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Diane M. Robins - One of the best experts on this subject based on the ideXlab platform.
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the krab zinc finger protein rsl1 regulates Sex and tissue specific promoter methylation and dynamic hormone responsive chromatin configuration
Molecular and Cellular Biology, 2012Co-Authors: Christopher J. Krebs, David C Schultz, Diane M. RobinsAbstract:Over 400 Kruppel-associated box zinc finger proteins (KRAB-ZFPs) are encoded in mammalian genomes. While KRAB-ZFPs strongly repress transcription in vitro, little is known about their biological function or gene targets in vivo. Regulator of Sex Limitation 1 (Rsl1), one of the first KRAB-Zfp genes assigned a physiological role, accentuates Sex-biased liver gene expression, most dramatically for mouse Sex-limited protein (Slp), which provides an in vivo reporter of KRAB-ZFP function. Slp is induced in males in the liver and kidney by growth hormone (GH) and androgen, respectively. In the liver but not kidney, the Rsl1 genotype correlates with methylation of a CpG dinucleotide in the Slp promoter that is demethylated at puberty. RSL1 binds 2 kb upstream of the Slp promoter, both in vitro and in vivo, within an enhancer containing response elements for STAT5b. Chromatin immunoprecipitation (ChIP) assays demonstrate that RSL1 recruits KAP1/TRIM28, the corepressor for KRAB action in vitro, to this enhancer. Slp induction requires rapid cycling of STAT5b in chromatin. Remarkably, RSL1 simultaneously binds adjacent to STAT5b with a reciprocal binding pattern that limits hormonal response. These experiments demonstrate a surprisingly dynamic interplay between a hormonal activator, STAT5b, and a KRAB-ZFP repressor and provide unique insights into KRAB-ZFP epigenetic mechanisms.
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regulator of Sex Limitation krab zinc finger proteins modulate Sex dependent and independent liver metabolism
Physiological Genomics, 2009Co-Authors: Christopher J. Krebs, Shaema M Khan, James W Macdonald, Meredith Sorenson, Diane M. RobinsAbstract:Kruppel-related zinc finger proteins (KRAB-zfps) comprise the largest mammalian transcription factor family, but their specific functions are largely unknown. Two KRAB-zfps, regulator of Sex-Limitation (Rsl) 1 and Rsl2, repress expression of the mouse Sex-limited protein (Slp) gene, the hallmark of Rsl activity, as well as some other male-predominant liver genes. This phenotype suggests Rsl modifies Sex-specific transcription. The scope of Rsl control was determined by expression profiling of liver RNA from wild-type (wt), rsl, and transgenic mice with hepatic overexpression of Rsl1 or Rsl2. About 7.5% of the liver transcriptome was Rsl-responsive. More genes in males than females were affected by the loss of Rsl (e.g., in rsl mice), whereas Rsl overexpression altered more transcripts in females than males. Rsl dramatically repressed some female-predominant genes, but most were modestly (1.25- to 2-fold) influenced. In males, most Rsl-responsive genes unexpectedly expressed at lower levels in rsl than wt, suggesting not all are direct targets of Rsl repression. Gene Ontology analysis showed Rsl targets enriched in pathways of cholesterol, steroid, and lipid metabolism, linking Rsl to energy balance. In accord with this, blood glucose levels were less in male rsl than wt mice, and less responsive to fasting and refeeding. rsl mice were also leaner than wt, consistent with their hepatic regulation of phosphoenolpyruvate carboxykinase 1 and stearoyl-Coenzyme A desaturase 1. Altogether, Rsl's effect on Sexually dimorphic and metabolically sensitive liver gene expression suggests a role for KRAB-zfps as broad genetic modulators of individual adaptation.
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Expansion and diversification of KRAB zinc-finger genes within a cluster including Regulator of Sex-Limitation 1 and 2.
