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PubMed2004

Effects of a quantitative trait locus for muscle hypertrophy from Belgian Texel sheep on carcass conformation and muscularity.

A QTL for muscle hypertrophy has been identified in the Belgian Texel breed. A population of F2 and backcross lambs created from crosses of Belgian Texel rams with Romanov ewes was studied. Effects on carcass traits and muscle development of the Belgian Texel breed polygenes and Belgian Texel single QTL were compared. In both cases, carcass conformation and muscularity were improved. The Texel polygenic environment improved conformation mainly through changes in skeletal frame shape. Segments were shorter and bone weight lower. Muscles were more compact, shorter, and thicker. The single QTL affected muscle development. Thickness and weight of muscles were increased. Composition in myosin changed toward an increase of fast contractile type. The relative contribution of hind limb joint to carcass weight was increased. Differences in skeletal frame morphology among the three genotypes of the single QTL were small. Conformation scoring was mainly influenced by leg muscularity. Back and shoulder muscle development, which largely contributed to variability of muscularity, were less involved in the conformation scoring. Lastly, the QTL explains a small part of differences between these Belgian Texel and Romanov breeds for conformation or muscle development. A large part of genetic variability remains to be explored.

Animals↗
PubMed2006

Bayesian reanalysis of a quantitative trait locus accounting for multiple environments by scaling in broilers.

A Bayesian method was developed to handle QTL analyses of multiple experimental data of outbred populations with heterogeneity of variance between sexes for all random effects. The method employed a scaled reduced animal model with random polygenic and QTL allelic effects. A parsimonious model specification was applied by choosing assumptions regarding the covariance structure to limit the number of parameters to estimate. Markov chain Monte Carlo algorithms were applied to obtain marginal posterior densities. Simulation demonstrated that joint analysis of multiple environments is more powerful than separate single trait analyses of each environment. Measurements on broiler BW obtained from 2 experiments concerning growth efficiency and carcass traits were used to illustrate the method. The population consisted of 10 full-sib families from a cross between 2 broiler lines. Microsatellite genotypes were determined on generations 1 and 2, and phenotypes were collected on groups of generation 3 animals. The model included a polygenic correlation, which had a posterior mean of 0.70 in the analyses. The reanalysis agreed on the presence of a QTL in marker bracket MCW0058-LEI0071 accounting for 34% of the genetic variation in males and 24% in females in the growth efficiency experiment. In the carcass experiment, this QTL accounted for 19% of the genetic variation in males and 6% in females.

Animal Husbandry↗
PubMed2006

Quantitative genetic aspects of coat color in horses.

The aim of this study was to estimate genetic parameters for coat color in horses. Besides defining coat color classes (gray, chestnut, bay, and black), the phenotypes were also measured quantitatively according to standardized international procedures (Commission Internationale de l'Eclairage L*, a*, b*), where L* describes lightness, a* describes color saturation from red to green, and b* describes color saturation from yellow to blue. The total color saturation was derived from a* and b* and referred to as Chroma. A total of 294 horses from the breeds Lipizzan, Nonius, Arabian Pure Bred, Shagya Arabian, and Gidran were measured at neck, shoulder, and belly. Heritabilities (within and between breeds or color classes) and repeatabilities were estimated using REML from univariate animal models defined separately for gray and nongray horses. For gray horses, the estimated within-breed heritabilities for L* ranged from 0.45 to 0.49 and for a*, b*, and Chroma from 0.09 to 0.52, indicating moderate polygenic effect. For nongray horses, between-color class heritabilities were high (0.70 to 0.85) and within-color class heritabilities were negligible (except for L* measured on neck and belly, 0.21 and 0.34, respectively). Additionally, the importance of L* was described by the relation with the total melanin content of horse coat hair; for gray and nongray horses, a strong negative linear relationship was detected (P < 0.01). The spectrometric measures and the results of this study demonstrate a possible approach to the estimation of the polygenic component involved in coat color inheritance.

Animals↗
PubMed2001

Hypothesis. Bystanders or bad seeds? Many autoimmune-target cells may be transforming to cancer and signalling "danger" to the immune system.

