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PubMed1992

Associations of maternal and paternal direct and differential behavior with sibling relationships: contemporaneous and longitudinal analyses.

In this study we examined associations of 4 paternal direct and differential behaviors with concurrent and longitudinal assessments of sibling relationships, as well as the unique contributions of mothers' and fathers' behavior to the sibling relationship variables. Observational assessments of maternal and paternal direct and differential behavior, as well as observational and self-report assessments of sibling relationship quality, were obtained. Only one difference emerged between rates of maternal and paternal behavior toward the children; however, paternal behavior accounted for unique variance in sibling relationship quality more often than did maternal behavior. The results are discussed in terms of relative parental availability.

Birth Order↗
PubMed1989

Paternal and maternal alcohol consumption: effects on offspring in two strains of rats.

Long-Evans and Sprague-Dawley male rats were given liquid alcohol diets containing 35%, 17.5%, or 0% ethanol-derived calories (EDC). The latter two groups were pair fed to the higher alcohol diet group. A fourth group received lab chow and water ad libitum to assess the role of paternal undernutrition associated with alcohol consumption. After three or four weeks of diet consumption, these males were bred to females of the same strain. Pregnant females were divided into similarly treated alcohol groups and were fed these diets beginning on gestation Day 8, thus creating a factorial study with strain, paternal, and maternal alcohol consumption as main factors. Paternal alcohol consumption was associated with decreased litter size, decreased testosterone levels, and a strain-related effect on offspring activity. Offspring activity decreased for those sired by 35% and 17.5% EDC Long-Evans fathers. Activity also decreased for offspring sired by 17.5% EDC Sprague-Dawley fathers but increased for those sired by 35% EDC fathers. Paternal alcohol consumption did not affect postnatal mortality or passive avoidance learning of offspring. Maternal alcohol consumption was associated with lower birth weights, lower offspring weights at weaning, increased postnatal mortality, and poorer passive avoidance learning. However, offspring activity was not affected. In a separate study, levels of alcohol in the testes were found to be somewhat, but not significantly, lower than blood alcohol levels. DNA taken from sperm of Long-Evans males consuming alcohol, migrated farther under pulsed field electrophoresis than DNA from control fathers, suggestive of an alcohol-related effect on sperm DNA.

Alcohol Drinking↗
PubMed1995

Alloantibody responses to antigens recognized by rabbit antitrophoblast antisera in trophoblast and mononuclear cell (MNC) membranes by primary aborting women before and after paternal leukocyte immunization.

PROBLEM: Because shared allogeneic antigens are expressed on peripheral blood lymphocytes, as well as trophoblasts, it has been proposed that lymphocyte transfusions may appropriately sensitize recurrent spontaneous aborters (RSA) to trophoblast and lead to pregnancy conservation. The degree to which these responses are affected by this treatment, however, has not been defined. METHOD: SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analyses were used to study the alloantibody responses in RSA patients both before and after immunization with paternal leukocytes (MNC) against membrane proteins isolated from peripheral blood mononuclear cells (MNC), first trimester and full term chorionic villi (CV). RESULTS: A distinct set of antigens with apparent molecular weights of 32, 36, 41, 63, 65, and 85 kDa was identified in both MNC and trophoblast membranes by rabbit anti-trophoblast antisera. In addition, a 55 kDa protein was recognized by MNC membranes. Thirty-eight percent of primary RSA sera recognized this 55 kDa protein. After paternal MNC immunization, all primary RSA samples displayed increased reactivity or produced antibodies to this 55 kDa protein when compared with preimmunization sera. The protein was identified as MCP using a rabbit polyclonal anti-MCP antisera. In contrast, reactivity to the other antigens present in the membrane preparations decreased after paternal MNC immunization. CONCLUSION: Changes in immune reactivity in RSA patients after paternal MNC immunization suggest that immunization alters serum immune reactivity to MNC and trophoblast shared antigens.

Abortion, Habitual↗
PubMed1996

Anomalous inheritance of a paternally derived trophoblast antigen.

