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PubMed2003

Congenic strains of mice for verification and genetic decomposition of quantitative trait loci for femoral bone mineral density.

Peak femoral volumetric bone mineral density (femoral bone mineral density) in C57BL/6J (B6) 4-month-old female mice is 50% lower than in C3H/HeJ (C3H) and 34% lower than in CAST/EiJ (CAST) females. Genome-wide analyses of (B6 x C3H)F2 and (B6 x CAST)F2 4-month-old female progeny demonstrated that peak femoral bone mineral density is a complex quantitative trait associated with genetic loci (QTL) on numerous chromosomes (Chrs) and with trait heritabilities of 83% (C3H) and 57% (CAST). To test the effect of each QTL on femoral bone mineral density, two sets of loci (six each from C3H and CAST) were selected to make congenic strains by repeated backcrossing of donor mice carrying a given QTL-containing chromosomal region to recipient mice of the B6 progenitor strain. At the N6F1 generation, each B6.C3H and B6.CAST congenic strain (statistically 98% B6-like in genomic composition) was intercrossed to obtain N6F2 progeny for testing the effect of each QTL on femoral bone mineral density. In addition, the femoral bone mineral density QTL region on Chr 1 of C3H was selected for congenic subline development to facilitate fine mapping of this strong femoral bone mineral density locus. In 11 of 12 congenic strains, 6 B6.C3H and 5 B6.CAST, femoral bone mineral density in mice carrying c3h or cast alleles in the QTL regions was significantly different from that of littermates carrying b6 alleles. Differences also were observed in body weight, femoral length, and mid-diaphyseal periosteal circumference among these 11 congenic strains when compared with control littermates; however, these latter three phenotypes were not consistently correlated with femoral bone mineral density. Analyses of eight sublines derived from the B6.C3H-1T congenic region revealed two QTLs: one located between 36.9 and 49.7 centiMorgans (cM) and the other located between 73.2 and 100.0 cM distal to the centromere. In conclusion, these congenic strains provide proof of principle that many QTLs identified in the F2 analyses for femoral bone mineral density exert independent effects when transferred and expressed in a common genetic background. Furthermore, significant differences in femoral bone mineral density among the congenic strains were not consistently accompanied by changes in body weight, femur length, or periosteal circumference. Finally, decomposition of QTL regions by congenic sublines can reveal additional loci for phenotypes assigned to a QTL region and can markedly refine genomic locations of quantitative trait loci, providing the opportunity for candidate gene testing.

Alleles↗
PubMed2001

Familial aggregation of anxiety-related quantitative traits in generalized social phobia: clues to understanding "disorder" heritability?

Social phobia, particularly the generalized form, is strongly familial. Given the probable continuity from extremes of normative personality (e.g., shyness) to social phobia to personality disorder (e.g., avoidant personality disorder), it is unlikely that social phobia itself, at the level of an Axis I disorder, is transmitted. Rather, it seems more parsimonious, and in keeping with current notions about the structure and heritability of mental disorders, that one or more temperamental risk factors for social phobia is transmitted. The goal of this study was to explore this possibility by examining relevant quantitative traits in a family study of generalized social phobia (GSP). First-degree (n = 103) relatives of patients with DSM-IV GSP and 65 first-degree relatives of not socially phobic comparison subjects (NC) completed a panel of self-report questionnaires that included measures of trait anxiety, social anxiety, and personality. Regression analysis was used to examine associations between group membership (i.e., whether that family member was a first-degree relative of a GSP proband) and these measures. First-degree relatives of GSP probands scored significantly higher than first-degree relatives of not socially phobic probands on measures of trait anxiety and social anxiety and on the Harm Avoidance subscale of the TPQ. One large factor, accounting for 84% of the variance, was strongly associated with being a first-degree relative of a GSP proband. Quantitative traits elevated in probands with generalized social phobia are also elevated in their first-degree relatives. Future family and genetic studies of social phobia should consider the possibility that one or more traits (or some aggregation thereof) may better approximate the phenotype of interest. More extensive efforts at phenotype refinement should be undertaken before such studies proceed.

Adult↗
PubMed2004

Multiple quantitative trait loci mapping with cofactors and application of alternative variants of the false discovery rate in an enlarged granddaughter design.