Autoimmune-target cells in autoimmune disease (AID) are usually construed as constitutionally normal healthy cells. A related assumption is that other cells in the body of AID patients, except for certain immunocytes, are healthy cells. An implication of that view is that any systemic pathology in organ-specific AID is related to metabolic derangements secondary to tissue destruction. However, much data on target and other cells in AID suggest widespread primary cellular defects. In insulin-dependent diabetes mellitus (IDDM), for example, many "complications" such as atherosclerosis, premature arterial stiffening, senescence of fibroblasts in vitro, and exuberant growth of smooth muscle and mesangial cells in vivo are not strictly attributable to glucose elevation. Also unexplained is the similar appearance of IDDM beta-cells and cells from insulinoma and why the prodromal phase of IDDM has many insulinoma-like features. While AID target cells have often been likened to neoplastic cells, investigators have rarely explored the possibility that autoimmunity in AID is fundamentally antineoplastic. This is likely because the dominant ideas in oncology and immunology-somatic mutation and clonal deletion, respectively-have prevented explanations for how normal immunity could detect transforming cells not expressing non-self antigens. New and less conventional theories of cancer and immunity have facilitated such an explanation. I use Rubin's "epigenetic" aging model of carcinogenesis and Matzinger's "danger" model of immunity to integrate the immunological and oncological sides of AID. In particular, I postulate that individuals suffering from AID have inherited many foci of prematurely aging cells. Those inherently damaged cells adapt to in vivo challenges by beginning to transform into cancer cells. However, as long as those stressed cells have not fully transformed, they will continue to signal "danger" to the innate immune system. The clinical outcome of that struggle between incipient neoplasia and immunity will vary depending upon the degree of tumor-proneness and resistance of the individual. Borrowing from cancer geneticist Henry Lynch, I postulate that tumor-resistance is inherited as a quantitative polygenic trait in direct proportion to tumor-proneness. I further contend that tumor-proneness and immunity are linked polygenic traits such that the greater one's tumor-proneness, the more powerful his/her antitumor immunity. I point to the shared DNA repair deficiency of certain cancer-prone syndromes and HLA-linked AID, their occasional co-occurrence, and their demonstrably exceptional immunity against solid tumors. I propose that HLA-linked AID constitute "chronic hypersensitivity syndromes" due to immunity's largely hidden battle to suppress multiple incipient neoplastic microfoci. Much of the physiopathology of AID is explicable as a sustained systemic response to threatened neoplastic transformation.

Animals↗
PubMed1996

Hypertension, thermotolerance, and the "African gene": an hypothesis.

Hypertension is a polygenic disease of world-wide concern. So far, no polygenic disease has been solved at the genetic level. Ethnic differences in the prevalence of hypertension may suggest candidate genes worthy of study. A strong genetic predisposition to hypertension and target organ damage appears to correlate with African ancestry, referred to as "the African gene." Sub-Saharan Africans have endured the selective pressure of extreme heat for thousands of generations. Polymorphisms in the renin-angiotensin system, such as the recently described insertion/deletion polymorphism in the angiotensin I converting enzyme (ACE) gene, may predispose to hypertension and related disorders because of an advantage they confer in thermoregulation.

Angiotensin I↗
PubMed2026

Genomic background of gestation length and calving-related traits in Holstein cattle.

The reproductive success of cows directly influences the profitability of dairy farms. Reproductive traits, particularly calving-related traits, generally have low heritability but sufficient additive genetic variance to enable genetic progress through genomic selection. Thus, the primary objectives of this study were to estimate genetic parameters and perform single-step genome-wide association studies (ssGWAS) for calf size, calving ease, gestation length, and stillbirth in Holstein cattle. Variance components were estimated based on animal models and Bayesian inference using a data set containing 226,717 animals with phenotypic records, 15,761 animals genotyped with 45,101 SNP markers, and 461,819 animals in the pedigree. SNP effects were estimated using the single-step GBLUP method. For direct and maternal genetic effects, heritability estimates (posterior standard deviation) ranged from 0.001 (0.002) for gestation length in heifers to 0.16 (0.001) for gestation length in cows. Genetic correlations ranged from -0.57 (0.01) between calving ease and stillbirth in heifers to 0.74 (0.01) between gestation length evaluated in heifers and cows. The ssGWAS results supported a highly polygenic architecture for calving-related traits, with most genomic signals not reaching genome-wide significance. A genome-wide significant association was detected for calving ease in cows on BTA23, highlighting FARS2 as a positional candidate gene. The strongest GWAS signals for each trait harbored additional biologically important candidate genes, including NPPA, NPPB, BCHE, EPHA4, DLD, and GTF2I. Given the generally low heritability estimates and the predominantly polygenic architecture observed for these traits, genomic selection may contribute to the genetic improvement of calving-related traits in Holstein cattle, with potential benefits for cow welfare, calf survival, and overall dairy production efficiency.

dairy cattle↗
PubMed2004

Genomic approaches to identifying breast cancer susceptibility factors.