Genomics, 2005Co-Authors: Christopher J. Krebs, Shaema M Khan, Leslie K. Larkins, Diane M. RobinsAbstract:The genomic locus on mouse chromosome 13 called Regulator of Sex-Limitation (Rsl) accentuates Sex differences in hepatic gene expression. Females homozygous for variant rsl alleles express some otherwise male-specific liver proteins, such as Sex-limited protein (Slp), major urinary proteins (MUPs), and members of the cytochrome P450 (cyp) 2d subfamily. We recently identified mutations in two genes, Rsl1 and Rsl2, accounting for the rsl phenotype. These genes encode KRAB zinc-finger proteins (KRAB-ZFPs) and are embedded within a cluster of over 20 similar genes. Mammalian genomes contain over 200 KRAB-ZFP genes, which act biochemically to repress transcription, but the Rsl genes are the first to have their biological functions elucidated. Here we compare Rsl1 and Rsl2 with their neighboring genes, tracing a series of duplication, inversion, and gene conversion events that have created subfamilies within the locus. Polymorphisms among inbred mouse strains and feral species suggest that mutations responsible for the rsl phenotype arose during the creation of inbred strains. Comparisons among mouse, rat, and human sequences show that the Rsl genes, like members of certain other multigene families, have diversified in a species-specific manner. The targets of Rsl regulation also vary between species, occurring in gene families with functions in steroid and xenobiotic metabolism (Cyp2d), reproduction (MUPs), and immunity (Slp). This suggests that the Rsl locus in mouse, and comparable KRAB-ZFP genes in other mammals, may play a role in speciation via modulation of expression of genes influencing reproductive fitness or behavior.
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Regulator of Sex-Limitation (Rsl) encodes a pair of KRAB zinc-finger genes that control Sexually dimorphic liver gene expression.
Genes & development, 2003Co-Authors: Christopher J. Krebs, Kathryn M. Tullis, Leslie K. Larkins, Ryan Price, Raymond D. Miller, Diane M. RobinsAbstract:Sexually dimorphic expression of a broad array of liver proteins involved in reproduction and xenobiotic metabolism is induced at puberty by Sex-specific growth hormone patterns. An additional control of Sex-dependent gene expression is conferred by Regulator of Sex-Limitation (Rsl) alleles. In variant rsl mice, females inappropriately express the male Sex-limited protein, Slp. We recently showed that a panel of male-specific liver genes is repressed by Rsl, accentuating Sex differences in a hormone-independent manner. Here we map rsl to a region on Chromosome 13 comprised exclusively of KRAB (Kruppel-associated box) zinc-finger protein (ZFP) genes. Among eight Rsl candidate (Rslcan) genes within the critical genetic interval, the recent duplicates Rslcan-4 and Rslcan-9 both harbor mutations in rsl mice (partial deletion and splice-site inactivation, respectively). Transgenesis with bacterial artificial chromosome (BAC) clones encompassing Rslcan-4 restores male-specific MUP (major urinary protein) expression to rsl mice, whereas a BAC containing Rslcan-9 rescues Sex-specific expression of Slp and cytochrome P450 Cyp2d9. Thus, the Rslcan-4 and Rslcan-9 paralogs partitioned regulation of their target genes during evolution. This demonstrates the first biological role for a set of KRAB zinc-finger repressor proteins and reveals the molecular basis of a gene-silencing pathway critical for Sexual dimorphism.
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The regulator of Sex-Limitation gene, Rsl, enforces male-specific liver gene expression by negative regulation
Endocrinology, 2003Co-Authors: Kathryn M. Tullis, Christopher J. Krebs, Janet Y. Leung, Diane M. RobinsAbstract:Expression of a broad array of proteins is Sexually dimorphic in rodent liver, dependent on Sex-specific patterns of GH secretion. Mice carrying rsl (regulator of Sex Limitation) alleles, discovered as trans-acting loci affecting the mouse Sex-limited protein (Slp) gene, reveal an additional axis in male-specific gene regulation. Slp expresses in adult males, but in rsl homozygous mice, Slp is also expressed in females. In this study, we examined congenic rsl strains to determine rsl's site of action, breadth of targets, and interaction with hormonal induction. We show that rsl affects Slp in liver, but not kidney, and that Rsl acts on a spectrum of male-specific liver genes, including mouse urinary proteins and a cytochrome P450 expressed predominantly by males, Cyp 2d-9, but does not act on the female-prominent P450, Cyp 2a-4. Slp expression in hypophysectomized or Tfm/Y rsl mice reveals that Rsl action is independent of GH or androgen signaling. Further, parabiosis of Rsl and rsl mice does not alter expression patterns, consistent with rsl action being liver intrinsic. Finally, Slp expression initiates earlier in rsl mice, suggesting that Rsl operates before, as well as independently of, hormonal induction. This characterization suggests Rsl functions to repress transcription of a set of genes that have in common their hormonal induction in male liver, and thus accentuates Sexual dimorphism of liver gene expression.
