites. Clinical and epidemiological aspects of American trypanosomiasis infections and Chagas's disease and of cutaneous, mucocutaneous, disseminated and visceral leishmaniases, as well as genetic susceptibility studies have been initiated by Mexican scientists. In order to organize and coordinate the molecular epidemiology activities and support effective prevention and control programs against these diseases, political decision from the health, and academic authorities is urgently needed to adopt and support the research strategy for typing Trypanosoma and Leishmania species through exposition and biological markers (analysis of chromosomal DNA, ribosomal genes restriction patterns, DNA sequence, and DNA plasmids); the study of the membrane proteins and isoenzymes and monoclonal antibodies; detecting antigens and nucleic acids; defining susceptibility to infection with genetic markers, and searching for species, variants and mutant strains responsible for high virulence. The support for the establishment of a Reference Center for identification, cryopreservation and registration of parasites, vectors and reservoires is of paramount importance.

Animals↗

Application of mathematical tools for metabolic design of microbial ethanol production.

Many attempts to engineer cellular metabolism have failed due to the complexity of cellular functions. Mathematical and computational methods are needed that can organize the available experimental information, and provide insight and guidance for successful metabolic engineering. Two such methods are reviewed here. Both methods employ a (log)linear kinetic model of metabolism that is constructed based on enzyme kinetics characteristics. The first method allows the description of the dynamic responses of metabolic systems subject to spatiotemporal variations in their parameters. The second method considers the product-oriented, constrained optimization of metabolic reaction networks using mixed-integer linear programming methods. The optimization framework is used in order to identify the combinations of the metabolic characteristics of the glycolytic enzymes from yeast and bacteria that will maximize ethanol production. The methods are also applied to the design of microbial ethanol production metabolism. The results of the calculations are in qualitative agreement with experimental data presented here. Experiments and calculations suggest that, in resting Escherichia coli cells, ethanol production and glucose uptake rates can be increased by 30% and 20%, respectively, by overexpression of a deregulated pyruvate kinase, while increase in phosphofructokinase expression levels has no effect on ethanol production and glucose uptake rates.

Bacteriological Techniques↗

Population genetics of Plasmodium falciparum within a malaria hyperendemic area.

Serotyping with monoclonal antibodies was used to estimate the number and frequencies of allelic variants of two merozoite surface proteins, MSP1 and MSP2, and an exported protein Exp-1, in a sample of 344 clinical isolates of Plasmodium falciparum from an urban region of The Gambia. Represented among the isolates were 36, 8 and 2 alleles of the MSP1, MSP2 and Exp-1 loci respectively. Relative frequencies of these alleles remained stable in the parasite population over the 2 years of the study. A computer program was used to calculate from the frequencies of individual alleles at the three loci, the probable number of different genotypes in samples from the population, assuming random assortment among the loci. No significant difference was found between the expected and the observed genotype diversity. It is concluded that recombination among unlinked loci is a common consequence of sexual reproduction of P. falciparum in The Gambia. Slightly lower genotype diversity was observed in each of two villages, which may be a consequence of smaller population size compared with the urban region.

Alleles↗