The majority of the genetic variants underlying susceptibility to breast cancer are yet to be discovered. Genome-wide linkage analyses, utilizing anonymous genetic markers, have been successful at identifying two genes, BRCA1 and BRCA2, which account for a sizeable fraction of the clearly inherited forms of breast cancer occurring in autosomal dominant Mendellian patterns. Mutations in these genes, however, account for less than (1/4) of the total genetic component of breast cancer susceptibility and the remaining component is likely to be polygenic in nature - the interaction of mutations in multiple genes, each with a weak effect, in combination with environmental influences. The identification of these polygenes will likely require the study of large numbers of unrelated subjects with and without breast cancer in case-control association studies. Until the time when complete genome sequence information is feasible for all study subjects, interim strategies involving a subset of all common genetic variation (primarily single nucleotide polymorphisms, SNPs) are being planned. Assuming the common disease-common variant theory of complex disease susceptibility, studying a very dense set of genetic markers is likely to identify breast cancer susceptibility genes by virtue of including either the biologically relevant variant, or one closely correlated with it due to linkage disequilibrium.

Journal Article↗
PubMed2006

Identification of genetic markers associated with Gyrodactylus salaris resistance in Atlantic salmon Salmo salar.

Gyrodactylus salaris Malmberg, 1957 is a freshwater monogenean ectoparasite of salmonids, first recorded in Norway in 1975 and responsible for extensive epizootics in wild Atlantic salmon Salmo salar L. The susceptibility of different populations of Atlantic salmon to G. salaris infection differs markedly, with fish from the Baltic being characterised as relatively resistant whereas those from Norway or Scotland are known to be (extremely) susceptible. Resistance to Gyrodactylus infection in salmonids has been found to be heritable and a polygenic mechanism of control has been hypothesised. The current study utilises a 'Quantitative trait loci' (QTL) screening approach in order to identify molecular markers linked to QTL influencing G. salaris resistance in B1 backcrosses of Baltic and Scottish salmon. Infection patterns in these fish exhibited 3 distinct types; susceptible (exponential parasite growth), responding (parasite load builds before dropping) and resistant (parasite load never increases). B1 backcross fish were screened at 39 microsatellite markers and single marker-trait associations were examined using general linear modelling. We identified 10 genomic regions associated with heterogeneity in both innate and acquired resistance, explaining up to 27.3% of the total variation in parasite loads. We found that both innate and acquired parasite resistance in Atlantic salmon are under polygenic control, and that salmon would be well suited to a selection programme designed to quickly increase resistance to G. salaris in wild or farmed stocks.

Animals↗
PubMed1994

Poultry immunogenetics: which way do we go?

A major goal in poultry immunogenetics is the enhancement of innate immunoresponsiveness and resistance to disease. This may be pursued by studying either single genes or polygenic traits. The MHC is perhaps the best-characterized family of host genes that modulates response to a variety of antigens and pathogenic challenges. The association of different MHC alleles with disease resistance has been known for decades. But only recently has analysis at the DNA level opened new avenues of understanding and new opportunities for application of genetic variation in the MHC with immunoresponsiveness. An alternate approach to molecular analysis is selection for a desired phenotype controlled by polygenes. Several studies have illustrated the successful alteration of immunoresponsiveness by genetic selection for antibody production. Recently, a selection program based upon multiple traits of immune response was conducted. Results of this project demonstrated that selection on multiple immune-response traits altered immunophysiology, MHC allelic frequencies, and disease resistance. Several areas for future pursuits in poultry immunogenetics research are proposed.

Animal Husbandry↗
PubMed2026

Gene by environment interaction effects on the metabolic subtype of Polycystic Ovary Syndrome in Hispanic Community Health Study/Study of Latinos.