PROBLEM: Recurrent spontaneous abortion occurs in 1 in 500 random matings and usually results in abortion of all pregnancies. If absence of antibody to a paternally derived antigen caused abortion, the woman would be expected to make antibody to the other paternal antigen and abort only half her pregnancies. METHODS: Microvesicles were prepared from equine placentae. Acid-eluted IgG antibody was eluted from the polymorphic R80K antigen and used to type the residual R80K antigen on vesicles or on peripheral blood leucocytes. RESULTS: In several equine sibships all the half-sibs had the same paternal R80K alloantigen. In the extended horse family descended from the stallion Nearco, three allotypes were found. The allele present was usually the grandpaternal one, but exceptions are seen. Whichever allele is transmitted all the progeny have the same alloantigen (probability of this occurring by chance = 2(-45)). CONCLUSION: Because only one paternal allotype is present in all progeny, lack of antibody to the R80K antigen would result in loss of all pregnancies, not one half.

Alleles↗
PubMed1992

Paternal occupational lead exposure and congenital malformations.

STUDY OBJECTIVE: The aim was to investigate whether occupational exposure to lead in fathers is associated with congenital malformation in their children. DESIGN: The study was a retrospective case-control study, nested within the wives of men biologically monitored for inorganic lead. Information on pregnancy outcome was obtained from medical registers. SUBJECTS: Cases were defined as wives with malformed child during 1973-82. Three age matched controls were selected for each case from the wives who had given birth during 1973-1983. The final study population was 27 cases and 57 controls. MEASUREMENTS AND MAIN RESULTS: Paternal lead exposure was assessed with blood lead measurements and data obtained from a questionnaire. The response rate was 67% among the cases and 76% among the controls. The odds ratio (OR) of congenital malformation for paternal lead exposure was increased (OR 2.4, 95% confidence interval 0.9-6.5), although not reaching statistical significance. The odds ratios varied from 1.9 to 3.2, when adjusted for one potential confounding variable at a time. CONCLUSIONS: Because of the small numbers and low participation, this study offers limited support for the hypothesis that paternal lead exposure is associated with congenital malformation. Further epidemiological studies on the reproductive hazards of paternal lead exposure are needed.

Abnormalities, Drug-Induced↗
PubMed1991

Paternal origin of the chromosomal deletion resulting in Wolf-Hirschhorn syndrome.

DNA samples were obtained from children with Wolf-Hirschhorn syndrome and their parents to assist with gene mapping studies of 4p16.3 (the region known to contain the Huntington's disease gene). A panel of seven families was studied, using polymorphic DNA markers, to determine the parental origin of the chromosome abnormality resulting in Wolf-Hirschhorn syndrome. All seven cases were the result of de novo deletions or rearrangements of 4p and in each case the abnormality arose on the paternal chromosome. Analysis of the 3' hypervariable regions of the alpha globin and mucin loci indicated that non-paternity was unlikely to be an explanation for these results. A paternal age effect was not observed. The possibilities of an environmental influence or genetic imprinting require further consideration. This report extends information regarding the preponderance of the paternal origin of de novo structural deletion syndromes.

Adult↗
PubMed1997

Paternal transmission of congenital myotonic dystrophy.

We report a rare case of paternally transmitted congenital myotonic dystrophy (DM). The proband is a 23 year old, mentally retarded male who suffers severe muscular weakness. He presented with respiratory and feeding difficulties at birth. His two sibs suffer from childhood onset DM. Their late father had the adult type of DM, with onset around 30 years. Only six other cases of paternal transmission of congenital DM have been reported recently. We review the sex related effects on transmission of congenital DM. Decreased fertility of males with adult onset DM and contraction of the repeat upon male transmission contribute to the almost absent occurrence of paternal transmission of congenital DM. Also the fathers of the reported congenitally affected children showed, on average, shorter CTG repeat lengths and hence less severe clinical symptoms than the mothers of children with congenital DM. We conclude that paternal transmission of congenital DM is rare and preferentially occurs with onset of DM past 30 years in the father.

Adult↗
PubMed2005

Heteroplasmy and paternally oriented shift of the organellar DNA composition in barley-wheat hybrids during backcrosses with wheat parents.