Robert Plomin - One of the best experts on this subject based on the ideXlab platform.
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Sex differences and science: the etiology of science excellence
Journal of child psychology and psychiatry and allied disciplines, 2009Co-Authors: Claire M. A. Haworth, Philip S. Dale, Robert PlominAbstract:Background: Are there Sex differences in the etiology of high performance in science in childhood that could contribute to the under-representation of women in scientific careers? In this study the relative contributions of genetic and environmental influences on high performance in science in both boys and girls were assessed using standard twin analyses. Methods: The sample included 3000 twin pairs from the UK Twins Early Development Study (TEDS). Science performance ratings based on the UK National Curriculum were collected from teachers when the twins were 9, 10 and 12 years old. Science excellence was defined as performing above the 85th percentile. Sex-Limitation liability threshold models were used to assess Sex differences in etiology. Results: We found no evidence for quantitative or qualitative Sex differences in the etiology of science excellence, which was moderately heritable (30–50%), and influenced by both shared (40–56%) and non-shared (10–13%) environmental influences. Conclusions: Although boys and girls do not differ genetically in relation to school science performance per se, the under-representation of women in scientific careers may be due to attitudes rather than aptitudes.
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The Etiology of Behavior Problems in 7-Year-Old Twins: Substantial Genetic Influence and Negligible Shared Environmental Influence for Parent Ratings and Ratings by Same and Different Teachers
Journal of abnormal child psychology, 2005Co-Authors: Kimberly J. Saudino, Angelica Ronald, Robert PlominAbstract:Parent ratings of behavior problems in childhood show substantial genetic influence and modest shared environmental influence. However, few studies have compared these results to teacher ratings and no previous studies have compared same-teacher ratings to different-teacher ratings. 3,714 7-year-old twin pairs in the Twins Early Development Study were rated by parents and teachers on the Strengths and Difficulties Questionnaire. Substantial heritability and negligible shared environmental influence were found for data from all three raters for total behavior problems, hyperactivity, prosocial behavior, peer problems, conduct problems, and emotional symptoms. Sex-Limitation models revealed similar results for males and females, although there was some evidence for greater heritability for boys, especially when twins were rated by the same teacher.
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Genetic and gender influences on nocturnal bladder control--a study of 2900 3-year-old twin pairs.
Scandinavian journal of urology and nephrology, 2001Co-Authors: Richard J. Butler, Michael J. Galsworthy, Fruhling Rijsdijk, Robert PlominAbstract:Objective: The present study of over 2900 twin pairs born in England and Wales in 1994 examines the influences of genetics and gender on nocturnal bladder control at 3 years of age. Materials and Method: Parent report data was analysed in terms of means and components of variance, using a Sex-Limitation model to explore genetic and environmental variation within and between the Sexes. Results: Both genetics and gender are seen to influence acquisition: bladder control at 3 years is moderately heritable (24%), and girls show on average slightly increased acquisition compared with boys, even within opposite-Sex pairs. The SexLimitation modelling showed an interaction between genetic influence and gender whereby nocturnal bladder control was significantly more heritable in boys (33%) than girls (10%). Conclusions: Both genetics and gender are important and interacting factors in the aetiology of nocturnal bladder control.
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Sex differences in early verbal and non‐verbal cognitive development
Developmental Science, 2000Co-Authors: Michael J. Galsworthy, Ginette Dionne, Philip S. Dale, Robert PlominAbstract:The present study of over 3000 2-year-old twin pairs used a Sex-Limitation model to examine genetic and environmental origins of Sex differences in verbal and non-verbal cognitive ability. Girls scored significantly higher on both measures (p
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Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes.
American journal of medical genetics, 1999Co-Authors: Jose R. Fernandez, Robert Plomin, George P. Vogler, Lisa M. Tarantino, Sylvia Vignetti, Gerald E. McclearnAbstract:During the past half century, researchers have identified and examined Sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of Sex linkage and must, therefore, reflect some form of Sex Limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant Sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of Sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a Sex-exclusive phenotypic value for the RI strains and multivariate regression on Sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999.
