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PubMed2001

The neuroendocrine regulation of the human ovarian cycle.

The menstrual cycle is now thought to be mainly determined by the ovary itself, which sends various signals to the pituitary and the hypothalamus. The hypothalamus is an autonomous pacemaker, with a pulse frequency that is modulated by ovarian signals; in turn, it is indispensable to ovarian function. In women, the ovarian cycle produces a single mature oocyte each month from puberty to menopause. This follicle is rescued from atresia, the genetically controlled ovarian apoptosis (or "programmed cell death"), involving 99.9% of the follicles. Follicular growth and maturation are mostly independent of gonadotropins from the stage of primordial to antral follicles. A complete intraovarian paracrine system is implied in this gonadotropin-independent follicular growth and in the modulation of the action of gonadotropins in the ovary. Follicle-stimulating hormone (FSH) allows the rescue of a minority of follicles from atresia and is indispensable only for the final maturation of the preovulatory follicle during the follicular phase of the cycle. Luteinizing hormone (LH) is responsible for the final growth of the dominant follicle in the late follicular phase. the induction of ovulation during the LH peak, and the survival of the corpus luteum during the luteal phase. The cyclical variations of gonadotropins are under the control of ovarian steroids (estradiol and progesterone) and peptides (inhibins). The cycle length is determined by the duration of terminal follicular growth and by the fixed life span of the corpus luteum. The ovarian cycle can be monitored as well at the level of target tissues of steroids, such as the endometrium. In fact, the endometrial maturation is synchronized to follicular development, and this synchronization is indispensable for successful implantation of the embryo. The improving knowledge of follicular and endometrial physiology will allow the development of new treatments of infertility, the design of new contraceptive techniques, and a better tolerance of treatments using sex steroids.

Biological Clocks↗
PubMedDate not supplied

The sperm chromatin dispersion test: a simple method for the determination of sperm DNA fragmentation.

Sperm DNA fragmentation is being increasingly recognized as an important cause of infertility. We herein describe the Sperm Chromatin Dispersion (SCD) test, a novel assay for sperm DNA fragmentation in semen. The SCD test is based on the principle that sperm with fragmented DNA fail to produce the characteristic halo of dispersed DNA loops that is observed in sperm with non-fragmented DNA, following acid denaturation and removal of nuclear proteins. This was confirmed by the analysis of DNA fragmentation using the specific DNA Breakage Detection-Fluorescence In Situ Hybridization (DBD-FISH) assay, which allows the detection of DNA breaks in lysed sperm nuclei. Sperm suspensions either prepared from semen or isolated from semen by gradient centrifugation were embedded in an agarose microgel on slides and treated with 0.08 N HCl and lysing solutions containing 0.8 M dithiothreitol (DTT), 1% sodium dodecyl sulfate (SDS), and 2 M NaCl. Then, the slides were sequentially stained with DAPI (4',6-diamidino-2-phenylindole) and/or the Diff-Quik reagent, and the percentages of sperm with nondispersed and dispersed chromatin loops were monitored by fluorescence and brightfield microscopy, respectively. The results indicate that all sperm with nondispersed chromatin displayed DNA fragmentation, as measured by DBD-FISH. Conversely, all sperm with dispersed chromatin had very low to undetectable DBD-FISH labeling. SCD test values were significantly higher in patients being screened for infertility than in normozoospermic sperm donors who had participated in a donor insemination program. The coefficient of variation obtained using 2 different observers, either by digital image analysis (DIA) or by brightfield microscopy scoring, was less than 3%. In conclusion, the SCD test is a simple, accurate, highly reproducible, and inexpensive method for the analysis of sperm DNA fragmentation in semen and processed sperm. Therefore, the SCD test could potentially be used as a routine test for the screening of sperm DNA fragmentation in the andrology laboratory.

Acids↗
PubMed2002

Variation in the fatty acid binding protein 2 gene is not associated with markers of metabolic syndrome in patients with coronary heart disease.