Mitochondrial (mt) and chloroplast (ct) genome inheritance was studied in barley-wheat hybrids, as were their progenies obtained from backcrosses with different common wheat cultivars, by monitoring the composition of 4 mtDNA (coxI, a 5'-flanking region of cob, nad3-orf156, and 5'-upstream region of 18S/5S) and 2 ctDNA (simple-sequence repeat locus downstream of trnS and a 3'-flanking region of rbcL) loci. In male sterile F1 and BC1 plants, maternal barley mtDNA fragments were mainly detected and very low levels of paternal wheat fragments were occasionally detected by PCR in coxI, a 5'-flanking region of cob and nad3-orf156, whereas a 5'-upstream region of 18S/5S showed clear heteroplasmy, containing both maternal and paternal copies, with maternal copies prevailing. Plants showing such heteroplasmic mtDNA composition remained either semisterile or became completely sterile in the later backcross generations. Only maternal ctDNA copies were detected in these plants. In 3 stable, self-fertile, and vigourous lines obtained in the advanced backcross generations and possessing recombinant wheat nuclear genome, however, only mt- and ctDNA copies of wheat parents were detected; thus, the original alloplasmic condition appeared to be lost. Our results suggest that transmission followed by selective replication of the paternal wheat organellar DNA leads to a paternally oriented shift of the organellar DNA composition in barley-wheat hybrids, which correlates with the restoration of fertility and plant vigour. These 2 processes seem to be related to nucleocytoplasmic compatibility and to be under the control of the nuclear genome composition.

Chimera↗
PubMed1993

Somatic mosaicism for partial paternal isodisomy in Wiedemann-Beckwith syndrome: a post-fertilization event.

Genomic imprinting has been implicated in the aetiology of an overgrowth cancer-prone syndrome, the Wiedemann-Beck-with syndrome (WBS). We have demonstrated uniparental disomy (UPD) for paternal chromosome 11p markers in 5 out of 25 sporadic cases (20%). Delineation of the extent of the disomy region may help in understanding the mechanism and the stage, meiotic or mitotic, of disomy formation in this disease and in associated tumours. Our current studies in WBS patients with seventeen 11p and one 11q markers reveal paternal isodisomy, not heterodisomy, in the five cases. For one case we demonstrate unambiguously that partial isodisomy for 11p and somatic mosaicism for UPD resulted from a post-fertilization event. The restriction of isodisomy to part of 11p in another case, and somatic mosaicism for UPD in three other cases, suggest a mitotic recombinational event that must have occurred after fertilization. Mosaic phenotypes reflect the timing of their origin and the fate of the cells involved, as well as the cell-specific pattern of imprinting. Somatic mosaicism for UPD in four cases may thus explain the incomplete forms of WBS. The association of hemihypertrophy in sporadic WBS and even some cases of isolated hemihypertrophy. This is in agreement with a recent report of paternal isodisomy for 11p markers in a patient with hemihypertrophy, Wilms' tumour and adrenocortical carcinoma. Moreover, the risk of developing a tumour seems higher (50%) for patients with paternal 11p UPD than for WBS patients in general (7.5%).

Adult↗
PubMed1991

Timing of paternal Pgk-1 expression in embryos of transgenic mice.

In mouse development, the paternal allele of the X-linked gene Pgk-1 initiates expression on day 6, two days later than the maternal allele, which is activated on day 4. The different timing of expression of the maternal and paternal alleles may be determined by (i) imprinting of the chromosome region in which the gene resides, but not aimed specifically at the Pgk-1 gene; (ii) gene specific imprinting, acting on Pgk-1 irrespective of the chromosomal localization of the gene; (iii) an interplay between embryo cell differentiation, timing of X-inactivation and Pgk-1 expression, without the involvement of imprinting at the Pgk-1 locus itself (Fundele R., Illmensee, K., Jagerbauer, E. M., Fehlau, M. and Krietsch, W. K. (1987) Differentiation 35, 31-36). Our findings in transgenic mouse lines, carrying Pgk-1 on autosomes, indicate the importance of the X chromosomal location for the delayed expression of the paternal Pgk-1 allele, and are in agreement with the first of the explanations listed above. We propose that the late activation of the paternal Pgk-1 locus is a consequence of imprinting targeted at, and centered around, the X chromosome controlling element.