Christopher J. Krebs - One of the best experts on this subject based on the ideXlab platform.
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the krab zinc finger protein rsl1 regulates Sex and tissue specific promoter methylation and dynamic hormone responsive chromatin configuration
Molecular and Cellular Biology, 2012Co-Authors: Christopher J. Krebs, David C Schultz, Diane M. RobinsAbstract:Over 400 Kruppel-associated box zinc finger proteins (KRAB-ZFPs) are encoded in mammalian genomes. While KRAB-ZFPs strongly repress transcription in vitro, little is known about their biological function or gene targets in vivo. Regulator of Sex Limitation 1 (Rsl1), one of the first KRAB-Zfp genes assigned a physiological role, accentuates Sex-biased liver gene expression, most dramatically for mouse Sex-limited protein (Slp), which provides an in vivo reporter of KRAB-ZFP function. Slp is induced in males in the liver and kidney by growth hormone (GH) and androgen, respectively. In the liver but not kidney, the Rsl1 genotype correlates with methylation of a CpG dinucleotide in the Slp promoter that is demethylated at puberty. RSL1 binds 2 kb upstream of the Slp promoter, both in vitro and in vivo, within an enhancer containing response elements for STAT5b. Chromatin immunoprecipitation (ChIP) assays demonstrate that RSL1 recruits KAP1/TRIM28, the corepressor for KRAB action in vitro, to this enhancer. Slp induction requires rapid cycling of STAT5b in chromatin. Remarkably, RSL1 simultaneously binds adjacent to STAT5b with a reciprocal binding pattern that limits hormonal response. These experiments demonstrate a surprisingly dynamic interplay between a hormonal activator, STAT5b, and a KRAB-ZFP repressor and provide unique insights into KRAB-ZFP epigenetic mechanisms.
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regulator of Sex Limitation krab zinc finger proteins modulate Sex dependent and independent liver metabolism
Physiological Genomics, 2009Co-Authors: Christopher J. Krebs, Shaema M Khan, James W Macdonald, Meredith Sorenson, Diane M. RobinsAbstract:Kruppel-related zinc finger proteins (KRAB-zfps) comprise the largest mammalian transcription factor family, but their specific functions are largely unknown. Two KRAB-zfps, regulator of Sex-Limitation (Rsl) 1 and Rsl2, repress expression of the mouse Sex-limited protein (Slp) gene, the hallmark of Rsl activity, as well as some other male-predominant liver genes. This phenotype suggests Rsl modifies Sex-specific transcription. The scope of Rsl control was determined by expression profiling of liver RNA from wild-type (wt), rsl, and transgenic mice with hepatic overexpression of Rsl1 or Rsl2. About 7.5% of the liver transcriptome was Rsl-responsive. More genes in males than females were affected by the loss of Rsl (e.g., in rsl mice), whereas Rsl overexpression altered more transcripts in females than males. Rsl dramatically repressed some female-predominant genes, but most were modestly (1.25- to 2-fold) influenced. In males, most Rsl-responsive genes unexpectedly expressed at lower levels in rsl than wt, suggesting not all are direct targets of Rsl repression. Gene Ontology analysis showed Rsl targets enriched in pathways of cholesterol, steroid, and lipid metabolism, linking Rsl to energy balance. In accord with this, blood glucose levels were less in male rsl than wt mice, and less responsive to fasting and refeeding. rsl mice were also leaner than wt, consistent with their hepatic regulation of phosphoenolpyruvate carboxykinase 1 and stearoyl-Coenzyme A desaturase 1. Altogether, Rsl's effect on Sexually dimorphic and metabolically sensitive liver gene expression suggests a role for KRAB-zfps as broad genetic modulators of individual adaptation.
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Expansion and diversification of KRAB zinc-finger genes within a cluster including Regulator of Sex-Limitation 1 and 2.