BACKGROUND AND AIM: It has been suggested that the threonine (Thr) 54 allele of the intestinal fatty acid binding protein 2 (FABP2) gene is associated with insulin resistance and affects the fatty acid composition of serum lipids. Our aim was to investigate the frequency of the alanine (Ala) 54Thr polymorphism of the FABP2 gene in patients with coronary heart disease (CHD), and the association between the polymorphism and the markers of metabolic syndrome, serum lipid levels and the fatty acid profile of serum lipids. METHODS AND RESULTS: A total of 414 CHD patients (mean age 61 years, range 33-74) participated in the cross-sectional EUROASPIRE (European Action on Secondary Prevention through Intervention to Reduce Events) Study. Markers of metabolic syndrome included fasting plasma glucose concentration, serum high-density lipoprotein cholesterol and triglycerides (TG), waist circumference, the waist/hip ratio, body mass index (BMI) and blood pressure (BP). The frequency of the Thr54 allele was similar in the CHD patients (27.2%) and control subjects from two independent studies (27.8% and 28.7%). There were no significant differences in plasma glucose, serum lipids, BP, BMI, waist circumference or waist/hip ratio among the genotypes. Genotype frequency was not associated with the prevalence of diabetes or metabolic syndrome, but metabolic syndrome (as defined by National Cholesterol Education Program criteria) tended to be more frequent in subjects with the Thr/Thr genotype (p = 0.095). There were no differences in the fatty acid profiles of serum cholesteryl esters, TG or phospholipids among the genotypes. CONCLUSIONS: The Ala54Thr polymorphism of the FABP2 gene is not associated with CHD, markers of the metabolic syndrome, or the fatty acid profile of serum lipids in Finnish CHD patients.

Adult↗
PubMed2002

Genetics of resistance to anthracnose and identification of AFLP and RAPD markers linked to the resistance gene in PI 320937 germplasm of lentil (Lens culinaris Medikus).

Anthracnose, caused by Colletotrichum truncatum, is a major disease problem and production constraint of lentil in North America. The research was conducted to examine the resistance to anthracnose in PI 320937 lentil and to identify molecular markers linked to the resistance gene in a recombinant inbred line (RIL) population developed from a cross of Eston lentil, the susceptible parent, and PI 320937, the resistant parent. A total of 147 F(5:6) RILs were evaluated for resistance to anthracnose in the greenhouse using isolate 95B36 of C. truncatum. Bulked segregant analysis (BSA) strategy was employed and two contrasting DNA bulks were constructed based on greenhouse inoculation of F(5)-derived F(6) RILs. DNA from the parents and bulks were screened with 700 RAPD primers and seven AFLP primer combinations. Analysis of segregation data indicated that a major dominant gene was responsible for resistance to anthracnose while variations in the resistance level among RILs could be the influences of minor genes. We designate the major gene as LCt-2. MapMaker analysis produced two flanking RAPD markers OPEO6(1250) and UBC-704(700) linked to LCt-2 locus in repulsion (6.4 cM) and in coupling (10.5 cM), respectively. Also, three AFLP markers, EMCTTACA(350) and EMCTTAGG(375) in coupling, and EMCTAAAG(175) in repulsion, were linked to the LCt-2 locus. These markers could be used to tag the LCt-2 locus and facilitate marker-assisted selection for resistance to anthracnose in segregating populations of lentil in which PI 320937 was used as the source of resistance. Also, a broader application of the linked RAPD markers was also demonstrated in Indianhead lentil, widely used as a source of resistance to anthracnose in the breeding program at the Crop Development Centre, University of Saskatchewan. Further selection within the few F(5:6) lines should be effective in pyramiding one or several of the minor genes into the working germplasm of lentil, resulting in a more durable and higher level of resistance.

Chromosome Segregation↗
PubMed2003

Quantitative trait loci for lodging resistance, plant height and partial resistance to mycosphaerella blight in field pea (Pisum sativum L.).

With the development of genetic maps and the identification of the most-likely positions of quantitative trait loci (QTLs) on these maps, molecular markers for lodging resistance can be identified. Consequently, marker-assisted selection (MAS) has the potential to improve the efficiency of selection for lodging resistance in a breeding program. This study was conducted to identify genetic loci associated with lodging resistance, plant height and reaction to mycosphaerella blight in pea. A population consisting of 88 recombinant inbred lines (RILs) was developed from a cross between Carneval and MP1401. The RILs were evaluated in 11 environments across the provinces of Manitoba, Saskatchewan and Alberta, Canada in 1998, 1999 and 2000. One hundred and ninety two amplified fragment length polymorphism (AFLP) markers, 13 random amplified polymorphic DNA (RAPD) markers and one sequence tagged site (STS) marker were assigned to ten linkage groups (LGs) that covered 1,274 centi Morgans (cM) of the pea genome. Six of these LGs were aligned with the previous pea map. Two QTLs were identified for lodging resistance that collectively explained 58% of the total phenotypic variation in the mean environment. Three QTLs were identified each for plant height and resistance to mycosphaerella blight, which accounted for 65% and 36% of the total phenotypic variation, respectively, in the mean environment. These QTLs were relatively consistent across environments. The AFLP marker that was associated with the major locus for lodging resistance was converted into the sequence-characterized amplified-region (SCAR) marker. The presence or absence of the SCAR marker corresponded well with the lodging reaction of 50 commercial pea varieties.

