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At least 19 recordsLinked to original sources
PubMed1992

Parental imprinting studied by allele-specific primer extension after PCR: paternal X chromosome-linked genes are transcribed prior to preferential paternal X chromosome inactivation.

The preferential inactivation of the paternal X chromosome in extraembryonic cells during early mouse development is an example of parental imprinting, but it has not been studied at the transcriptional level because standard methods of measuring RNA levels do not allow detection of allele-specific RNAs in individual early embryos. We sought to determine whether the paternal allele of the X chromosome-linked gene for 3-phosphoglycerate kinase 1 (Pgk-1), which is located very near the center of X chromosome inactivation, is transcribed prior to differentiation of extraembryonic lineages. Previous reports indicated that in heterozygous embryos there is a delay in the appearance of the phosphoglycerate kinase 1 allozyme encoded by the paternal X chromosome until 2 days after the appearance of the corresponding maternal allozyme. We report results obtained by use of a reverse transcription/PCR-based method which allows the quantitative measurement of allele-specific RNA. The assay is sensitive enough for the quantitative analysis in single embryos of allele-specific transcripts differing by only one nucleotide. We have used this assay to analyze mouse embryos heterozygous at the Pgk-1 and Hprt [hypoxanthine (guanine) phosphoribosyltransferase] loci, and we find that individual 8-cell and blastocyst embryos express both Hprt and Pgk-1 paternal transcripts, as do pooled 2- to 4-cell embryos. These results are discussed in view of the apparent temporal delay in paternal expression of the Pgk-1 gene at the enzyme level.

Alleles↗
PubMed1975

Paternal loss (pal): a meiotic mutant in Drosophila melanogaster causing loss of paternal chromosomes.

The effects of a male-specific meiotic mutant, paternal los (pal), in D. melanogaster have been examined genetically. The results indicate the following: (1) When homozygous in males, pal can cause loss, but not nondisjunction, of any chromosome pair. The pal-induced chromosome loss produces exceptional progeny that apparently failed to receive one, or more, paternal chromosomes and, in addition, mosaic progeny during whose early mitotic divisions one or more paternal chromosomes were lost. (2) Only paternally derived chromosomes are lost. (3) Mitotic chromosome loss can occur in homozygous pal+progeny of pal males. (4) Chromosomes differ in their susceptibility to pal-induced loss. The site responsible for the insensitivity vs. sensitivity of the X chromosome to pal mapped to the basal region of the X chromosome at, or near, the centromere. From these results, it is suggested that pal+acts in male gonia to specify a product that is a component of, or interacts with, the centromeric region of chromosomes and is necessary for the normal segregation of paternal chromosomes. In the presence of pal, defective chromosomes are produced and these chromosomes tend to get lost during the early cleavage divisions of the zygote. (5) The loss of heterologous chromosome pairs is not independent; there are more cases of simultaneous loss of two chromosomes than expected from independence. Moreover, an examination of cases of simultaneous somatic loss of two heterologs reveals an asymmetry in the early mitotic divisions of the zygote such that when two heterologs are lost at a somatic cleavage division, almost invariably one daughter nucleus fails to get either, and the other daughter nucleus receives its normal chromosome complement. It is suggested that this asymmetry is not a property of pal but is rather a normal process that is being revealed by the mutant. (6) The somatic loss of chromosomes in the progeny of pal males allows the construction of fate maps of the blastoderm. Similar fate maps are obtained using data from gynandromorphs and from marked Y chromosome (nonsexually dimorphic) mosaics.

Animals↗
PubMed1978

[Paternity index. Application to a sample of 48 trios presumptive father-mother-child. Study of the relationship between the probability of paternity and the percentage of exclusion].

Two different indices are of interest in paternity diagnosis. 1. The proportion of men whose paternity is excluded by mother and child phenotypes. 2. The posterior probability of paternity, obtained by a bayesian process from the phenotypes of putative father, mother and child. These two indices are different, and it is proposed that the first one be used for gauging the value of the second. Two examples of the method are given: first, a sample of 48 putative father-mother-child trios, observed in the probability of paternity versus proportion of excluded men plane at different steps on the laboratory examinations, second, the figure obtained for a child for whom two putative fathers were at examination.

Paternity↗
PubMed1991

[Diagnosis of paternity by deduction of the probable genotype of the deceased person from the relatives--in addition to the examination of the Essen-Möller value and diagnosis of paternity based on the probability distribution of log (Y/X)].