The experimental power of a granddaughter design to detect quantitative trait loci (QTL) in dairy cattle is often limited by the availability of progeny-tested sires, by the ignoring of already identified QTL in the statistical analysis, and by the application of stringent experimentwise significance levels. This study describes an experiment that addressed these points. A large granddaughter design was set up that included sires from two countries (Germany and France), resulting in almost 2000 sires. The animals were genotyped for markers on nine different chromosomes. The QTL analysis was done for six traits separately using a multimarker regression that included putative QTL on other chromosomes as cofactors in the model. Different variants of the false discovery rate (FDR) were applied. Two of them accounted for the proportion of truly null hypotheses, which were estimated to be 0.28 and 0.3, respectively, and were therefore tailored to the experiment. A total of 25 QTL could be mapped when cofactors were included in the model-7 more than without cofactors. Controlling the FDR at 0.05 revealed 31 QTL for the two FDR methods that accounted for the proportion of truly null hypotheses. The relatively high power of this study can be attributed to the size of the experiment, to the QTL analysis with cofactors, and to the application of an appropriate FDR.

Animals↗
PubMed2026

Integration of Genome-Wide Association Studies With Single-Cell and Bulk Expression Quantitative Trait Locus to Identify Stroke Susceptibility Genes.

BACKGROUND: Previous studies have integrated genome-wide association studies with expression quantitative trait locus (eQTL) data from bulk tissues to identify stroke susceptibility genes. However, eQTL data exhibit high cell-type specificity, and genetic variants may have distinct effects across stroke subtypes. METHODS: We applied the summary-data-based Mendelian randomization (MR) method to integrate eQTL data from 7 brain cell types with genome-wide association studies data for 5 stroke phenotypes (stroke, ischemic stroke, cardioembolic stroke, large artery stroke, and small vessel stroke). Results were compared with summary-data-based MR using eQTL data from 49 tissues in the Genotype-Tissue Expression project. Robustness of significant single-cell summary-data-based MR associations was assessed via MR and colocalization analyses. Further evaluations included single-cell RNA-seq differential expression, protein-protein interaction, druggability, and phenome-wide association studies. RESULTS: Single-cell summary-data-based MR identified many novel significant genes not detected using bulk tissue eQTL data. Validated associations revealed 2 stroke risk genes (LRCH1, ICA1L), 3 stroke protective genes (AHI1, LYRM9, CENPQ), 2 large artery stroke risk genes (LIPA, ELL), and 1 ischemic stroke protective gene (CENPQ). Single-cell RNA-seq showed significantly increased LIPA expression in mouse stroke samples compared with controls. Protein-protein interaction and druggability analyses, along with phenome-wide association studies, prioritized LIPA and LRCH1 as potential therapeutic targets for stroke while indicating possible adverse effects. CONCLUSIONS: Integrating single-cell eQTL with stroke-subtype genome-wide association studies uncovers novel cell-type-specific causal genes and highlights promising therapeutic targets, advancing understanding of stroke pathogenesis.

Genome-Wide Association Study↗
PubMed2006

Quantitative trait loci x maternal cytoplasmic environment interaction for development rate in Oncorhynchus mykiss.

Effects of maternal cytoplasmic environment (MCE) on development rate in rainbow trout were evaluated within a quantitative trait loci (QTL) analysis framework. Previous research had identified QTL for development rate in doubled haploid (DH) progeny produced from a cross between the Oregon State University (OSU) and the Swanson (SW) River rainbow trout clonal lines. In this study, progeny for QTL mapping were produced from a cross between the OSU and Clearwater (CW) River clonal lines. Doubled haploids were produced from the OSU x CW F1 by androgenesis using eggs from different females (or MCEs); with androgenesis, the maternal nuclear genome was destroyed by irradiation and diploidy was restored by blocking the first embryonic cleavage by heat shock. All embryos were incubated at the same temperature and development rate quantified as time to hatch. Using a linkage map constructed primarily with AFLP markers, QTL mapping was performed, including MCE covariates and QTL x MCE effects in models for testing. The major QTL for development rate in the OSU x SW cross overlaps with the major QTL found in this OSU x CW cross; effects at this locus were the same across MCEs. Both MCE and QTL x MCE effects contribute to variability in development rate, but QTL x MCE were minor and detected only at small-effect QTL.

Animals↗
PubMed1998

Quantitative trait loci affecting peak bone mineral density in mice.