Animals↗
PubMed1997

Differential H4 acetylation of paternal and maternal chromatin precedes DNA replication and differential transcriptional activity in pronuclei of 1-cell mouse embryos.

In the mouse embryo, transcriptional activation begins during S/G2 phase of the first cell cycle when paternal and maternal chromatin are still in separate nuclear entities within the same cytoplasm. At this time, the male pronucleus exhibits greater transcriptional activity than the female pronucleus. Since acetylation of histones in the nucleosome octamer exerts a regulatory influence on gene expression, we investigated changes in histone acetylation during the remodeling of paternal and maternal chromatin from sperm entry through to minor genome activation and mitosis. We found (1) neither mature sperm nor metaphase II maternal chromatin stained for hyperacetylated histone H4; (2) immediately following fertilization, hyperacetylated H4 was associated with paternal but not maternal chromatin while, in parthenogenetically activated oocytes, maternal chromatin became hyperacetylated; (3) in zygotes, differential levels and patterns of hyperacetylated H4 between male and female pronuclei persisted throughout most of G1 with histone deacetylases and acetyltransferases already active at this time; (4) when transcriptional differences are observed in S/G2, male and female pronuclei have equivalent levels of H4 hyperacetylation and DNA replication was not required to attain this equivalence and (5) in contrast to the lack of H4 hyperacetylation on gametic chromatin, chromosomes at the first mitosis showed distinct banding patterns of H4 hyperacetylation. These results suggest that sperm chromatin initially out-competes maternal chromatin for the pool of hyperacetylated H4 in the oocyte, that hyperacetylated H4 participates in the process of histone-protamine exchange in the zygote, and that differences in H4 acetylation in male and female pronuclei during G1 are translated across DNA replication to transcriptional differences in S/G2. Prior to fertilization, neither paternal nor maternal chromatin show memory of H4 hyperacetylation patterns but, by the end of the first cell cycle, before major zygotic genome activation at the 2-cell stage, chromosomes already show hyperacetylated H4 banding patterns.

Acetylation↗
PubMed1997

Roles of the imprinted gene Igf2 and paternal duplication of distal chromosome 7 in the perinatal abnormalities of androgenetic mouse chimeras.

Mouse chimeras made with androgenetic (two paternal genomes) ova or embryonic stem cells frequently die at the perinatal stage and exhibit a range of defects, the most noticeable being a pronounced overgrowth of rib cartilage. Excess concentrations of IGFII, a potent mitogen, has been suggested to play a major role in these defects, as androgenetic cells possess two active paternal copies of the imprinted Igf2 gene, rather than one inactive maternal and one active paternal copy as in normal cells. Here, we show that chimeras made with androgenetic embryonic stem cells, homozygous for an Igf2 null mutation, do not develop rib cartilage hyperplasia, demonstrating the dependence of this defect on Igf2 activity produced by androgenetic cells. In contrast, in these same chimeras, many other defects, including whole body overgrowth and perinatal death, are still prevalent, indicating that the abnormal expression of one or more imprinted genes, other than Igf2, is also capable of inducing most of the defects of androgenetic chimeras. Many of these genes may reside on distal chromosome 7, as we also show that perinatal chimeras made with embryonic stem cells possessing paternal duplication of distal chromosome 7 exhibit a range of defects similar to those of androgenetic chimeras. The relevance of these findings for the human imprinting-related disorder, Beckwith-Wiedemann syndrome, is discussed.

Animals↗
PubMed1998

The paternal allele of the H19 gene is progressively silenced during early mouse development: the acetylation status of histones may be involved in the generation of variegated expression patterns.