Genomics, 2005Co-Authors: Christopher J. Krebs, Shaema M Khan, Leslie K. Larkins, Diane M. RobinsAbstract:The genomic locus on mouse chromosome 13 called Regulator of Sex-Limitation (Rsl) accentuates Sex differences in hepatic gene expression. Females homozygous for variant rsl alleles express some otherwise male-specific liver proteins, such as Sex-limited protein (Slp), major urinary proteins (MUPs), and members of the cytochrome P450 (cyp) 2d subfamily. We recently identified mutations in two genes, Rsl1 and Rsl2, accounting for the rsl phenotype. These genes encode KRAB zinc-finger proteins (KRAB-ZFPs) and are embedded within a cluster of over 20 similar genes. Mammalian genomes contain over 200 KRAB-ZFP genes, which act biochemically to repress transcription, but the Rsl genes are the first to have their biological functions elucidated. Here we compare Rsl1 and Rsl2 with their neighboring genes, tracing a series of duplication, inversion, and gene conversion events that have created subfamilies within the locus. Polymorphisms among inbred mouse strains and feral species suggest that mutations responsible for the rsl phenotype arose during the creation of inbred strains. Comparisons among mouse, rat, and human sequences show that the Rsl genes, like members of certain other multigene families, have diversified in a species-specific manner. The targets of Rsl regulation also vary between species, occurring in gene families with functions in steroid and xenobiotic metabolism (Cyp2d), reproduction (MUPs), and immunity (Slp). This suggests that the Rsl locus in mouse, and comparable KRAB-ZFP genes in other mammals, may play a role in speciation via modulation of expression of genes influencing reproductive fitness or behavior.
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Regulator of Sex-Limitation (Rsl) encodes a pair of KRAB zinc-finger genes that control Sexually dimorphic liver gene expression.
Genes & development, 2003Co-Authors: Christopher J. Krebs, Kathryn M. Tullis, Leslie K. Larkins, Ryan Price, Raymond D. Miller, Diane M. RobinsAbstract:Sexually dimorphic expression of a broad array of liver proteins involved in reproduction and xenobiotic metabolism is induced at puberty by Sex-specific growth hormone patterns. An additional control of Sex-dependent gene expression is conferred by Regulator of Sex-Limitation (Rsl) alleles. In variant rsl mice, females inappropriately express the male Sex-limited protein, Slp. We recently showed that a panel of male-specific liver genes is repressed by Rsl, accentuating Sex differences in a hormone-independent manner. Here we map rsl to a region on Chromosome 13 comprised exclusively of KRAB (Kruppel-associated box) zinc-finger protein (ZFP) genes. Among eight Rsl candidate (Rslcan) genes within the critical genetic interval, the recent duplicates Rslcan-4 and Rslcan-9 both harbor mutations in rsl mice (partial deletion and splice-site inactivation, respectively). Transgenesis with bacterial artificial chromosome (BAC) clones encompassing Rslcan-4 restores male-specific MUP (major urinary protein) expression to rsl mice, whereas a BAC containing Rslcan-9 rescues Sex-specific expression of Slp and cytochrome P450 Cyp2d9. Thus, the Rslcan-4 and Rslcan-9 paralogs partitioned regulation of their target genes during evolution. This demonstrates the first biological role for a set of KRAB zinc-finger repressor proteins and reveals the molecular basis of a gene-silencing pathway critical for Sexual dimorphism.
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The regulator of Sex-Limitation gene, Rsl, enforces male-specific liver gene expression by negative regulation
Endocrinology, 2003Co-Authors: Kathryn M. Tullis, Christopher J. Krebs, Janet Y. Leung, Diane M. RobinsAbstract:Expression of a broad array of proteins is Sexually dimorphic in rodent liver, dependent on Sex-specific patterns of GH secretion. Mice carrying rsl (regulator of Sex Limitation) alleles, discovered as trans-acting loci affecting the mouse Sex-limited protein (Slp) gene, reveal an additional axis in male-specific gene regulation. Slp expresses in adult males, but in rsl homozygous mice, Slp is also expressed in females. In this study, we examined congenic rsl strains to determine rsl's site of action, breadth of targets, and interaction with hormonal induction. We show that rsl affects Slp in liver, but not kidney, and that Rsl acts on a spectrum of male-specific liver genes, including mouse urinary proteins and a cytochrome P450 expressed predominantly by males, Cyp 2d-9, but does not act on the female-prominent P450, Cyp 2a-4. Slp expression in hypophysectomized or Tfm/Y rsl mice reveals that Rsl action is independent of GH or androgen signaling. Further, parabiosis of Rsl and rsl mice does not alter expression patterns, consistent with rsl action being liver intrinsic. Finally, Slp expression initiates earlier in rsl mice, suggesting that Rsl operates before, as well as independently of, hormonal induction. This characterization suggests Rsl functions to repress transcription of a set of genes that have in common their hormonal induction in male liver, and thus accentuates Sexual dimorphism of liver gene expression.