Peak bone mass is a major determinant of risk of osteoporotic fracture. Family and twin studies have found a strong genetic component to the determination of bone mineral density (BMD). However, BMD is a complex trait whose expression is confounded by environmental influences and polygenic inheritance. The number, locations, and effects of the individual genes contributing to natural variation in this trait are all unknown. Experimental animal models provide a means to circumvent complicating environmental factors, and the development of dense genetic maps based on molecular markers now provides opportunities to resolve quantitative genetic variation into individual regions of the genome influencing a given trait (quantitative trait loci, QTL). To begin to identify the heritable determinants of BMD, we have examined genetically distinct laboratory mouse strains raised under strict environmental control. Mouse whole-body bone mineral content by dual-energy X-ray absorptiometry (DXA) correlated strongly with skeletal calcium content by ashing, and peak whole-body BMD by DXA in female mice occurred at approximately 80-90 days of age. We therefore determined mean body weight and peak whole body BMD values in 12-week-old female mice from a panel of 24 recombinant inbred (RI) BXD strains, derived from a cross between C57BL/6 and DBA/2 progenitors. The distribution of body weight and BMD values among the strains clearly indicated the presence of strong genetic influences on both of these traits, with an estimated narrow sense heritability of 60% and 35%, respectively. The patterns of differences in body weight and peak whole body BMD in the BXD strains were then integrated with a large database of genetic markers previously defined in the RI BXD strains to generate chromosome map sites for QTL. After correction for redundancy among the significant correlations, QTL analysis of the BXD RI strain series provisionally identified 10 chromosomal sites linked to peak bone mass development in the female. Several of the identified sites map near genes encoding hormones, structural proteins, and cell surface receptors that are intricately involved in skeletal homeostasis. Four QTL for body weight were also identified. One of these loci was also strongly linked to inherited variation in BMD. This finding suggests that body weight and peak BMD may be influenced by linked genes or perhaps by common genes with pleiotropic effects. Our phenotyping in the RI BXD strains has allowed us to map a number of specific genetic loci strongly related to the acquisition of peak BMD. Confirmation of these findings will likely result in the understanding of which genes control skeletal health.

Absorptiometry, Photon↗
PubMedDate not supplied

[DNA-marking of quantitative traits in corn].

Methods of ISSR- and RAPD-analyses were used for marking quantitative trait loci (QTLs) determining the development of some morphological and biological traits in maize. Specificity of marker locus alleles was established for certain levels of polygenic trait phenotype manifestation. Criteria of marker locus informativity are discussed. A possibility of marker-assisted selection for valuable genotypes with desired for breeding trait values was demonstrated.

Alleles↗
PubMed2004

Quantitative trait loci analysis for growth and carcass traits in a half-sib family of purebred Japanese Black (Wagyu) cattle.

We used a half-sib family of purebred Japanese Black (Wagyu) cattle to locate economically important quantitative trait loci. The family was composed of 348 fattened steers, 236 of which were genotyped for 342 microsatellite markers spanning 2,664 cM of 29 bovine autosomes. The genome scan revealed evidence of 15 significant QTL (<5% chromosome-wise level) affecting growth and carcass traits. Of the 15 QTL, six QTL were significant at the 5% experiment-wise level and were located in bovine chromosomes (BTA) 4, 5, and 14. We analyzed these three chromosomes in more detail in the 348 steers, with an average marker interval of 1.2 cM. The second scan revealed that the same haplotype of the BTA 4 region (52 to 67 cM) positively affected LM area and marbling. We confirmed the QTL for carcass yield estimate on BTA 5 in the region of 45 to 54 cM. Five growth-related QTL located on BTA 14, including slaughter and carcass weights, were positively affected by the same region of the haplotype of BTA 14 (29-51 cM). These data should provide a useful reference for further marker-assisted selection in the family and positional cloning research. The research indicates that progeny design with moderate genotyping efforts is a powerful method for detecting QTL in a purebred half-sib family.

Animals↗
PubMed2005

Ecotype allelic variation in C-to-U editing extent of a mitochondrial transcript identifies RNA-editing quantitative trait loci in Arabidopsis.