Ascomycota↗
PubMed2001

Biochemical and morphological changes in herniated human intervertebral disc.

The molecular and morphologic features of herniated human intervertebral disc tissues are of particular importance to clarify the pathogenesis. The present study analyzed the biochemical and morphological features of herniated intervertebral disc tissues to determine the constituent factors responsible for intervertebral disc herniation. A total of 32 herniated disc specimens and 4 control disc samples were analyzed. Collagen subunit composition, collagenase activity, lipid peroxidation level, caspase-3 activity, metal levels, morphologic studies, and genetic analysis were performed on herniated disc tissues of chronic (group A) and acute (group B) group and compared with findings of control group. Nick translation analysis in situ revealed apoptotic-positive stained DNA fragments as black-brown spots in herniated disc tissues. The presence of type II collagen in control disc samples and its absence in herniated samples were confirmed immunohistochemically. The increased caspase-3 activity, the apoptotic-positive stained DNA fragments, and the electron microscopic findings suggest enhanced programmed cell death in herniated discs. The significant increase in lipid peroxidation levels and collagenase activity, and the low metal levels suggest the enhancement of cell death signals in herniated discs, caused by oxygen stress. Linkage analysis of herniated disc tissues in Japanese individuals may suggest ethnic variation. These findings may be helpful in understanding the pathogenesis of herniated disc disease.

Adolescent↗
PubMed2004

Effects of long-term negative energy balance with exercise on plasma lipid and lipoprotein levels in identical twins.

Plasma lipid and lipoprotein concentrations were measured before and after a 58,000kcal (244MJ) negative energy balance protocol induced entirely by supervised endurance exercise over a 93-day period in seven pairs of young sedentary and healthy male monozygotic twins. The negative energy balance induced significant changes in all measures of body weight and composition except fat free mass. The mean weight loss was 5.0+/-0.6kg, and it was entirely accounted for by the loss of body fat. In response to the program, improvement in the plasma lipid profile was seen including decreases in plasma total (P=0.028) and low density lipoprotein (LDL) (P=0.004) cholesterol; total cholesterol/high density lipoprotein (HDL) cholesterol ratio (P=0.002); and HDL apolipoprotein A-I concentration (P=0.062). Statistically significant within-pair resemblance was found for the changes in total and very low density lipoprotein (VLDL) cholesterol; total, VLDL and LDL triglycerides, and total, VLDL and LDL apolipoprotein B. The findings suggest that favorable changes in the lipid profile can be obtained through chronic negative energy balance achieved by clamping daily energy intake and adding daily moderate intensity exercise even in persons with relatively normal lipid levels at baseline. Furthermore, within-pair resemblance among twin brothers strongly suggests that genetic differences partially account for the variation in the response of lipids and lipoproteins to the negative energy balance protocol.

Adolescent↗
PubMed2005

Integrative genetic analysis of transcription modules: towards filling the gap between genetic loci and inherited traits.