Richard J. Rose - One of the best experts on this subject based on the ideXlab platform.
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Genetic and Environmental Factors in Breakfast Eating Patterns
Behavior Genetics, 2004Co-Authors: Anna Keski-rahkonen, Jaakko Kaprio, Richard J. Viken, Aila Rissanen, Richard J. RoseAbstract:Despite many studies on the prevalence of breakfast eating, we know little about factors that determine breakfast eating patterns. Our aim was to find out to which extent breakfast eating frequency is influenced by genetic and environmental factors using twin and twin-family models in a population sample of 16-year-old twins ( n = 5250) and their parents ( n = 4663). In common effects Sex-Limitation models, additive genetic effects explained 41% (95% CI: 21–63%) of the variance in breakfast eating in girls and 66% (95% CI: 47–79%) in boys, and common environmental effects 45% (95% CI: 23–62%) in girls and 14% (95% CI: 5–29%) in boys. Of twin-family models, phenotypic assortment models fitted the data best. Heritability estimates increased somewhat (72%, 95% CI: 46–98% in girls and 63%, 95% CI: 38–89%) in boys. Common family environment remained substantial in both Sexes. Cultural transmission was nonsignificant. The relative influence of genetic and family factors on adolescent breakfast eating frequency differs by Sex and is generation-specific.
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Genetic and Environmental Influences on the Relationship between Aggression and Hyperactivity-impulsivity as Rated by Teachers and Parents
Twin research : the official journal of the International Society for Twin Studies, 2004Co-Authors: Elina Vierikko, Lea Pulkkinen, Jaakko Kaprio, Richard J. RoseAbstract:This study examined genetic and environmental contributions to the covariance between aggression and hyperactivity-impulsivity as rated by twins' teachers and parents. Sex-differences in these genetic and environmental contributions and rater bias/sibling interaction effects were of interest as well. Part of an ongoing nation-wide twin-family study of behavioral development and health habits, the sample consisted of 1636 Finnish twin pairs ascertained from five consecutive and complete twin birth cohorts. Data were collected at ages 11-12, using teacher and parental rating forms of the Multidimensional Peer Nomination Inventory. Bivariate analyses were performed using structural equation modeling allowing Sex-Limitation effects. Results show that, in addition to significant genetic and environmental influences specific to each behavior, aggression and hyperactivity-impulsivity share common genetic and environmental etiology. Results provide evidence that both genetic and environmental factors are important in creating the observed correlation between aggression and hyperactivity-impulsivity.
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Genetic and environmental influences on pubertal development: longitudinal data from Finnish twins at ages 11 and 14.
Developmental psychology, 2004Co-Authors: Brian Mustanski, Lea Pulkkinen, Jaakko Kaprio, Richard J. Viken, Richard J. RoseAbstract:To study sources of individual differences in pubertal development, the authors fit a Sex-Limitation common factor model to data reported, at ages 11 and 14 years, by 1,891 twin pairs on items that comprise the Pubertal Development Scale (PDS; A. C. Petersen, L. Crockett, M. Richards, & A. Boxer, 1988). The model divides variation into a general pubertal factor and item-specific variation and, in addition, decomposes it into constituent sources. In both boys and girls, genetic influences made the largest contribution to variance common to PDS items. Genetic and nonshared environmental factors accounted for variation specific to PDS items in boys, whereas for girls, common environmental influences were added for growth spurt and menarcheal status. For both common and item-specific variation, genetic effects were partially Sex specific. Subsidiary analyses found accelerated maturation in both boys and girls who at age 14 were reared in father-absent homes.