In higher plants, RNA editing is a posttranscriptional process that converts C to U in organelle mRNAs. Although RNA editing in mitochondria occurs much more frequently than in chloroplasts, editing of exogenously supplied RNA substrates in vitro and in organello has shown that editing in the two organelles shares some common features. In particular, the 20 nucleotides upstream of the editing site play an important role in specifying the C to be edited. Biochemical approaches have allowed the identification of features of cis-sequences necessary for RNA editing to occur, but have failed to identify any of the components of the mitochondrial editing machinery. In order to implement a genetic approach for identification of editing factors, we have identified a polymorphism in the editing efficiency of a mitochondrial site between two ecotypes of Arabidopsis (Arabidopsis thaliana), Columbia (Col) and Landsberg erecta (Ler). In rosette leaves, an editing site within the ccb206 mitochondrial gene is more highly edited in Col than in Ler. Depending on the development stage and tissue analyzed, the difference in editing extent varies between the two ecotypes; for example, in floral buds, editing extent does not differ. Single-point regression analysis of the editing efficiency in a sample of recombinant inbred lines derived from a cross between Col and Ler allowed the identification of two quantitative trait loci controlling this trait. A member of the pentatricopeptide repeat protein family that carries a putative mitochondrial transit sequence has been identified near a major quantitative trait locus on chromosome 4.

Alleles↗
PubMed2004

Quantitative trait loci affecting knockdown resistance to high temperature in Drosophila melanogaster.

Knockdown resistance to high temperature is an ecologically important trait in small insects. A composite interval mapping was performed on the two major autosomes of Drosophila melanogaster to search for quantitative trait loci (QTL) affecting knockdown resistance to high temperature (KRHT). Two dramatically divergent lines from geographically different thermal environments were artificially selected on KRHT. These lines were crossed to produce two backcross (BC) populations. Each BC was analysed for 200 males with 18 marker loci on chromosomes 2 and 3. Three X-linked markers were used to test for X-linked QTL in an exploratory way. The largest estimate of autosome additive effects was found in the pericentromeric region of chromosome 2, accounting for 19.26% (BC to the low line) and 29.15% (BC to the high line) of the phenotypic variance in BC populations, but it could represent multiple closely linked QTL. Complete dominance was apparent for three QTL on chromosome 3, where heat-shock genes are concentrated. Exploratory analysis of chromosome X indicated a substantial contribution of this chromosome to KRHT. The results show that a large-effect QTL with dominant gene action maps on the right arm of chromosome 3. Further, the results confirm that QTL for heat resistance are not limited to chromosome 3.

Animals↗
PubMed2000

Selective genotyping with epistasis can be utilized for a major quantitative trait locus mapping in hypertension in rats.

Epistasis used to be considered an obstacle in mapping quantitative trait loci (QTL) despite its significance. Numerous epistases have proved to be involved in quantitative genetics. We established a backcross model that demonstrates a major QTL for hypertension (Ht). Seventy-eight backcrossed rats (BC), derived from spontaneously hypertensive rats (SHR) and normotensive Fischer 344 rats, showed bimodal distribution of systolic blood pressure (BP) values and a phenotypic segregation ratio consistent with 1:1. In this backcross analysis, sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase (Serca) II heterozygotes showed widespread bimodality in frequency distribution of BP values and obviously demonstrated Ht. First, in genome-wide screening, Mapmaker/QTL analysis mapped Ht at a locus between D1Mgh8 and D1Mit4 near Sa in all 78 BC. The peak logarithm of the odds (LOD) score reached 5.3. Second, Serca II heterozygous and homozygous BC were analyzed separately using Mapmaker/QTL. In the 35 Serca II heterozygous BC, the peak LOD score was 3.8 at the same locus whereas it did not reach statistical significance in the 43 Serca II homozygotes. Third, to map Ht efficiently, we selected 18 Serca II heterozygous BC with 9 highest and 9 lowest BP values. In these 18 BC, the peak LOD score reached 8.1. In 17 of the 18, D1Mgh8 genotypes (homo or hetero) qualitatively cosegregated with BP phenotypes (high or low) (P < 0.0001, by chi-square analysis). In conclusion, selective genotyping with epistasis can be utilized for a major QTL mapping near Sa on chromosome 1 in SHR.

Animals↗
PubMedDate not supplied

Parallel computing in interval mapping of quantitative trait loci.

Linear regression analysis is considered the least computationally demanding method for mapping quantitative trait loci (QTL). However, simultaneous search for multiple QTL, the use of permutations to obtain empirical significance thresholds, and larger experimental studies significantly increase the computational demand. This report describes an easily implemented parallel algorithm, which significantly reduces the computing time in both QTL mapping and permutation testing. In the example provided, the analysis time was decreased to less than 15% of a single processor system by the use of 18 processors. We indicate how the efficiency of the analysis could be improved by distributing the computations more evenly to the processors and how other ways of distributing the data facilitate the use of more processors. The use of parallel computing in QTL mapping makes it possible to routinely use permutations to obtain empirical significance thresholds for multiple traits and multiple QTL models. It could also be of use to improve the computational efficiency of the more computationally demanding QTL analysis methods.