1) The present paper deals with the general formulas of paternity probability, applicable to any cases where the putative man and/or the plaintive mother are deceased, using the blood types of various relatives. Two typical examples are described. 2) Bayes's theorem is applied to the calculation of probability of paternity using the Essen-Möller's formula, in which a putative father is to be compared with any one of the men in the general population whose blood types are unidentified. Statistically, those men are supposed to have any one of several blood types, depending on the frequency of occurrence of those types. This means that their blood types include the blood type of the putative father. According to Bayes's theorem, however, probability calculations are valid only when the two types to be compared are mutually exclusive. Consequently, the theorem should not be applied to probability calculations using the Essen-Möller's formula. 3) A new basis of judgement for the diagnosis of paternity is proposed using the probability distribution of the relative frequencies of log (Y/X) for true father and that for non-father.

Blood Group Antigens↗
PubMed1977

[Calculation of the Chance of paternity exclusion and of the probability of paternity for the HLA system (author's transl)].

The genetics of the serological defined SD antigens of the HLA system, which are governed by three closely linked loci (HLA-A, HLA-B and HLA-C) situated on the chromosome C6, are described. Regarding patermity testing, only the antigens coded by the loci HLA-A and HLA-B are used routinely up to now. Because of the strong linkage disequilibrium between these two loci, they cannot be considered as independent. The influence of the linkage disequilibrium on the calculation of the chance of paternity exclusion and of the plausibility of paternity is discussed and demonstrated in several examples.

Adult↗
PubMed1977

[Calculation of the probability of paternity and of the chance of paternity exclusion for the HLA system using only the typing results from the child and the putative father (author's transl)].

A method for the calculation of the probability of paternity for the HLA system using only the typing results from the child and the putative father, without taking into account the data of the mother, is presented. Furthermore, the usability of the formulas by Mayr and Pausch (Z. Immun.-Forsch. 150, 447 (1975)) for the computation of the chance of paternity exclusion in such cases is demonstrated.

Austria↗
PubMed2026

Monitoring the fate of paternal mitochondria and their elimination in rice zygotes.

Mitochondria are preferentially transmitted from the maternal plant in most angiosperms, including rice, and paternal mitochondria are generally eliminated during microgametogenesis and/or in zygotes. The mechanism by which paternal mitochondria are eliminated progresses during plant reproductive processes. In the present study, we examined the distribution of paternal mitochondria in rice sperm cells and zygotes produced through the in vitro fertilization (IVF) of isolated rice gametes. Male gametes of rice possess mitochondria with nucleoids, suggesting the potential transfer of paternal mitochondria and their DNA into zygotes on fertilization and subsequent selective elimination of paternal mitochondria in the zygote. To intensively monitor the fate of rice paternal mitochondria in zygotes immediately after gamete fusion, time-lapse observations were conducted in paternal mitochondria labeled with GFP from rice zygotes produced using an IVF system. The results showed that the paternal mitochondria are progressively degraded during the early developmental stage at 1 to 3 h after fusion (HAF), leaving a small number of paternal mitochondria at 6 HAF. The remaining paternal mitochondria were considered to be degraded in later developmental-stage zygotes because paternal mitochondrial DNA-derived single-nucleotide polymorphisms were not detected in the sequencing reads of genomic DNA prepared from inter-subspecific hybrid rice. In addition, treatment with autophagy inhibitors stabilized the paternal mitochondria in zygotes. This suggests that the autophagy-dependent massive and selective elimination machinery for male mitochondria functions in rice zygotes immediately after gamete fusion and supports the strict maternal inheritance of mitochondria in rice.

Oryza↗
PubMed2026

Associations Between Paternal Pre-Conceptional Body Mass Index and Lifestyle Factors and Offspring Weight Development.

BACKGROUND: Evidence suggests that pre-conceptional paternal factors, including BMI and diet, may influence offspring development. OBJECTIVES: We examined the associations between paternal BMI, dietary protein intake, glycemic index (GI), smoking and alcohol consumption and offspring development during the first 5 years of life. METHODS: This secondary analysis of an RCT included 162 father-child pairs from pregnancies among women with pre-pregnancy overweight or obesity. Paternal characteristics were reported at gestational week 15, reflecting the preceding 3 months. Offspring anthropometry was measured at birth, 6 and 18 months, 3 and 5 years. Associations were examined using linear mixed models and linear regression models. RESULTS: No consistent associations were found between paternal characteristics and offspring outcomes from birth to 3 years. At age 5, higher paternal BMI was associated with higher offspring BMI z-score (β = 0.07 (CI: 0.03; 0.10)), fat mass index (β = 0.07 kg/m2 (CI: 0.02; 0.12)) and fat-free mass index (β = 0.05 kg/m2 (CI: 0.01; 0.08)). Lower paternal protein intake was associated with higher offspring BMI z-score (β = 0.54 (CI: 0.07; 1.01)) and fat-free mass index (β = 0.60 kg/m2 (CI: 0.13; 1.07)), while moderately higher protein intake was associated with higher waist-to-height ratio (β = 0.03 (CI: 3.00 × 10-3; 0.05)). Higher paternal GI was associated with lower offspring BMI z-score (β = -0.04 (CI: -0.08; -2.14-10-3)) at age 5. Smoking and alcohol were not associated with offspring outcomes. CONCLUSION: Paternal BMI was associated with offspring outcomes at age 5 years, while findings for paternal dietary factors were less consistent.