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The heritability of depressive symptoms : multiple informants and multiple measures
Journal of child psychology and psychiatry and allied disciplines, 2002Co-Authors: Minna Happonen, Lea Pulkkinen, Jaakko Kaprio, Jaap Van Der Meere, Richard J. Viken, Richard J. RoseAbstract:Background: Earlier research suggests large rater differences in heritability estimates of children's depressive symptoms in the context of significant age and Sex-Limitation effects. Methods: With data from an ongoing, population-based twin-family study, we estimated genetic and environmental influences on children's depression with models allowing for Sex-specific effects. Our assessments of twins included self-reports and ratings made by their classmate peers, their parents and their teachers, allowing estimates of genetic and environmental effects with data from different informants. Model-fitting used maximum likelihood estimation of log-transformed data from a sample of 1,366 11- and 12-year-old twin pairs. Results: Estimates of additive genetic effects were significant for both boys and girls across all four informants, and, standardized to reflect the percentage of phenotypic variance accounted for, those estimates ranged from .28 to .71. Significant effects from common environmental sources were found in ratings of teachers and parents, where, typically, one individual rated both co-twins, but neither in peer nominations nor self-ratings. The correlation of teacher and parent ratings was modest, and bivariate model-fitting found no correlation in either genetic or shared environmental effects between teacher and parental ratings. At this young age, Sex-Limitation effects were found only in teacher ratings, where genetic effects were greater in girls than in boys. Conclusions: Results underscore the utility of using multiple informants to measure children's behavior and provide a foundation for follow-up of these twins in later adolescence.
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Sex differences in genetic and environmental factors contributing to body-height.
Twin research : the official journal of the International Society for Twin Studies, 2001Co-Authors: Karri Silventoinen, Jaakko Kaprio, Richard J. Viken, Eero Lahelma, Richard J. RoseAbstract:Sex differences in the heritability of self-reported body-height in two Finnish twin cohorts were studied by using Sex-Limitation models. The first cohort was born in 1938-1949 (N = 4873 twin pairs) and the second in 1975-1979 (N = 2374 twin pairs). Body-height was greater in the younger cohort (difference of 3.1 cm for men and 2.9 cm for women). The heritability estimates were higher among men (h2 = 0.87 in the older cohort and h2 = 0.82 in the younger cohort) than women (h2 = 0.78 and h2 = 0.67, respectively). Sex-specific genetic factors were not statistically significant in either cohort, suggesting that the same genes contribute to variation in body height for both men and women. The stronger contribution of environmental factors to body-height among women questions the hypothesis that women are better buffered against environmental stress, at least for this phenotype.
Yoon-mi Hur - One of the best experts on this subject based on the ideXlab platform.
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Perceived Family Cohesion Moderates Environmental Influences on Prosocial Behavior in Nigerian Adolescent Twins.
Twin research and human genetics : the official journal of the International Society for Twin Studies, 2017Co-Authors: Yoon-mi Hur, Jeanette Taylor, Hoe-uk Jeong, Min-seo Park, Brett C. HaberstickAbstract:Research shows that perceived family cohesion is positively related to prosocial behavior in adolescents. In this study, we investigated heritability of prosocial behavior (PB) and perceived family cohesion (FC) among Nigerian twins attending public schools in Lagos State, Nigeria (mean age = 14.7 years, SD = 1.7 years), and explored the issue of whether children's perception of cohesive family environment moderated genetic and environmental influences on (PB). The PB scale of the Strengths and Difficulties Questionnaire and the FC scale of the Family Adaptability and Cohesion Evaluation Scale III were completed by 2,376 twins (241 monozygotic (MZ) male, 354 MZ female, 440 dizygotic (DZ) male, 553 DZ female, and 788 opposite-Sex DZ twins). A general Sex-Limitation and the bivariate genotype by environment interaction (G×E) models were applied to the data. The general Sex-Limitation model showed no significant Sex differences, indicating that additive genetic and non-shared environmental influences were, 38% (95% CI = 31, 46) and 62% (95% CI = 54, 69) for PB and 33% (95% CI = 24, 40) and 67% (95% CI = 60, 76) for FC in both Sexes. These estimates were similar to those found in Western and Asian twin studies to date. The correlation between PB and FC was 0.36. The best-fitting bivariate G×E model indicated that FC significantly moderated non-shared environmental influence unique to PB (E×E interaction). Specifically, non-shared environmental contributions to PB were highest when FC was lowest, and decreased as the levels of FC increased. However, genetic variances in PB were stable across all levels of FC. These findings suggest that FC reduces individual differences in PB by changing non-shared environmental experiences rather than genetic factors in PB.