Algorithms↗
PubMed2003

Identification of a quantitative trait locus for ileitis in a spontaneous mouse model of Crohn's disease: SAMP1/YitFc.

BACKGROUND & AIMS: The SAMP1/Yit mouse strain develops spontaneous ileitis with histologic features of Crohn's disease. Disease expression in the SAMP1/YitFc subline (SAMP1/Fc) is partially inhibited by outcross to C57BL/6J (B6) mice, suggesting complex genetic control of disease susceptibility with both dominant and recessive determinants. We performed a genetic analysis of a (B6 x SAMP1/Fc)F(2) cross to localize the genes regulating intestinal inflammation in this model. METHODS: A genome-wide scan was performed using a panel of microsatellite loci determined to be informative for this cross. Quantitative trait loci were identified with Map Manager QT using a serial regression approach. Positional candidate genes were selectively sequenced at the genomic level to identify potential susceptibility genes for functional screening. RESULTS: A genome-wide scan of (B6 x SAMP1/Fc)F(2) mice identified a SAMP-derived quantitative trait loci with additive effects on chromosome 9 in a region likely to have been inherited from the AKR mouse strain. The candidate interval contains several genes of interest because of their potential role in either immune system function, intestinal epithelial function, or both. Suggestive evidence for additional loci was also observed on chromosomes 6 and X. CONCLUSIONS: The SAMP1/Fc allele for a locus, designated Ibdq1, promotes inflammation-associated epithelial damage in these mice. Consistent with persistent mild ileitis in (B6 x SAMP1/Fc)F(1) mice, this locus appears to function in an additive fashion. Two genes in this interval, encoding the interleukin 10 receptor alpha chain and interleukin 18, are excellent candidates for Ibdq1.

Alleles↗
PubMed2000

Deficiency mapping of quantitative trait loci affecting longevity in Drosophila melanogaster.

In a previous study, sex-specific quantitative trait loci (QTL) affecting adult longevity were mapped by linkage to polymorphic roo transposable element markers, in a population of recombinant inbred lines derived from the Oregon and 2b strains of Drosophila melanogaster. Two life span QTL were each located on chromosomes 2 and 3, within sections 33E-46C and 65D-85F on the cytological map, respectively. We used quantitative deficiency complementation mapping to further resolve the locations of life span QTL within these regions. The Oregon and 2b strains were each crossed to 47 deficiencies spanning cytological regions 32F-44E and 64C-76B, and quantitative failure of the QTL alleles to complement the deficiencies was assessed. We initially detected a minimum of five and four QTL in the chromosome 2 and 3 regions, respectively, illustrating that multiple linked factors contribute to each QTL detected by recombination mapping. The QTL locations inferred from deficiency mapping did not generally correspond to those of candidate genes affecting oxidative and thermal stress or glucose metabolism. The chromosome 2 QTL in the 35B-E region was further resolved to a minimum of three tightly linked QTL, containing six genetically defined loci, 24 genes, and predicted genes that are positional candidates corresponding to life span QTL. This region was also associated with quantitative variation in life span in a sample of 10 genotypes collected from nature. Quantitative deficiency complementation is an efficient method for fine-scale QTL mapping in Drosophila and can be further improved by controlling the background genotype of the strains to be tested.

Animals↗
PubMed2006

Genome-wide scan to identify quantitative trait loci for baseline resting heart rate and its response to endurance exercise training: the HERITAGE Family Study.

Evidence of a genetic component for resting heart rate (RHR) has been found. Quantitative trait loci (QTLs) for baseline RHR have been reported, but not for RHR training response. It is of interest to identify QTLs that may harbor genes influencing RHR variation at baseline and in response to regular exercise training. Here, a multipoint variance components linkage scan using 654 markers was performed to search for QTLs that influence RHR adjusted for several covariates at baseline and in response to 20 weeks of endurance training (post-training minus baseline) in 99 White and 127 Black families in the HERITAGE Family Study. Potentially interesting linkages were revealed on 4 q and 11 p for baseline RHR, and on 1 q and 21 q for RHR training response in Whites. The QTLs on 2 q, 6 q, 7 q, 12 q, 14 q, and 15 q for baseline RHR, and on 3 p, 20 p and 21 q for RHR training response were found in Blacks. Promising linkages (lod scores >or= 1.75, p or= 135/80 mm Hg) subset of 40 White families suggesting a pleiotropic gene for BP and RHR with interactions. In conclusion, among QTLs on 1 q, 2 p, 3 p, 4 q, and 11 p that replicated across subsamples and studies, 11 p is most promising for dense mapping and association studies in HERITAGE and other cohorts.

