Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PATERNITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2006

Peg1/Mest in obese adipose tissue is expressed from the paternal allele in an isoform-specific manner.

Paternally expressed 1 (Peg1)/mesoderm specific transcript (Mest) is an imprinted gene, which is only transcribed from the paternal (father's) allele. In some human cancer tissues, an alternatively spliced variant of PEG1/MEST mRNA using a different promoter of a distinct first exon is expressed from both paternal and maternal alleles. We previously reported that Peg1/Mest expression was markedly up-regulated in obese adipose tissue in mice. Moreover, transgenic overexpression of Peg1/Mest in the adipose tissue resulted in the enlargement of adipocytes in size. Given the potential pathophysiologic relevance in obesity, we examined the nature of increased expression of Peg1/Mest in obese adipose tissue. In obese adipose tissue, expression of Peg1/Mest was increased, but not that of other imprinted genes tested. The transcription rate of Peg1/Mest was increased in obese adipose tissue. We found at least four isoforms of mouse Peg1/Mest generated by use of the alternative first exons. We also demonstrated that the abundantly expressed Peg1/Mest in obese adipose tissue retained monoallelic expression. This is the first report of monoallelic induction of Peg1/Mest in adult tissues.

Adipocytes↗
PubMed2003

Prenatal prediction of infant atopy by maternal but not paternal total IgE levels.

BACKGROUND: The atopic history of parents has long been used to predict infant atopy. However, bias from questionnaires of allergic history are also frequently suspected, because a large number of vasomotor rhinitis, intrinsic asthma, and seborrheic dermatitis cases are probably misinterpreted to be atopic diseases. OBJECTIVE: We attempted to identify a risk factor other than parental atopic history to predict elevated infant IgE levels and infant atopy. METHODS: A total of 655 core families were prenatally recruited, and finally 545 families completed the study for the prospective analysis of infant atopy at 6 months of age. Atopic history and blood samples of parents were collected in the third trimester during pregnancy. Cord blood (CB) was collected immediately after birth. Infant blood samples and history of infant eczema were collected in the 6-month physical checkup clinic. Blood total IgE and specific IgE levels were determined by use of the Pharmacia CAP system. RESULTS: In univariate analysis, maternal, but not paternal, atopic history correlated with elevated CB IgE levels and the occurrence of infant eczema. Elevated maternal, but not paternal, total IgE levels (>150 KU/L) significantly correlated with increases of CB IgE levels (median, 0.54 vs 0.17 KU/L, P <.001), infant IgE levels (log-transformed mean values, 1.32 +/- 0.51 vs 1.13 +/- 0.51 KU/L, P <.001), and infant eczema (P =.008). Multivariate logistical regression analysis, however, showed that only maternal total IgE levels correlated with CB and infant IgE levels and the development of infant eczema. CONCLUSIONS: The maternal, but not paternal, total IgE level correlates with elevated infant IgE levels and infant atopy. This provides a high specificity (83%) and a sensitivity of 34% for prediction of infant atopy. This suggests that maternal factors, placental factors, or both have an impact on perinatal allergic sensitization.

Eczema↗
PubMed2005

Asymmetry in histone H3 variants and lysine methylation between paternal and maternal chromatin of the early mouse zygote.

In mammalian fertilization, the paternal genome is delivered to the secondary oocyte by sperm with protamine compacted DNA, while the maternal genome is arrested in meiotic metaphase II. Thus, at the beginning of fertilization, the two gametic chromatin sets are strikingly different. We elaborate on this contrast by reporting asymmetry for histone H3 type in the pre-S-phase zygote when male chromatin is virtually devoid of histone H3.1/3.2. Localization of the histone H3.3/H4 assembly factor Hira with the paternal chromatin indicates the presence of histone H3.3. In conjunction with this, we performed a systematic immunofluorescence analysis of histone N-tail methylations at position H3K4, H3K9, H3K27 and H4K20 up to the young pronucleus stage and show that asymmetries reported earlier are systematic for virtually all di- and tri-methylations but not for mono-methylation of H3K4 and H4K20, the only marks studied present in the early male pronucleus. For H4K20 the expanding male chromatin is rapidly mono-methylated. This coincides with the formation of maternally derived nucleosomes, a process which is observed as early as sperm chromatin decondensation occurs. Absence of tri-methylated H3K9, tri-methylated H4K20 and presence of loosely anchored HP1-beta combined with the homogenous presence of mono-methylated H4K20 suggests the absence of a division of the paternal chromatin in eu- and heterochromatin. In summary the male, in contrast to female G1 chromatin, is uniform and contains predominantly histone H3.3 as histone H3 variant.