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Heritability of central corneal thickness in Chinese: the Guangzhou Twin Eye Study.
Investigative ophthalmology & visual science, 2008Co-Authors: Yingfeng Zheng, Guofu Huang, Jian Zhang, Bin Liu, Yoon-mi HurAbstract:PURPOSE. To assess the heritability of central corneal thickness (CCT) in Chinese children in a classic twin study. METHODS. Twins aged 8 to 16 years were recruited from the Guangzhou Twin Registry. Pachymetry data were obtained by one operator using the same imaging system. Zygosity was confirmed by genotyping with 16 polymorphic markers in all same-Sex twin pairs. The CCT of the right eyes was chosen as the trait of interest in the analysis. Heritability was assessed by a general Sex-Limitation model, using Mx software (University of Richmond, Virginia). RESULTS. Four hundred forty-nine twin pairs were available for data analyses, including 131 pairs of monozygotic boys (MZM), 44 pairs of dizygotic boys (DZM), 166 pairs of monozygotic girls (MZF), 31 pairs of dizygotic girls (DZF), and 77 pairs of opposite-Sex dizygotic (OSDZ) twins. Twin correlations for CCT were 0.90 for MZM, 0.92 for MZF, 0.56 for DZM, 0.61 for DZF, and 0.44 for OSDZ twins. A Sex-Limitation model combining additive genetic and unique environmental factors produced the best fit for the data. Heritability estimates for CCT were 0.88 (95% confidence interval [CI]: 0.84-0.91) in the boys and 0.91 (95% CI: 0.89-0.93) in the girls. Unique environmental effects explained only 0.12 (95% CI: 0.09 - 0.16) and 0.09 (95% CI: 0.07-0.11) of the variance in CCT in the boys and the girls, respectively. CONCLUSIONS. Additive genetic effects appear to be the major contributor to the variation of CCT in Chinese population. Heritability of CCT appears to be slightly greater in the girls than in the boys.
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Sex difference in heritability of BMI in South Korean adolescent twins.
Obesity (Silver Spring Md.), 2007Co-Authors: Yoon-mi HurAbstract:Twin studies of BMI on the basis of Asian twins are extremely rare. Eight hundred eighty-eight pairs of twins [279 monozygotic (MZ) and 82 dizygotic (DZ) pairs of male twins, 319 MZ and 82 DZ pairs of female twins, and 126 opposite-Sex pairs of DZ twins] completed items concerning height and weight through a mail and a telephone survey. A general Sex-Limitation model was applied to the data. Heritability estimate was greater among women than among men. However, there was little evidence of Sex-specific genes. Under the best-fitting model, additive genetic variances were 82% [95% confidence interval (CI): 72% to 95%] for men and 87% (95% CI: 77% to 99%) for women; shared environmental variances were negligible in both men and women. These estimates of genetic and environmental factors in BMI found among South Korean adolescent twins were broadly in the range of those reported in previous studies of BMI based on Western twin samples.
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Nonadditive genetic effects on hostility in South Korean adolescent and young adult twins.
Twin research and human genetics : the official journal of the International Society for Twin Studies, 2006Co-Authors: Yoon-mi HurAbstract:Hostility has been shown to be a vulnerability marker for various health problems. The present study examined genetic and environmental contributions to individual differences in hostility in South Korean adolescent and young adult twins. Seven hundred and nineteen same- and opposite-Sex twin pairs aged from 13 to 23 years completed a hostility scale. The scalar Sex-Limitation model was applied to the data. The best fitting model indicated that 34% of the total variation of hostility was attributable to genetic factors operating in a nonadditive manner. The remaining 66% of the variance was associated with nonshared environmental influences and measurement error. These findings were largely consistent with results from previous twin studies of personality based on Caucasian twins, rendering support for the pervasive influence of genetic nonadditivity on human personality traits and the generalization of the heritability of personality across human populations.