Black People↗
PubMed2002

QTL Express: mapping quantitative trait loci in simple and complex pedigrees.

QTL Express is the first application for Quantitative Trait Locus (QTL) mapping in outbred populations with a web-based user interface. User input of three files containing a marker map, trait data and marker genotypes allows mapping of single or multiple QTL by the regression approach, with the option to perform permutation or bootstrap tests.

Chromosome Mapping↗
PubMed2005

Studies of variations of the cyclin-dependent kinase inhibitor 1C and the cyclin-dependent kinase 4 genes in relation to type 2 diabetes mellitus and related quantitative traits.

CDK4 is involved in the regulation of body weight, pancreatic beta-cell proliferation, insulin responsiveness, and diabetes pathogenesis. CDK4 activity is inhibited by CDKN1C, which is regulated by insulin. In addition, CDKN1C plays an important role in beta-cell proliferation and is involved in the pathogenesis of the Beckwith-Wiedemann syndrome, a disorder characterized by neonatal hyperinsulinaemic hypoglycaemia and pre- and post-natal overgrowth. The aim of this study was to investigate if variations in the proximal promoter and the coding region of the CDKN1C and CDK4 genes are associated with type 2 diabetes or changes in related quantitative phenotypes among glucose-tolerant subjects. Mutation analyses of the two genes in 62 type 2 diabetic patients resulted in the discovery of seven variants of CDKN1C and two variants of CDK4. In a case-control study comprising 717 type 2 diabetic patients and 518 glucose-tolerant subjects the most frequent variants did not show any difference in allele frequencies between the type 2 diabetic patients and the control subjects. However, in two genotype-quantitative trait correlation studies involving 206 glucose-tolerant offspring of type 2 diabetic patients and 359 young, healthy subjects the CDKN1C del171APVA variant associated with increased birth weight (P=0.05 and P=0.05). Furthermore, the same variant tended to be associated with decreased basal glucose oxidation among 16 genotypically discordant dizygotic twins (P=0.03). In a genotype-quantitative trait study involving 500 middle-aged glucose-tolerant subjects the CDK4 IVS2-31G-->A variant was associated with an increased waist circumference (P=0.03) and waist-to-hip ratio (P=0.02) and altered fasting plasma glucose (P=0.03). However, these later findings could not be replicated in additional studies. In conclusion, variants in CDKN1C may contribute to the inter-individual variation in birth weight.

Aged↗
PubMed1997

Towards the quantitative traits regulation: fountain theory implications in comparative and developmental biology.

A fountain mechanism of quantitative regulation of gene expression level during development is proposed. The mechanism is based on postulated ability of a special class of RNA molecules, so called fountain RNAs (fRNAs), to induce passive and selective ionic channels in the internal nuclear membrane. Ions diffuse via channel from the nuclear lumen into the chromatin compartment. An RNA-dependent battery of ion channels is assumed to produce < > of ions in close vicinity to the corresponding genes. An ion atmosphere, in its turn, locally changes the chromatin configuration and effectiveness of transcription and processing of transcripts. Hence this mechanism can be used to change genes productivity. It is a basic mechanism of quantitative traits regulation. A passive selective ion flux periodically stops after a threshold ion concentration induces local chromatin compactization and arrests the activity of ion channels in a given chromatin compartment. This process serves as a basis for many cellular biorhythms that are relatively temperature-independent because of the passive nature of ion channel. It is postulated that eukaryotes became eukaryotes just to obtain this fountain mechanism that allows them to perform gradual quantitative modulation of corresponding genes expression levels. The fountain mechanism is partly responsible for dominance and heterosis, X-chromosome inactivation, gene position effects, and some other epigenetic events. It plays an important role in embryonic and post-embryonic development. A significant portion of the former < > DNA can be referred to as fDNA involved in the proposed mechanism functioning. Genomic rearrangements of fDNA could lead to micro- and macroevolutionary changes in the animal and plant kingdoms. The pivotal evolutionary function of transposons could reside in their ability to contain and relocate fDNA along the chromosomes.

Animals↗