Polycystic Ovary Syndrome (PCOS) is a common polygenic endocrine disorder that is heterogenous in clinical presentation across genetic ancestry groups. PCOS is characterized by an array of symptoms such as hyperandrogenism, impaired mental health, and metabolic dysregulation. Studying the interaction of environmental factors (such as diet, physical activity, anxiety, and depression) with genetic variants on PCOS and its subtypes in populations with high cardiometabolic burden, e.g., Hispanic/Latinas, could aid in unraveling pathophysiological and genetic pathways through which PCOS functions. We sought to study gene by environment interactions with PCOS and its metabolic subtype (mPCOS) in a sample of US Hispanic/Latina female adults from the Hispanic Community Heath Study/Study of Latinos. In this large community-based study, we derived PCOS using self-reported condition and menstrual cycle information. We classified females with PCOS as having mPCOS if they had high metabolic impairment (fasting glucose, fasting insulin, or body mass index higher than the 75th percentile). There were 451 individuals with PCOS and 221 of them had mPCOS in our sample. We found that PCOS and mPCOS were significantly associated with hyperglycemia and high triglycerides in this population. While a polygenic risk score derived in European ancestry did not generalize to Hispanic/Latina females with PCOS, we identified the best proxy genetic variants in this population in known PCOS regions and investigated their interactions with four environment variables (diet, physical activity, anxiety and depression). Associations with known PCOS loci were generalized in our study at STAG3L4 and CACNA1G genomic regions. We observed GxE interactions between variants in/near three genes and physical activity on PCOS and mPCOS, including FGGY, FAT1, and PTHLH. Additionally, we noted interactions between diet and a variant in FANCC on PCOS, and diet and a variant near CMAS on both PCOS and mPCOS. We also detected GxE interactions between anxiety and depression and a variant in FGGY on PCOS, and depression and a variant near FBP1 on mPCOS. Our results point to potential protective effects of physical activity in females with PCOS and could inform future research on the mitigating effects of lifestyle management on PCOS genetic risk in Hispanic/Latino populations.

GxE↗
PubMed2003

CD4+ T cell-associated pathophysiology critically depends on CD18 gene dose effects in a murine model of psoriasis.

In a CD18 hypomorphic polygenic PL/J mouse model, the severe reduction of CD18 (beta(2) integrin) to 2-16% of wild-type levels leads to the development of a psoriasiform skin disease. In this study, we analyzed the influence of reduced CD18 gene expression on T cell function, and its contribution to the pathogenesis of this disease. Both CD4(+) and CD8(+) T cells were significantly increased in the skin of affected CD18 hypomorphic mice. But only depletion of CD4(+) T cells, and not the removal of CD8(+) T cells, resulted in a complete clearance of the psoriasiform dermatitis. This indicates a central role of CD4(+) T cells in the pathogenesis of this disorder, further supported by the detection of several Th1-like cytokines released predominantly by CD4(+) T cells. In contrast to the CD18 hypomorphic mice, CD18 null mutants of the same strain did not develop the psoriasiform dermatitis. This is in part due to a lack of T cell emigration from dermal blood vessels, as experimental allergic contact dermatitis could be induced in CD18 hypomorphic and wild-type mice, but not in CD18 null mutants. Hence, 2-16% of CD18 gene expression is obviously sufficient for T cell emigration driving the inflammatory phenotype in CD18 hypomorphic mice. Our data suggest that the pathogenic involvement of CD4(+) T cells depends on a gene dose effect with a reduced expression of the CD18 protein in PL/J mice. This murine inflammatory skin model may also have relevance for human polygenic inflammatory diseases.

Animals↗
PubMed2000

Relationship between the severity of alcoholic liver cirrhosis and the metabolism of caffeine in 226 patients.

OBJECTIVES: To evaluate the polygenic regulated caffeine metabolism in a group of 226 patients with liver alcoholic cirrhosis classified according to the Child score. METHODS: Over a 14-year period an hepatic function test, using caffeine as probe drug, has been systematically associated to the usual clinical and biochemical investigations performed in patients with liver alcoholic cirrhosis. "Caffeine test" consisted in a 200 mg caffeine oral intake. Urines were collected over 24 hours: caffeine (137X), 1-7 dimethylxanthine (17X), 1-3 dimethylxanthine (13X), 1-3 dimethylurate (13U), 3-7 dimethylxanthine (37X), 1-7 dimethylurate (17U), 1-methylxanthine (1X), 1-methylurate (1U), 7-methylxanthine (7X), 3-methylxanthine (3X), and 5-acetylamino-6-formylamino-3-methyluracyl (AFMU) were analyzed by high performance liquid chromatography (HPLC). Total and individual metabolite urinary elimination rates were expressed in micromol/24 hours. Enzyme activities were evaluated from the following urinary metabolites ratios: (AFMU+1U+1X)/17U for CYPIA2, 17U/17X for CYP2A6, AFMU/(AFMU+ 1U+1X) for NAT-2, 1U/1X for XO. RESULTS: Compared to healthy subjects, whatever the Child score, caffeine metabolism was reduced by half in patients with alcoholic cirrhosis. The main cause was the decreased CYP1A2 activity. On the other hand, XO and CYP2A6 activities were increased and NAT-2 activity remained unchanged in slow acetylators (SA) and decreased in rapid acetylators (RA) Child B and C. Bimodality of NAT-2 distribution was unclear, but a right assignment of RA and SA phenotype in cirrhotic patients, confirmed by comparison with genotype, was obtained, using the antimode value of NAT-2 distribution used in healthy subjects. At last, there was an interindividual variability in caffeine metabolism as great as in the usual laboratory parameters. CONCLUSION: Metabolism of caffeine is decreased in patients with alcoholic liver cirrhosis. This decrease paralleled the modifications of the usual laboratory tests and does not bring additional information on the severity of the disease. But the equilibrium between the various metabolic pathways of caffeine is impaired. Beyond the changes of a specific enzymatic activity, this must be taken into account particularly for drugs whose metabolism is of the polygenic regulation type.