Humans↗
PubMed1991

Lymphocytotoxins in sera from highly sensitized multiparous dialysis patients: antibody class, relationship with the HLA and with paternal antigens.

1. Sera from 11 highly sensitized multiparous dialysis patients were studied in order to define the target antigens, antibody class and relationship with paternal HLA class I antigens of the underlying lymphocytotoxic antibodies. All sera contained lymphocytotoxic antibodies to over 70% of a panel of lymphocytes from 24 donors (panel reactivity greater than 70%). 2. Inhibition of cytotoxic activity against paternal lymphocytes by monoclonal antibodies to HLA framework determinants indicated that all 11 sera contained lymphocytotoxic antibodies to paternal class I antigens. In addition, five sera contained lymphocytotoxic antibodies to paternal class II antigens. 3. In order to determine the extent to which lymphocytotoxic antibodies were directed to paternal antigens, the panel reactivity of sera was compared before and after absorption with paternal peripheral blood lymphocytes. Over 50% of panel reactivity was absorbed from eight out of 11 sera, and in three of these 11 over 80% was absorbed. In the majority of patients this change in panel reactivity could be ascribed to binding of lymphocytotoxic antibodies to specific paternal class I antigens. 4. Digestion of sera with dithiothreitol had no significant effect on panel reactivity, indicating that the lymphocytotoxic antibodies were of immunoglobulin G class. 5. No sera reacted with either autologous lymphocytes or K562 cells, indicating an absence of autoantibodies. 6. These studies imply that panel-reactive lymphocytotoxic antibodies in the sera of highly sensitized multiparous patients are those which mediate hyperacute renal allograft rejection. Their development may be related to secondary humoral responses to antigens in blood transfusions from donors who share paternal class I specificities.

Adult↗
PubMed1978

Down syndrome, paternal age, maternal age and birth order.

Recent cytogenetic evidence has shown that trisomy 21 can arise, perphaps even in substantial proportion, from paternal nondisjunction. The statistical association between Down syndrome incidence and maternal age, paternal age and birth order has been studied in a sample of over 4000 cases. The size of this sample made it possible to control for the effect of maternal age by single years of age during the search for a paternal age effect and vice versa, and the importance of such stringent control is emphasized. The maternal age association was confirmed with an extremely high degree of statistical significance while no independent effect of paternal age was found; indeed, the rates at paternal ages over 45 years appear to be nearly constant. After adjusting for the effects of parental age, a significant inverse association of birth order with incidence was noted. It also appears that the incidence among very young mothers may be high: for maternal ages 15 years and less the rates seem to be equivalent to those found at 30 or 35 years. In order to help answer the question of whether the maternal age association is the result of increasing rates of nondisjunction or of some other mechanism (for example, an age related defect in a spontaneous abortion screening mechanism), the proportion of cases due to maternal and paternal nondisjunction at different parental ages must be determined.

Adolescent↗
PubMed2026

Risk of neurodevelopmental disorders associated with paternal use of valproate during spermatogenesis: a living meta-analysis-version 1.

OBJECTIVE: To evaluate the association of paternal use of valproate during spermatogenesis compared with paternal use of lamotrigine or levetiracetam on offspring risk of neurodevelopmental disorders (NDDs). METHODS: Eligibility criteria: observational, peer-reviewed studies reporting neurodevelopmental outcomes of children exposed to paternal monotherapy use of valproate vs lamotrigine or levetiracetam during spermatogenesis. INFORMATION SOURCES: the databases PubMed, Embase, Cochrane Library and Web of Science were systematically searched from January 1995 to October 2025.Synthesis of results and risk of bias: a random-effects model was used to estimate pooled HRs and 95% CI, with heterogeneity assessed using I2 statistic for any NDD.We present a meta-analysis of observational, peer-reviewed studies reporting neurodevelopmental outcomes of children exposed to paternal monotherapy use of valproate versus lamotrigine or levetiracetam during spermatogenesis. Given the major regulatory implications of paternal valproate safety, the recent emergence of new population-based data, and the expectation of further large studies, we designed this work as a living systematic review and meta-analysis that will be updated as new eligible evidence becomes available. RESULTS: We identified three eligible studies based on data from (1) Norway and Sweden, (2) Norway and Taiwan and (3) Denmark. As two studies included Norwegian data, their results are referred to as 'Norway 1' and 'Norway 2' for clarity. In the meta-analysis of data from Denmark, Sweden and Norway 1, the pooled HR of offspring NDDs was 1.05 (95% CI 0.87 to 1.27; I2=0.0%), and in meta-analysis of data from Denmark, Sweden and Norway 2, it was 1.03 (95% CI 0.85 to 1.24; I2=0.0%).In the meta-analysis including Taiwan, Denmark, Sweden and Norway 1, the pooled HR was 1.06 (95% CI 0.88 to 1.27; I2=0.0%), and when including data from Taiwan, Denmark, Sweden and Norway 2, the pooled HR was 1.04 (95% CI 0.87 to 1.25; I2=0.0%). CONCLUSIONS: In this living meta-analysis, we found no evidence that paternal exposure to valproate compared with lamotrigine/levetiracetam during spermatogenesis was associated with increased risk of NDDs in offspring.