Genetic loci that regulate inherited traits are routinely identified using quantitative trait locus (QTL) mapping methods. However, the genotype-phenotype associations do not provide information on the gene expression program through which the genetic loci regulate the traits. Transcription modules are 'self-consistent regulatory units' and are closely related to the modular components of gene regulatory network [Ihmels, J., Friedlander, G., Bergmann, S., Sarig, O., Ziv, Y. and Barkai, N. (2002) Revealing modular organization in the yeast transcriptional network. Nat. Genet., 31, 370-377; Segal, E., Shapira, M., Regev, A., Pe'er, D., Botstein, D., Koller, D. and Friedman, N. (2003) Module networks: identifying regulatory modules and their condition-specific regulators from gene expression data. Nat. Genet., 34, 166-176]. We used genome-wide genotype and gene expression data of a genetic reference population that consists of mice of 32 recombinant inbred strains to identify the transcription modules and the genetic loci regulating them. Twenty-nine transcription modules defined by genetic variations were identified. Statistically significant associations between the transcription modules and 18 classical physiological and behavioral traits were found. Genome-wide interval mapping showed that major QTLs regulating the transcription modules are often co-localized with the QTLs regulating the associated classical traits. The association and the possible co-regulation of the classical trait and transcription module indicate that the transcription module may be involved in the gene pathways connecting the QTL and the classical trait. Our results show that a transcription module may associate with multiple seemingly unrelated classical traits and a classical trait may associate with different modules. Literature mining results provided strong independent evidences for the relations among genes of the transcription modules, genes in the regions of the QTLs regulating the transcription modules and the keywords representing the classical traits.

Animals↗
PubMed2006

The use of capillary blood samples in a large scale screening approach for the detection of beta-thalassemia and hemoglobin variants.

Hemoglobinopathies are priority genetic diseases for prevention programs in at-risk populations. We implemented an accurate and simple methodology to identify hemoglobin (Hb) variants and to quantify HbA2 and HbF in capillary blood samples stored at room temperature for up to 7 days after collection. This methodology is particularly indicated for screening for carriers in primary care medical centers in which facilities for collecting venous blood are not available.

Capillaries↗
PubMed1988

Dyslexia subtypes: genetics, behavior, and brain imaging.

This study was designed to identify inherited subtypes of specific dyslexia and to characterize these types by a variety of studies. A previous linkage study in large three-generation families resulted in a LOD score of 3.24 at a 13% recombination frequency between dyslexia and normal variations for the short arm of chromosome 15. The odds for linkage with chromosome 15 markers are better than 1,000 to 1. We estimate that 30% of an extended series of families show linkage to chromosome 15 polymorphisms. Other linkages remain to be identified. PET scanning is being used to examine measures of regional cerebral glucose metabolism during two types of reading by (adult) dyslexics and normal readers. MRI is also being used to examine pertinent brain structures. Behavioral tests are also in progress. The long-term goals of this study are to develop specific genetic and other diagnostic techniques that can be used to test children before beginning school and to develop sufficient understanding of the abnormal brain function of each subtype so that specific and effective remedial programs can be developed.

Brain↗
PubMed2003

Improving the Arabidopsis genome annotation using maximal transcript alignment assemblies.

The spliced alignment of expressed sequence data to genomic sequence has proven a key tool in the comprehensive annotation of genes in eukaryotic genomes. A novel algorithm was developed to assemble clusters of overlapping transcript alignments (ESTs and full-length cDNAs) into maximal alignment assemblies, thereby comprehensively incorporating all available transcript data and capturing subtle splicing variations. Complete and partial gene structures identified by this method were used to improve The Institute for Genomic Research Arabidopsis genome annotation (TIGR release v.4.0). The alignment assemblies permitted the automated modeling of several novel genes and >1000 alternative splicing variations as well as updates (including UTR annotations) to nearly half of the approximately 27 000 annotated protein coding genes. The algorithm of the Program to Assemble Spliced Alignments (PASA) tool is described, as well as the results of automated updates to Arabidopsis gene annotations.

Algorithms↗
PubMed1991

Genetic and environmental modulations of chromosomal stability: their roles in aging and oncogenesis.