Aryl Hydrocarbon Hydroxylases↗
PubMed2001

Caffeine metabolism in a group of 67 patients with primary biliary cirrhosis.

OBJECTIVE: To evaluate the polygenic regulated caffeine metabolism in a group of 67 patients with a documented primary biliary cirrhosis (PBC) classified according to the histologic stage proposed by Scheuer. METHODS: Over a 14-year period, drug liver metabolism, using caffeine as a probe drug, has been systematically carried out in addition to the usual clinical, histological and biochemical investigations performed in patients with PBC. The "Caffeine test" consisted of a 200 mg caffeine oral intake. Urines were collected over 24 hours: caffeine (137X), 1-7-dimethylxanthine (17X), 1-3-dimethylxanthine (13X), 1-3-dimethylurate (13U), 3-7-dimethylxanthine (37X), 1-7-dimethylurate (17U), 1-methylxanthine (1X), 1-methylurate (1U), 7-methylxanthine (7X), 3-methylxanthine (3X), and 5-acetylamino-6-formylamino-3-methyluracyl (AFMU) were analyzed by high performance liquid chromatography (HPLC). Total and individual metabolite urinary elimination rates were expressed in micromol/24 hours. Enzyme activities were evaluated from the following urinary metabolite ratios: (AFMU+1U+1X)/17U for CYP1A2, 17U/17X for CYP2A6, AFMU/(AFMU+U+ 1X) for NAT-2, 1U/1X for XO. RESULTS: Compared to healthy subjects, patients with PBC presented a reduced metabolism of caffeine due to a decreased CYP1A2 activity, all the more important since the patients had an advanced histological stage. This picture was nearly identical to the observed picture in chronic liver diseases from various origins. PBC affected the various metabolic pathways of caffeine in a differential manner. CYP1A2 activity was decreased but XO and mainly CYP2A6 activities were increased as shown by the raised urinary ratio 17U/total metabolite elimination. In contrast to the described loss of bimodality of the NAT-2 index distribution in patients with alcoholic cirrhosis, we found a clear-cut, bimodal distribution in patients with PBC, without a high incidence of slow acetylator status. CONCLUSION: Metabolism of caffeine is strongly and differentially disturbed in patients with PBC and apparently not exactly in the same way as that in alcoholic cirrhosis which is more often taken as an index of chronic liver disease. This suggests the need for caution with medicines whose metabolism is under polygenic regulation. Because of the relationships between caffeine metabolism modifications and histological stages, the caffeine test might be used along with the usual tests to safely follow-up the evolution of the disease.

Administration, Oral↗
PubMed2026

Diverse mediators of cancer predisposition uncovered by germline whole genome sequencing of unexplained familial cancers.

Cancer frequently clusters in families due to shared environment and genetics. However, many familial cancer cases lack a clinically recognized pathogenic germline variant (PGV). We analyzed germline genomes and family history from 2,726 individuals without a PGV in the All of Us Research Program, including 1,496 cases across 18 cancer types with extensive family history and 1,230 family history-negative, cancer-free controls. We identified allelic series of rare structural variants inactivating MSH2 in individuals with phenotypes consistent with Lynch syndrome and BRCA1 in breast cancer. Cancer polygenic risk scores were enriched in cases and correlated with patterns of cancer diagnoses within families. Exome-wide rare variant analyses nominated six candidate predisposition genes, including TSTD2 and BRAT1 in thyroid and breast cancer, respectively. Overall, polygenic risk and rare variants impacting known genes explained a median of 5% of unexplained familial cancers, increasing to 11% when including newly nominated risk factors.

