scholarly journals Focusing on parental origin of aneuploidy: does paternal age impact aneuploidy rates in embryos?

2019 ◽  
Vol 112 (3) ◽  
pp. e16
Author(s):  
Katrina Merrion ◽  
Diane Ahern ◽  
Jessica Adsit ◽  
Katherine L. Howard ◽  
Dusan Kijacic ◽  
...  
Keyword(s):  
Paternal Age ◽  
Parental Origin

scholarly journals Molecular Analysis of Nondisjunction in Mice Heterozygous for a Robertsonian Translocation

Genetics ◽  
2002 ◽  
Vol 161 (3) ◽  
pp. 1219-1224
Author(s):  
Lara A Underkoffler ◽  
Laura E Mitchell ◽  
A Russell Localio ◽  
Shannon M Marchegiani ◽  
Justin Morabito ◽  
...  
Keyword(s):  
Molecular Analysis ◽  
Robertsonian Translocation ◽  
Metacentric Chromosome ◽  
Paternal Age ◽  
Chromosome 7 ◽  
Parental Origin ◽  
Molecular Genotyping ◽  
Factors Influencing ◽  
Meiotic Nondisjunction ◽  
Acrocentric Chromosomes

Abstract A Robertsonian translocation results in a metacentric chromosome produced by the fusion of two acrocentric chromosomes. Rb heterozygous mice frequently generate aneuploid gametes and embryos, providing a good model for studying meiotic nondisjunction. We intercrossed mice heterozygous for a (7.18) Robertsonian translocation and performed molecular genotyping of 1812 embryos from 364 litters with known parental origin, strain, and age. Nondisjunction events were scored and factors influencing the frequency of nondisjunction involving chromosomes 7 and 18 were examined. We concluded the following: The frequency of nondisjunction among 1784 embryos (3568 meioses) was 15.9%.Nondisjunction events were distributed nonrandomly among progeny. This was inferred from the distribution of the frequency of trisomics and uniparental disomics (UPDs) among all litters.There was no evidence to show an effect of maternal or paternal age on the frequency of nondisjunction.Strain background did not play an appreciable role in nondisjunction frequency.The frequency of nondisjunction for chromosome 18 was significantly higher than that for chromosome 7 in males.The frequency of nondisjunction for chromosome 7 was significantly higher in females than in males. These results show that molecular genotyping provides a valuable tool for understanding factors influencing meiotic nondisjunction in mammals.

Parental breeding age effects on descendants’ longevity interact over two generations in matrilines and patrilines

2019 ◽  
Author(s):  
Zac Wylde ◽  
Foteini Spagopoulou ◽  
Amy K Hooper ◽  
Alexei A Maklakov ◽  
Russell Bonduriansky
Keyword(s):  
Maternal Age ◽  
First Generation ◽  
Age Effects ◽  
Population Variation ◽  
Paternal Age ◽  
Interactive Effects ◽  
Competitive Environment ◽  
Larval Diet ◽  
Negative Effects ◽  
Two Generations

Individuals within populations vary enormously in mortality risk and longevity, but the causes of this variation remain poorly understood. A potentially important and phylogenetically widespread source of such variation is maternal age at breeding, which typically has negative effects on offspring longevity. Here, we show that paternal age can affect offspring longevity as strongly as maternal age does, and that breeding age effects can interact over two generations in both matrilines and patrilines. We manipulated maternal and paternal ages at breeding over two generations in the neriid fly Telostylinus angusticollis. To determine whether breeding age effects can be modulated by the environment, we also manipulated larval diet and male competitive environment in the first generation. We found separate and interactive effects of parental and grandparental ages at breeding on descendants’ mortality rate and lifespan in both matrilines and patrilines. These breeding age effects were not modulated by grandparental larval diet quality or competitive environment. Our findings suggest that variation in maternal and paternal ages at breeding could contribute substantially to intra-population variation in mortality and longevity.