Animals↗
PubMed2005

Is maternal smoking more determinant than paternal smoking on the respiratory symptoms of young children?

BACKGROUND: It is generally accepted that maternal smoking has more detrimental effects than paternal smoking on the respiratory health of children. The objective of this study was to assess the effects of postnatal exposure due to the smoking behaviour by father and mother in the home, and prenatal exposure from maternal smoking during pregnancy, on the respiratory symptoms in children. METHODS: The parents of 484 children, aged 3-6 years, completed a questionnaire about smoking and respiratory symptoms in children. Bivariate and logistic regression analyses were used to examine the associated factors with respiratory symptoms. RESULTS: The final model of logistic regression analysis showed that prenatal exposure by maternal smoking during pregnancy increased the risk of wheezing with colds (adjusted OR=2.00, 95% CI:1.13-3.55) with respect to those children whose mothers reported no smoking during pregnancy. Postnatal exposure by maternal smoking in the home, in the presence of the child, increased the risk of cough with phlegm (adjusted OR=2.79, 95% CI:1.23-6.30) with respect to those children whose mothers did not smoke in their presence. Paternal smoking was associated with wheezing and cough in the bivariate analysis, but did not remain significant in the multivariate analysis. CONCLUSIONS: Our results underline a greater influence of exposure to maternal smoking (prenatal and postnatal) than postnatal paternal smoking on the development of respiratory symptoms in young children.

Air Pollution, Indoor↗
PubMed2005

Effect of testicular biopsy in childhood on spermatogenesis, fertility, and paternity in adulthood--a mouse model study.

OBJECTIVES: To study the effect of testicular biopsy in childhood on spermatogenesis, fertility, and paternity in subsequent adulthood using an animal model. Considerable controversy exists as to whether testicular biopsy should be performed in children. METHODS: Four-week-old male ICR mice were subjected to unilateral testicular biopsy (group 1), bilateral biopsy (group 2), or a sham operation (group 3). At 8 weeks of age, the testicular weight, seminiferous tubular diameter, and manifestation of apoptosis were examined. The motility of sperm obtained from the epididymides of the same testes was also examined. Fertility and paternity was assessed in each mouse by housing it with 2 age-matched females for 2 weeks. RESULTS: No significant differences were found in the testicular weight, mean seminiferous tubular diameter, or number of apoptotic germ cells between the biopsied and unbiopsied side in group 1 or between groups 2 and 3. No significant differences were noted in the average sperm motility rate between the biopsied (30.5% +/- 14.5%) and unbiopsied side (35.8% +/- 19.2%) in group 1, or between groups 2 (37.6% +/- 18.0%) and 3 (39.3% +/- 10.0%). All females who coupled with the male mice in all groups became pregnant. The average number of offspring from the 2 female mice was not significantly different among the three groups (group 1, 13.1 +/- 2.3; group 2, 12.3 +/- 2.0; and group 3, 11.3 +/- 3.0). CONCLUSIONS: The spermatogenesis, fertility, and paternity of mature mice were unaffected by testicular biopsy in childhood.

Age Factors↗
PubMed2001

Paternally inherited transgenes are down-regulated but retain low activity during early embryogenesis in Arabidopsis.

We investigated the timing of transgene activation after fertilisation in Arabidopsis following crosses and using two transgenic promoters (from the AtCYCB1 and AtLTP1 genes). Using both a transactivation system and direct transcriptional fusion to drive beta-glucuronidase reporter expression, reciprocal crosses showed a lack of expression of the paternal components. This is consistent with a lack of paternal genome activity previously reported during early seed development in Arabidopsis [Viella-Calzada et al. (2000) Nature 404, 91-94]. However, transactivation experiments of the BARNASE gene gave evidence that at least some paternal loci retain transcriptional activity, though at a low level, during early embryogenesis.

Arabidopsis↗
PubMedDate not supplied

Paternal and maternal major histocompatibility complex class I antigens are expressed co-dominantly by equine trophoblast.