The primary objective of this review is to suggest a major role of cytogenetic pathology in the genesis of both the neoplastic phenotype and the senescent phenotype of aging mammalian organisms. It is hypothesized that allelic variation at a number of genetic loci that have the potential to modulate various types of chromosomal mutation could account, in part, for species-specific variations in maximum life-span potentials and the times of onset of characteristic age-related neoplasms. As a corollary to this proposition, attention is directed to the potential importance of environmental clastogens and aneugens as both oncogenic and "gerontogenic" agents. By way of introduction, a series of definitions of our subject material is given (aging, oncogenesis, proliferative homeostasis, point mutation, chromosomal mutation, epimutation, mutagens, clastogens, aneugens, gerontogens). There follows a defense of the view that there is a tight coupling of abnormalities in proliferative homeostasis (including atrophies, hyperplasias, benign neoplasias and malignant neoplasias) with intrinsic biological aging. This view differs from those of other authors who either: 1) believe that, to qualify as a bona fide component of aging, the phenotype in question (in this case, neoplasia) must be "genetically programmed" or 2) insist that the rate of development of the neoplastic phenotype should parallel species-specific Gompertz kinetics for the survival of the population of organisms. After briefly reviewing the classification of chromosomal lesions, we consider evidence for constitutional genetic determinants of chromosomal stability, oncogenesis, and some other aspects of the senescent phenotype, both with respect to interspecific and intraspecific differences. The discussion will include the recent evidence characterizing a human segmental progeroid syndrome (Werner's syndrome) as a deletor mutator strain. A summary of research on environmental chemical clastogens and aneugens is given, showing both discordances and concordances of such assays with assays for point mutagens. An analysis of the literature indicates that there is no statistical evidence for the positive correlations when substances showing effects only at comparatively high concentrations (greater than 1 mM) are excluded from the analysis. Brief mention is also made of the roles of viral agents and ionizing radiation in the genesis of chromosomal mutations. Finally, some possible pathogenetic mechanisms common to chromosomal mutagenicity, oncogenicity and gerontogenicity are considered, including chemical free radicals (active oxygen species), DNA transposition, DNA amplification, DNA glycation, virally induced cell fusion, posttranslational modifications of centromeric and mitotic spindle proteins, and alterations in the metabolism of telomeric DNA.

Aging↗
PubMed2006

The sorry state of F2 hybrids: consequences of rapid mitochondrial DNA evolution in allopatric populations.

Through the processes of natural selection and genetic drift, allopatric populations diverge genetically and may ultimately become reproductively incompatible. In cases of prezygotic reproductive isolation, candidate systems for speciation genes logically include genes involved in mate or gamete recognition. However, where only postzygotic isolation exists, candidate speciation genes could include any genes that affect hybrid performance. We hypothesize that because mitochondrial genes frequently evolve more rapidly than the nuclear genes with which they interact, interpopulation hybridization might be particularly disruptive to mitochondrial function. Understanding the potential impact of intergenomic (nuclear and mitochondrial) coadaptation on the evolution of allopatric populations of the intertidal copepod Tigriopus californicus has required a broadly integrative research program; here we present the results of experiments spanning the spectrum of biological organization in order to demonstrate the consequences of molecular evolution on physiological performance and organismal fitness. We suggest that disruption of mitochondrial function, known to result in a diverse set of human diseases, may frequently underlie reduced fitness in interpopulation and interspecies hybrids in animals.

Animals↗
PubMed2003

Fugu ESTs: new resources for transcription analysis and genome annotation.

The draft Fugu rubripes genome was released in 2002, at which time relatively few cDNAs were available to aid in the annotation of genes. The data presented here describe the sequencing and analysis of 24,398 expressed sequence tags (ESTs) generated from 15 different adult and juvenile Fugu tissues, 74% of which matched protein database entries. Analysis of the EST data compared with the Fugu genome data predicts that approximately 10,116 gene tags have been generated, covering almost one-third of Fugu predicted genes. This represents a remarkable economy of effort. Comparison with the Washington University zebrafish EST assemblies indicates strong conservation within fish species, but significant differences remain. This potentially represents divergence of sequence in the 5' terminal exons and UTRs between these two fish species, although clearly, complete EST data sets are not available for either species. This project provides new Fugu resources, and the analysis adds significant weight to the argument that EST programs remain an essential resource for genome exploitation and annotation. This is particularly timely with the increasing availability of draft genome sequence from different organisms and the mounting emphasis on gene function and regulation.

Animals↗
PubMed1992

Lymphocytotoxic strains of feline leukemia virus induce apoptosis in feline T4-thymic lymphoma cells.