Transcriptional silencing can reflect heritable, epigenetic inactivation of genes, either singly or in groups, during the life-time of an organism. This phenomenon is exemplified by parent-of-origin-specific inactivation events (genomic imprinting) for a subset of mammalian autosomal genes, such as H19. Very little is known, however, about the timing and mechanism(s) of silencing of the paternal H19 allele during mouse development. Using a novel in situ approach, we present evidence that the silencing of the paternal H19 allele is progressive in the trophectodermal lineage during early mouse development and generates variegated expression patterns. The silencing process apparently involves recruitment of histone deacetylases since the mosaic paternal-specific H19 expression reappears in trichostatin A-treated mouse conceptuses, undergoing in vitro organogenesis. Moreover, the paternal H19 alleles of PatDup.d7 placentas, in which a region encompassing the H19 locus of chromosome 7 is bipaternally derived, partially escape the silencing process and are expressed in a variegated manner. We suggest that allele-specific silencing of H19 share some common features with chromatin-mediated silencing in position-effect variegation.

Acetylation↗
PubMed2006

Paternal chromosome segregation during the first mitotic division determines Wolbachia-induced cytoplasmic incompatibility phenotype.

The most common Wolbachia-induced phenotype in insects is cytoplasmic incompatibility (CI), which occurs when sperm from infected males fertilize eggs from uninfected females. CI produces distinct phenotypes in three closely related haplo-diploid species of the genus Nasonia: mortality in N. longicornis and N. giraulti, and conversion to male development in N. vitripennis. We demonstrate that the majority of CI-induced mortality occurs during embryogenesis and that the pattern of paternal chromosome segregation during the first mitosis is a good predictor of CI phenotype. In N. giraulti and N. longicornis, the paternal chromosomes mis-segregate, producing abnormal nuclei connected by chromatin bridges. Consequently, these embryos arrest development with very few and abnormal nuclei. In contrast, the paternal genome in N. vitripennis is either not segregated or mis-segregates to one of the two daughter nuclei. Consequently, these embryos continue development utilizing the maternally derived haploid nuclei, resulting in male offspring. The latter class is the first documented example of asymmetric mitotic segregation of abnormal chromosomes. We conclude that in haplo-diploids, CI-induced embryonic lethality occurs only when abnormal paternal genome segregation affects both products of the first mitotic division. This is the first study to associate differences in types of CI with specific cytological defects.

Animals↗
PubMed2002

Child sexual abuse victims' perception of paternal support as a significant predictor of coping style and global self-worth.

One hundred eighty-eight female participants (44 victims and 144 non-victims of CSA) from a 4-year university were recruited. The first objective examined the difference between victims and non-victims on measures of perceived social support, coping strategies, and global self-worth. Victims were more likely to report lower maternal support than non-victims of CSA. Additionally, victims who were perpetrated by a family member were more likely to report lower maternal support than those who were perpetrated by a non-family member. The second objective investigated the impact of victimization and several mediating factors on global self-worth. Victimization indirectly related to global self-worth through paternal support. Additional analyses examining non-victims showed significant direct relations between paternal, friend, and campus support leading to global self-worth. For victims, paternal support indirectly related to global self-worth through emotion- focused coping. These results indicate that paternal support and coping strategies may be important for later psychological adjustment in victims of CSA.

Adaptation, Psychological↗
PubMed2001

Peripubertal paternal EtOH exposure.