Invasive equine trophoblast cells of the chorionic girdle express high levels of paternally inherited Major Histocompatibility Complex (MHC) class I antigens prior to migration into the endometrium to form the so-called endometrial cups. Three groups of experiments were performed to determine if maternally inherited MHC class I antigens are expressed on chorionic girdle cells. Results indicated that maternally and paternally inherited MHC class I antigens are co-dominantly expressed by cells of the invasive equine trophoblast, and therefore, that the expression of polymorphic equine MHC class I genes does not appear to be affected by genomic imprinting in this tissue. The demonstration that cells of the chorionic girdle were immunogenic supports the hypothesis that invasion of the maternal endometrium by chorionic girdle cells stimulates the production of anti-paternal alloantibodies normally observed in early horse pregnancy. The co-dominant expression of MHC class I antigens by invasive chorionic girdle cells has important implications for the mechanism of recognition of allogeneic fetal MHC class I antigens by the maternal immune system.

Animals↗
PubMed2000

Paternal investment and the human mating system.

Paternal investment has long been considered responsible for the evolution of predominantly monogamous marriage in humans. However, male-male competition resulting in mate-guarding and male coercion could be equally important. In this review, I use a comparative approach to examine the effect of variation in human paternal investment on our mating system. I conclude paternal investment is important but so too is mate-guarding. I propose a model of our mating system incorporating both factors. Variation in the mating system is explained by variation in male resource control and contribution, resulting in ecologically imposed monogamy or polygyny, as predicted by the polygyny threshold model, as well as variation in male-male competition for status, resulting in socially imposed monogamy or polygyny.

Journal Article↗
PubMed2002

The importance of paternal care on pup survival and pup growth in Peromyscus californicus when required to work for food.

We examined paternal care in the monogamous California mouse when wheel running was necessary to obtain food. Paternal and maternal care, pup survival and feeding were compared in litters with single females (Male Absent) and paired females (Male Present) under three different foraging requirements. When wheel running was required for obtaining food (Wheel Contingent), the male's presence significantly increased pup survival. There were no significant effects of the male's presence on pup survival in the No Wheel (standard laboratory housing with ad lib food) or Wheel Noncontingent (running wheel with ad lib food) groups. Males may have indirectly increased pup survival by helping generate food through wheel running and then subsequently spending less time eating than females. While females reduced the time spent in parental care as pups aged, males increased the time spent in parental care as pups aged. Thus as pups became larger and more expensive to rear, the male increased parental care. These results indicate that paternal care benefits pup survival more under conditions where the parents must forage to obtain food than when food is provided ad lib in the standard laboratory environment.

Journal Article↗
PubMed1997

Paternal repression of the imprinted mouse Igf2r locus occurs during implantation and is stable in all tissues of the post-implantation mouse embryo.

The insulin-like growth factor type 2 receptor, also known as the cation independent mannose-6-phosphate receptor (Igf2r) is an imprinted gene, which is repressed on the paternally inherited allele in midgestation mouse embryos. We have used a LacZ reporter gene, targeted into the endogenous gene, to investigate the developmental timing, tissue specificity and stability of the repression of the paternal allele. The LacZ expression pattern in pre- and post-implantation embryos, confirmed that Igf2r shows monoallelic expression only after implantation. We show here, additionally, that Igf2r shows biallelic expression in all cells of the preimplantation embryo at E4.5, and, that monoallelic expression is clearly present in all tissues at E6.5, in the early post-implantation embryo. Imprinted expression is maintained in later embryonic development and no tissue was observed to escape imprinting up to E13.5 of development. Thus, for Igf2r, the onset of monoallelic expression occurs in all cells during the implantation period and paternal repression is maintained in all tissues of the late developing embryo.

Alleles↗
PubMedDate not supplied

The human homologue (PEG3) of the mouse paternally expressed gene 3 (Peg3) is maternally imprinted but not mutated in women with familial recurrent hydatidiform molar pregnancies.