Humans↗
PubMed2026

Beckwith-Wiedemann spectrum exhibiting a 46,XY karyotype caused by genome-wide paternal uniparental heterodisomy: a case report.

BACKGROUNDS: Patients with genome-wide paternal uniparental disomy (GWpUPD) usually exhibit clinical features of Beckwith-Wiedemann syndrome (BWS) and a 46,XX karyotype, with all chromosomes showing isodisomy. To date, male patients with GWpUPD and a complete 46,XY karyotype, specifically involving heterodisomy, have not been described. RESULTS: We report a male infant exhibiting classical BWS clinical features. DNA methylation analyses showed paternal-specific methylation across multiple imprinted loci, suggesting GWpUPD. Genetic analysis of autosomes and sex chromosomes indicated two distinct paternal genomes in peripheral blood leukocytes, whereas a normal biparental genome was detected in other tissues under chimeric conditions. These findings indicated that the patient had genome-wide paternal uniparental heterodisomy (GWpUPhD). The SNP array revealed the presence of one copy of the X chromosome and one copy of the Y chromosome, the patient is a chimera composed of 46,XY biparental cells (with maternal X) and 46,XY GWpUPhD cells (with paternal X). CONCLUSIONS: This is the first report of a male patient with a GWpUPhD chimera. We propose a potential mechanism of GWpUPhD formation. Our findings expand the molecular spectrum of GWpUPD and provide valuable insights into its pathogenesis in chimeric conditions. Furthermore, the potential for clinical manifestations unique to 46,XY heterodisomy warrants careful long-term follow-up.

Humans↗
PubMed1992

Influence of paternal characteristics on the risk of low birth weight.

The combined effects of maternal and paternal factors on the risk of delivering low birth weight (less than 2,500 g) and very low birth weight (less than 1,500 g) infants were examined among married parents. Using 1984-1988 natality data compiled by the National Center for Health Statistics, the authors found paternal education and race to have independent effects on the risks of low birth weight and very low birth weight after adjustment for maternal characteristics. The odds of low and very low birth weight decreased with increasing paternal education. Adjustment for paternal education decreased the effect of maternal education on the risks of low and very low birth weight. Additionally, the examination of paternal race led to the identification of a subgroup of married black women with lower risks of low and very low birth weight than married black mothers overall. These data suggest that paternal characteristics should be used, in addition to maternal characteristics, to describe the risks of low and very low birth weight.

Adult↗
PubMed1991

The examination of the ITI system in disputed paternities.

106 paternity cases with a total of 114 putative fathers were examined in the inter-alpha-trypsin inhibitor (ITI) system. Analysis was performed by isoelectric focusing (IEF) of untreated sera on polyacrylamide gels. From 39 paternity exclusions, determined in other genetic systems, 7 were confirmed in the ITI system. In 75 expertises the alleged man was not excluded from fatherhood; in 68 cases the probability of paternity was W greater than 99.73%. The practical exclusion rate in the ITI system was therefore calculated to be 10.45%. The theoretical exclusion rate was determined to be 19.3%. In one paternity case the alleged father and the child showed inverse homozygosity in the ITI system, while the man was not excluded from fatherhood in 28 additional marker systems. The calculated probability of his paternity was 99.99%. The assumption of an incomplete expression of the ITI phenotypes in infants is supported by a significant deviation between the observed and expected ITI distributions at population equilibrium.

Alpha-Globulins↗
PubMed1992

Two-man and two-sibling paternity cases.

Traditional genetic marker systems rarely fail to resolve paternity disputes when two or more men are accused, except when men are brothers. A sibling of the biologic father may not be excluded by these laboratory tests and sometimes yields calculated odds of paternity that are equal to or higher than the true male parent. Resolved two-brother cases were compared with resolved cases involving two unrelated men. In each case, the residual odds of paternity were determined for each man and the greater was divided by the lesser to produce a paternity fraction. The paternity fraction is a useful indicator of biologic parentage when it exceeds a value of 10 (log10 of-the-odds score greater than or equal to 1). Tests for alleles at highly heterozygous loci are indicated in initial laboratory evaluations of cases involving brothers. Human leukocyte antigen and variable number of tandem repeat polymorphisms appear suitable.

Alleles↗