Fetal alcohol syndrome usually implies effects on the offspring of maternal EtOH consumption during gestation, with fewer reports addressing the impact of paternal exposure on the progeny. One previous report has dealt with the impact of EtOH exposure on peripubertal male rats as a model of teenage drinking and the deleterious effects on the offspring. We report here findings examining the effect of 2 mo of EtOH feeding on male animals as they progressed through puberty on their ability to impregnate EtOH-naive female rats and characteristics of the subsequent litters. The EtOH-imbibing fathers weighed significantly less than pairfed controls and animals ingesting a non-EtOH liquid diet ad libitum. Nevertheless, they were able to mate successfully, although fecundity was significantly reduced. The number of successful pregnancies, defined as carried to term, was diminished from 92% in controls to 75% in EtOH-fed animals (p < 0.05). There was increased paternal testicular oxidative injury demonstrated by enhanced lipid peroxidation, protein oxidation, and decreased ratio of reduced to oxidized glutathione. The litter size of the EtOH-exposed males was reduced by 46%. The average litter size was 12.4+/-1.5 pups/litter in ad libitum animals, virtually identical to the 12.5+/-0.6 pups/litter in the pair fed controls. This is in sharp contrast to the 6.7+/-0.1 pups/litter from the paternal EtOH matings (p < 0.001). There was an increase in the average individual weight of pup offspring of paternally EtOH-exposed animals (p < 0.01 vs pair-fed controls and p < 0.05 vs ad libitum). Curiously, the male-to-female pup ratio was altered with a higher preponderance of male offspring from EtOH-fed fathers. There were no gross malformations noted among the pups. Insulin-like growth factor-1 levels in the pups at 10 d of age were unaltered between the groups. However, leptin was significantly elevated in the EtOH offspring. It appears that chronic EtOH exposure in the peripubertal fathers subsequently decreases fecundity and that this may be mediated by testicular oxidative injury, perhaps leading to accelerated germ cell apoptosis.

Animals↗
PubMed2001

Analysis of paternal alleles in nucleated red blood cells enriched from maternal blood.

The purpose of our study was to identify paternal alleles in NRBC enriched from maternal peripheral blood for detection of the presence of foetal cells in the maternal circulation and to establish a reliable non-invasive method which should allow following genetic testing. For enrichment of foetal cells from peripheral maternal blood we combined Ficoll-Paque density gradient centrifugation and MACS. Maternal leukocytes were firstly depleted using anti-CD14 and anti-CD45 microbeads. NRBC were sorted from the CD14-/CD45- fraction by positive selection using CD71 microbeads. Paternal alleles in the CD14-/CD45-/CD71+ fraction were indicated by the PCR method using HLA (DRB1, DQB1, DQA1) and Polymarker System (LDLR, GYPA, HBGG, D7S8, GC) as genetic markers. Different paternal alleles of studied 8 loci were detected in 13 out of 19 samples of cells enriched from maternal peripheral blood between the 13th and 36th week of gestation. Our results demonstrate that foetal cells enriched from maternal peripheral blood may be used as a source of foetal DNA for prenatal diagnosis, paternity testing and other application.

Alleles↗
PubMed1999

Hyperinsulinism caused by paternal-specific inheritance of a recessive mutation in the sulfonylurea-receptor gene.

Neonatal hyperinsulinism (HI) is a genetic disorder of pancreatic beta-cells characterized by failure to suppress insulin secretion in the presence of hypoglycemia, resulting in brain damage or death if not adequately treated. Germline mutations in four genes have been associated with HI. Some patients have focal regions of beta-cell proliferation (focal HI). Seventy HI probands in whom at least one SUR-1 mutation was identified were studied. Clinical data from patients with two SUR-1 mutant alleles were compared with those from patients with single paternally inherited mutations. Thirty-seven probands were homozygous or compound heterozygous for SUR-1 mutations. In 33 probands, only a single mutation was identified, and in 31, the parental origin of the proband could be determined; in 29, the mutation was on the paternal allele (P < 0.0002). For three of these, pancreatic tissue was available and showed focal beta-cell hyperplasia. DNA extracted from the focal lesion and adjacent normal pancreas revealed loss of the maternal chromosome 11p15, resulting in reduction to homozygosity for the SUR-1 mutation within the focal lesion only. Using the Tdt-mediated dUTP nick end labeling (TUNEL) reaction, apoptotic beta-cells were identified exclusively within the focal region. At diagnosis, disease severity was similar in patients with paternally inherited mutations and those with two mutations. For patients who did not undergo surgery, those with only paternal mutations entered clinical remission within 16 +/- 6.2 months, compared with 48 +/- 23 months for those with two SUR-1 mutations (P = 0.001). In conclusion, we identified a novel mechanism to explain the pathophysiology of focal HI and provide evidence to suggest that this entity may be self-limiting, since affected beta-cells undergo apoptosis.

ATP-Binding Cassette Transporters↗