Journal Article↗
PubMed2026

Type 2 diabetes genetics in 125,000 admixed adults from Mexico City.

Type 2 diabetes (T2D) is a highly heritable, polygenic disease with over 600 loci identified through genome-wide association studies (GWAS). However, despite possessing unique genetic variation shaped by demographic history and admixture, Latin American populations remain markedly underrepresented in global genomic research. To address this gap, we conducted genome- and exome-wide analyses of 19,431 T2D cases and 105,611 controls from the Mexico City Prospective Study (MCPS). We identified 86 independent GWAS associations, including 21 novel signals, 15 of which replicated in external cohorts. Risk alleles at novel loci were enriched in individuals with Indigenous American ancestry. Exome analyses revealed rare and ultra-rare missense variants with substantial risk effects at HNF1A and GCK, as well as a protein-damaging variant in SLC30A8 that reduced T2D risk by 45% in carriers. Integrative analyses indicate that T2D genetic architecture in Mexico is predominantly driven by common regulatory variation acting in the endocrine pancreas. Polygenic risk scores strongly stratified T2D risk and transferred to Indigenous Mexican populations. These findings demonstrate the power of large-scale genetic discovery in diverse populations to refine disease architecture and identify loci with potential therapeutic relevance.

Journal Article↗
PubMedDate not supplied

[Mode of inheritance of idiopathic generalized non-myoclonic epilepsy in families investigated by studying members with idiopathic epilepsy with tonic-clonic crises on waking. Antioquia, Colombia].

In attempt to identify the possible role of mayor genes, multifactorial inheritance, and cohort effects in the susceptibility to idiopathic epilepsy with generalized tonic clonic seizures of the awakening type (GTCS), complex segregation analysis was performed in 196 nuclear families ascertained through affected with probands with idiopathic epilepsy with GTCS belonging to the Paisa community of Antioquia (Colombia). Models postulating no transmission, single mayor locus (dominant and recessive) only, and multifactorial component only, were rejected. The models postulating no polygenic component to transmission, and no transmission of the major effect were also rejected. Thus far, complex segregation analysis suggested that a major autosomal codominant allele together with a multifactorial component (mixed model) best explains clustering of idiopathic epilepsy with GTCS in families of the Paisa community. The deficit of transmission of heterozygotes (0.17) is compatible with the existence of epistasis acting on a major gene whose frequency was estimated to be 0.0211. Its transmission variance accounts for 81% of the susceptibility to idiopathic epilepsy with GTCS. The complementary variance (19%) is due to polygenic component.

Adolescent↗
PubMed1975

The genetic contribution to coronary heart disease through lipoprotein concentrations.

Many factors both genetic and environmental contribute to the liability to coronary heart disease and one of the genetically determined risk factors is the concentration of lipoproteins in the blood. The evidence so far is that serum cholesterol level is polygenically determined, but that in a minority of the population it is determined by a single mutant gene of large effect. There is evidence that the risk of coronary death for affected individuals is very high and that the condition warrants a maximum effort at identification and treatment. For the remainder of the population whose hyperlipidaemia is polygenically determined, the liability to coronary heart disease might be substantially reduced by simple and appropriate environmental measures aimed at reducing the total liability. The measures if correctly applied should effectively improve the population risks of early coronary death.

Cholesterol↗
PubMed1975

Dental variation among populations. An anthropologic view.

There is considerable variation between and within populations with regard to tooth size, age of eruption, congenitally missing teeth, and crown morphology. These differences are a reflection of the ongoing process of evolution. The genetic basis for this variation is best explained by a polygenic model of inheritance. Even though tooth morpholoyg and agenesis have discontinuous distributions - usually evidence of single gene transmission - they are also polygenic traits and are examples of "quasi-continuous" characteristics. These are traits which exhibit phenotypic discontinuity at the end of a continuous distribution. Postnatal conditions such as nutrition, disease, or climate seem to have little influence on normal dental variation. Most of the environmental factors which affect the dentition occur during the prenatal period. In particular the quality of the intrauterine environment appears to be most important. This suggests that good prenatal nutrition and medical care are needed for a normal and healthy dentition.

Africa↗