Parental origin of diabetes-associated HLA types in sibling pairs with type I diabetes

Diabetes ◽  
1994 ◽  
Vol 43 (12) ◽  
pp. 1462-1468 ◽  
Author(s):  
S. C. Bain ◽  
B. R. Rowe ◽  
A. H. Barnett ◽  
J. A. Todd
Keyword(s):  
Type I Diabetes ◽  
Parental Origin ◽  
Type I ◽  
Sibling Pairs

Offspring sex ratio in moose Alces alces in relation to paternal age: an experiment

2004 ◽  
Vol 10 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Bernt-Erik Sæther ◽  
Erling J. Solberg ◽  
Morten Heim ◽  
John E. Stacy ◽  
Kjetill S. Jakobsen ◽  
...  
Keyword(s):  
Sex Ratio ◽  
Alces Alces ◽  
Paternal Age ◽  
Offspring Sex Ratio ◽  
Offspring Sex

scholarly journals Development of thalamus mediates paternal age effect on offspring reading: A preliminary investigation

2021 ◽  
Author(s):  
Zhichao Xia ◽  
Cheng Wang ◽  
Roeland Hancock ◽  
Maaike Vandermosten ◽  
Fumiko Hoeft
Keyword(s):  
Preliminary Investigation ◽  
Age Effect ◽  
Paternal Age ◽  
Paternal Age Effect

The relative and interactive impact of multiple risk factors in schizophrenia spectrum disorders: a combined register-based and clinical twin study

2021 ◽  
pp. 1-11
Author(s):  
C. Lemvigh ◽  
R. Brouwer ◽  
R. Hilker ◽  
S. Anhøj ◽  
L. Baandrup ◽  
...  
Keyword(s):  
Risk Factors ◽  
Environmental Factors ◽  
Childhood Trauma ◽  
Cannabis Use ◽  
Paternal Age ◽  
Interactive Effects ◽  
Polygenic Risk Score ◽  
Multiple Risk Factors ◽  
Schizophrenia Spectrum ◽  
Multiple Risk

Abstract Background Research has yielded evidence for genetic and environmental factors influencing the risk of schizophrenia. Numerous environmental factors have been identified; however, the individual effects are small. The additive and interactive effects of multiple risk factors are not well elucidated. Twin pairs discordant for schizophrenia offer a unique opportunity to identify factors that differ between patients and unaffected co-twins, who are perfectly matched for age, sex and genetic background. Methods Register data were combined with clinical data for 216 twins including monozygotic (MZ) and dizygotic (DZ) proband pairs (one or both twins having a schizophrenia spectrum diagnosis) and MZ/DZ healthy control (HC) pairs. Logistic regression models were applied to predict (1) illness vulnerability (being a proband v. HC pair) and (2) illness status (being the patient v. unaffected co-twin). Risk factors included: A polygenic risk score (PRS) for schizophrenia, birth complications, birth weight, Apgar scores, paternal age, maternal smoking, season of birth, parental socioeconomic status, urbanicity, childhood trauma, estimated premorbid intelligence and cannabis. Results The PRS [odds ratio (OR) 1.6 (1.1–2.3)], childhood trauma [OR 4.5 (2.3–8.8)], and regular cannabis use [OR 8.3 (2.1–32.7)] independently predicted illness vulnerability as did an interaction between childhood trauma and cannabis use [OR 0.17 (0.03–0.9)]. Only regular cannabis use predicted having a schizophrenia spectrum diagnosis between patients and unaffected co-twins [OR 3.3 (1.1–10.4)]. Conclusion The findings suggest that several risk factors contribute to increasing schizophrenia spectrum vulnerability. Moreover, cannabis, a potentially completely avoidable environmental risk factor, seems to play a substantial role in schizophrenia pathology.

scholarly journals The Evolution of Genomic Imprinting

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1283-1295 ◽  
Author(s):  
Atsushi Mochizuki ◽  
Yasuhiko Takeda ◽  
Yoh Iwasa
Keyword(s):  
Growth Factor ◽  
Genomic Imprinting ◽  
Parental Origin ◽  
Coding Region ◽  
Placental Development ◽  
Genetic Conflict ◽  
Multiple Partners ◽  
Zygotic Gene ◽  
Mammalian Genes ◽  
Maternal Resources

Abstract In some mammalian genes, the paternally and maternally derived alleles are expressed differently: this phenomenon is called genomic imprinting. Here we study the evolution of imprinting using multivariate quantitative genetic models to examine the feasibility of the genetic conflict hypothesis. This hypothesis explains the observed imprinting patterns as an evolutionary outcome of the conflict between the paternal and maternal alleles. We consider the expression of a zygotic gene, which codes for an embryonic growth factor affecting the amount of maternal resources obtained through the placenta. We assume that the gene produces the growth factor in two different amounts depending on its parental origin. We show that genomic imprinting evolves easily if females have some probability of multiple partners. This is in conflict with the observation that not all genes controlling placental development are imprinted and that imprinting in some genes is not conserved between mice and humans. We show however that deleterious mutations in the coding region of the gene create selection against imprinting.

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