OBJECTIVES: We mapped a locus for autosomal recessive molar pregnancies with biparental genomic contribution to chromosome 19q13.4 between D19S924 and D19S890. This 5-Mb region is homologous to proximal mouse chromosome 7 and contains a cluster of Krüppel-type zinc finger genes, including the human homologue of the mouse imprinted genes: the paternally expressed gene 3 (PEG3) and the maternally expressed Zim1 genes. We analyzed the PEG3 gene for mutations in women with familial recurrent hydatidiform moles and to determine its imprinting status in humans. METHODS: We used database searches and screened cDNA libraries to find the complete genomic structure of PEG3. Polymerase chain reaction (PCR) amplification and direct sequencing of coding exons and flanking introns were performed on genomic DNA from the affected women. Allele-specific methylation and expression were studied by methylation-sensitive Southern analysis of a 5' located CpG island and by reverse-transcription PCR of total lymphoblast-derived RNA of normal individuals who were informative for two expressed polymorphisms. RESULTS: We did not detect any mutations in the coding region of PEG3 in the affected women. We observed allele-specific methylation of the CpG island and expression from the paternal allele in two independent informative pedigrees. CONCLUSION: Consistent with the findings in the mouse, the human PEG3 gene is expressed from the paternal allele. Our data support that PEG3 is not mutated in women with familial recurrent hydatidiform moles, although mutations in the regulatory regions that might affect imprinting or transcriptional level of the gene could not be evaluated.

Animals↗
PubMed2000

Perceptions of paternal resemblance predict family violence.

Fifty-five men participating in a domestic violence treatment program agreed to complete a questionnaire and rate the degree to which their children looked like them. Ratings of paternal resemblance were positively correlated with the self-reported quality of the men's relationships with their children and inversely proportional to the severity of injuries suffered by their spouses. Analogous results were also found for the men's experience with their parents. We suggest that these results reflect men's use of paternal resemblance to assess paternity.

Journal Article↗
PubMed2000

Does paternal uncertainty explain discriminative grandparental solicitude? A cross-cultural study in Greece and Germany.

Recent research on kin investment as a reproductive strategy is based on the idea that differences in grandparental caregiving directly reflect degrees of differential grandpaternal versus grandmaternal certainty. In a cross-cultural study in Greece and Germany, 544 subjects (318 Greeks, 208 Germans, 18 of other origins) were asked for an assessment of their grandparents' (GPs') caregiving. In Germany and urban Greece (modern Western societies), the maternal GPs were rated as more intensive caregivers than the paternal GPs, but this was not the case in rural Greece, where paternal GPs provided more care. However, in all groups, grandmothers were more caring than grandfathers. Thus, contrary to previous theory and research, these two effects must be clearly distinguished, and may be explained by (1) more intense female caregiving in humans (as in other viviparous mammals) and (2) a socially engendered favoring of maternal relatives in Western industrial societies as opposed to the favoring of paternal GPs seen in the patrilateral culture of rural Greece.

Journal Article↗
PubMed2004

Degradation of paternal mitochondria after fertilization: implications for heteroplasmy, assisted reproductive technologies and mtDNA inheritance.

Maternal inheritance of mitochondrial DNA has long been regarded as a major paradox in developmental biology. While some confusion may still persist in popular science, research data clearly document that the paternal sperm-borne mitochondria of most mammalian species enter the ooplasm at fertilization and are specifically targeted for degradation by the resident ubiquitin system. Ubiquitin is a proteolytic chaperone that forms covalently linked polyubiquitin chains on the targeted proteinaceous substrates. The polyubiquitin tag redirects the substrate proteins to a 26-S proteasome, a multi-subunit proteolytic organelle. Thus, specific proteasomal inhibitors reversibly block sperm mitochondrial degradation in ooplasm. Lysosomal degradation and the activity of membrane-lipoperoxidating enzyme 15-lipoxygenase (15-LOX) may also contribute to sperm mitochondrial degradation in the ooplasm, but probably is not crucial. Prohibitin, the major protein of the inner mitochondrial membrane, appears to be ubiquitinated in the sperm mitochondria. Occasional occurrence of paternal inheritance of mtDNA has been suggested in mammals including humans. While most such evidence has been widely disputed, it warrants further examination. Of particular concern is the documented heteroplasmy, i.e. mixed mtDNA inheritance after ooplasmic transplantation. Intracytoplasmic sperm injection (ICSI) has inherent potential for delaying the degradation of sperm mitochondria. However, paternal mtDNA inheritance after ICSI has not been documented so far.

DNA, Mitochondrial↗
PubMed1996

A new case of Beckwith-Wiedemann syndrome with an 11p15 duplication of paternal origin [46,XY,-21,+der(21), t(11;21)(p15.2;q22.3)pat].