Feline leukemia retrovirus (FeLV) strains with subgroup C env genes kill feline T4 lymphoma 3201 cells by 7 to 12 days after in vitro inoculation, whereas FeLV strains with subgroup A env genes do not. Neither FeLV-A nor FeLV-C kill feline fibroblasts. FeLV-C, but not FeLV-A, is replicated to higher titer by 3201 cells and productive infection precedes death by 3 to 7 days. Transcriptional activity of the FeLV-C long terminal repeat, as assessed by chloramphenicol acetyltransferase activity, is high in feline lymphoid cells but low in feline fibroblasts. Activity of the FeLV-A long terminal repeat is moderate in both cell types. FeLV-C-infected cells form aggregates 1 to 4 days before dying; ultrastructurally, virus particles can be seen approximating the clustered cells. Dying cells demonstrate nuclear condensation, surface blebbing, and fragmentation. DNA fragmentation and laddering compatible with apoptosis occur 1 to 2 days before massive cell death. In FeLV-C-infected 3201 cells, a shift from phospholipid to neutral lipid incorporation of [14C]oleic acid, increases in palmitic acid proportions and decreases in linoleic acid proportions occur 1 to 2 days before peak killing. Exposure of 3201 cells to ultraviolet-inactivated FeLV-KT (200-800 micrograms/10(6) cells) causes cytostasis within 2 days and death within 4 days. Blebbing and nuclear condensation occur but clusters do not form. The induction of programmed cell death in feline thymic lymphoma cells by subgroup C feline retroviruses may be relevant to the pathogenesis of FeLV-induced thymic atrophy, paracortical lymphoid depletion and acquired immunodeficiency in vivo.

Animals↗
PubMed1979

[Genetic program aid thanatogenesis].

The paper develops the thesis on the association between the genetic pattern of the organism, the nature of its diseases and the mode of its dying. Four variants of relationships between the gentic and environmental factors are discussed and in each of them the importance of these factors in tanatogenesis is evaluated. The arguments are presented in favour of the concept that genetic pattern of the organism is the most essential inner cause of the diseases and the death in the majority of cases except the situations in which extreme environmental factors are involved.

Accidents↗
PubMed1984

Analysis of variability in albumin content of sister hepatoma cells and a model for geometric phenotypic variability (quantitative shift model).

A model (quantitative shift model) is presented that can account for the phenomenon termed geometric phenotypic variability in which quantitative variation occurs along a square root 2-fold geometric series. The model is based on data for variability in albumin content in hepatoma cells and has three basic assumptions: (i) The albumin genes on each chromosome are active and under independent quantitative regulation. (ii) The rate of albumin gene transcription per cell is the sum of the rates of transcription of the genes of each chromosome. (iii) The mechanism that controls the rate of transcription is highly variable so that at each cell cycle there is a high probability (P = 0.1-0.3) that on the newly synthesized chromatid the rate of transcription of the albumin gene will be different from that of the old chromatid. However, if the rate is different, it will usually be either half or twice the levels of the old chromatid. A computer program was developed based on the model that can generate quantitative diversity in single cells that mimics the pattern of variability in albumin content between sister hepatoma cells, among cells in clonal colonies, and in cell populations where the periodicities in single-cell distributions are compared by Fourier transform analysis. It was determined that the rate of phenotypic variability is indirectly proportional to the magnitude of the quantitative shift in albumin content and that it can be as high as 0.3 per cell per generation. Also, the square root 2 factor in geometric phenotypic variability appears to be an average of a family of values and not the actual value of the smallest quantal shift.

Animals↗
PubMed2006

Evidence for a large-scale population structure of Arabidopsis thaliana from genome-wide single nucleotide polymorphism markers.

Population-based methods for the genetic mapping of adaptive traits and the analysis of natural selection require that the population structure and demographic history of a species are taken into account. We characterized geographic patterns of genetic variation in the model plant Arabidopsis thaliana by genotyping 115 genome-wide single nucleotide polymorphism (SNP) markers in 351 accessions from the whole species range using a matrix-assisted laser desorption/ionization time-of-flight assay, and by sequencing of nine unlinked short genomic regions in a subset of 64 accessions. The observed frequency distribution of SNPs is not consistent with a constant-size neutral model of sequence polymorphism due to an excess of rare polymorphisms. There is evidence for a significant population structure as indicated by differences in genetic diversity between geographic regions. Accessions from Central Asia have a low level of polymorphism and an increased level of genome-wide linkage disequilibrium (LD) relative to accessions from the Iberian Peninsula and Central Europe. Cluster analysis with the structure program grouped Eurasian accessions into K = 6 clusters. Accessions from the Iberian Peninsula and from Central Asia constitute distinct populations, whereas Central and Eastern European accessions represent admixed populations in which genomes were reshuffled by historical recombination events. These patterns likely result from a rapid postglacial recolonization of Eurasia from glacial refugial populations. Our analyses suggest that mapping populations for association or LD mapping should be chosen from regional rather than a species-wide sample or identified genetically as sets of individuals with similar average genetic distances.

Arabidopsis↗