We present a new case of 11p15 duplication (trisomy 11p15) in a boy (46,XY,-21,+der(21), t(11;21)(p15.2;q22.3)] suffering from Beckwith-Wiedemann syndrome (BWS), whose phenotypically normal father carries a balanced translocation between chromosomes 11 and 21[46,XY, t(11;21)(p15.2;q22.3)]. The paternal grandmother has the same balanced translocation and is also clinically normal. BWS was suspected when the boy was 6 months old because of gigantism, macroglossia, visceromegaly, ear lobe creases and abdominal distention. Apart from the characteristic BWS phenotype, the boy has other features which are almost exclusively observed in 11p trisomy (high forehead with frontal upsweep of hair, wide central nose bridge, slightly beaked nose, chubby cheeks and severe mental retardation). So far, at least eight cases of 11p15 duplication have been described as patients with BWS. In six of these, the duplication was due to inheritance of a translocated or rearranged paternal chromosome. This was also the case in our patient. In the two other previously published cases, the 11p15 duplications were de novo, but in one of these, DNA analysis has subsequently shown that the duplication was of paternal origin. We discuss our observations in relation to the above-mentioned previous cases of 11p15 duplication and the possible role of genomic imprinting in the etiology of BWS.

Beckwith-Wiedemann Syndrome↗
PubMed1992

Further observation of paternal transmission of Drosophila mitochondrial DNA by PCR selective amplification method.

By designing 3' ends of primers in PCR (polymerase chain reaction), a specific DNA fragment was selectively amplified in the presence of a 10(3)-fold excess of highly homologous (sequence difference ca. 2%) opponent DNA. This technique was applied in detecting paternal leakage of mitochondrial DNA (mtDNA) in intraspecific crosses of Drosophila simulans and interspecific crosses of Drosophila simulans and Drosophila mauritiana. The mtDNA types of their progeny were analysed by selective amplification of the paternal mtDNA fragment possessing a polymorphic restriction site and detecting its cleaved fragments. Paternal mtDNA was detected in the progeny of 14 out of 16 crosses. The present result indicates small but frequent inheritance of sperm mtDNA in Drosophila, which is supportive to our previous finding.

Animals↗
PubMed2001

The battle of the sexes after fertilization: behaviour of paternal and maternal chromosomes in the early mammalian embryo.

In the early diploid mammalian embryo, a father's chromosomes don't mix with the mother's until some time after fertilization. This topological genome separation is preserved up to the four-cell embryo stage and then gradually disappears. Unlike maternal DNA, sperm DNA arrives in an almost crystalline structure, heavily modified with methylcytosines (MeCs), which keep genes inactive. Compartmentalization of the nucleus according to parental origin may make it easier for the cellular machinery of the fertilized egg to revive the paternal chromosomes and to control paternal gene expression. Active zygotic demethylation of the paternal genome by a putative demethylase in the egg is a striking example for the battle of the sexes at the genomic level and beyond the single-gene level. It has important implications for genomic imprinting, and the establishment of genetic totipotency in fertilized eggs and in somatic cells during mammalian cloning.

Animals↗
PubMedDate not supplied

Interaction between the Xce locus and imprinting of the paternal X chromosome in mouse yolk-sac endoderm.

In female eutherian mammals preferential inactivation of the paternally derived X chromosome (XP) takes place in certain extra-embryonic tissues such as mouse yolk-sac endoderm, chorionic ectoderm and trophoblast and has been demonstrated both biochemically and cytologically. This is thought to be due to the paternal X chromosome being 'imprinted', that is, somehow marked as different, during either male gametogenesis or fertilization, causing primary nonrandom X-inactivation in tissues that differentiate early, such as trophectoderm and primitive endoderm, from which yolk-sac endoderm is derived. Different alleles of the X-chromosome controlling element, Xce locus, centrally located on the mouse X chromosome, also cause primary nonrandom X-chromosome inactivation in embryonic tissues which would otherwise show random inactivation. The work reported here was designed to elucidate whether the nonrandom inactivation of the imprinted XP in yolk-sac endoderm could be modified, or even overridden, by the effect of different Xce alleles. Using the modified Kanda method we have therefore studied the proportion of cells at metaphase with the XP inactive in separated yolk-sac endoderm and mesoderm of mouse embryos heterozygous for a marker X chromosome (Cattanach's translocation) carrying different Xce alleles on XP and XM. The results show that the extreme Xcec allele, when present on the paternally derived X, can significantly reduce the proportion of inactive XP seen in yolk-sac endoderm compared with controls. This is the first evidence that imprinting of XP is not an 'all or none' event but can be modified by a 'strong' allele at the Xce locus, and is another indication that the Xce locus may represent the inactivation centre.

Alleles↗