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Maternal Expression (maternal + expression)

Distribution by Scientific Domains

Life Sciences	85%

Selected Abstracts

Maternal expression and function of the Drosophila sox gene Dichaete during oogenesis

DEVELOPMENTAL DYNAMICS, Issue 10 2006
Ashim Mukherjee
Abstract Members of the Sox family of DNA-binding HMG domain proteins have been shown to regulate gene transcription in a wide range of developmental processes, including sex determination, neurogenesis, and chondrogenesis. However, little is known about their potential functions in developing germline tissues. In Drosophila, the Sox protein Dichaete (a.k.a., Fish-hook) is a member of the SoxB subgroup whose HMG domain shares strong sequence similarity to that of vertebrate Sox2. Dichaete exhibits dynamic expression in embryonic and larval stages and has pleiotropic functions in a variety of tissues. In this study, we extend analyses of Dichaete function and show that expression of Dichaete protein is detected in the developing oocyte during early to mid stages of oogenesis. Strikingly, Dichaete exhibits cytoplasmic distribution and is not detected in the oocyte nucleus. Germline mosaic analyses revealed that the Dichaete gene has maternal functions that influence dorsal/ventral patterning of the egg chamber. Dichaete mutant eggs exhibit defects in formation of the dorsal appendages, differentiation of dorsal/anterior follicle cells, and mislocalization of Gurken protein and gurken mRNA. Dichaete protein was shown to possess RNA-binding capabilities, suggesting a direct post-transcriptional role in regulating RNA functions. Developmental Dynamics 235:2828,2835, 2006. © 2006 Wiley-Liss, Inc. [source]

Differential expression of CaMK-II genes during early zebrafish embryogenesis

DEVELOPMENTAL DYNAMICS, Issue 1 2007
Sarah C. Rothschild
Abstract CaMK-II is a highly conserved Ca2+/calmodulin-dependent protein kinase expressed throughout the lifespan of all vertebrates. During early development, CaMK-II regulates cell cycle progression and "non-canonical" Wnt-dependent convergent extension. In the zebrafish, Danio rerio, CaMK-II activity rises within 2 hr after fertilization. At the time of somite formation, zygotic expression from six genes (camk2a1, camk2b1, camk2g1, camk2g2, camk2d1, camk2d2) results in a second phase of increased activity. Zebrafish CaMK-II genes are 92,95% identical to their human counterparts in the non-variable regions. During the first three days of development, alternative splicing yields at least 20 splice variants, many of which are unique. Whole-mount in situ hybridization reveals that camk2g1 comprises the majority of maternal expression. All six genes are expressed strongly in ventral regions at the 18-somite stage. Later, camk2a1 is expressed in anterior somites, heart, and then forebrain. Camk2b1 is expressed in somites, mid- and forebrain, gut, retina, and pectoral fins. Camk2g1 appears strongly along the midline and then in brain, gut, and pectoral fins. Camk2g2 is expressed early in the midbrain and trunk and exhibits the earliest retinal expression. Camk2d1 is elevated early at somite boundaries, then epidermal tissue, while camk2d2 is expressed in discrete anterior locations, steadily increasing along either side of the dorsal midline and then throughout the brain, including the retina. These findings reveal a complex pattern of CaMK-II gene expression consistent with pleiotropic roles during development. Developmental Dynamics 236:295,305, 2007. © 2006 Wiley-Liss, Inc. [source]

CYTONUCLEAR INTERACTIONS CAN FAVOR THE EVOLUTION OF GENOMIC IMPRINTING

EVOLUTION, Issue 5 2009
Jason B. Wolf
Interactions between cytoplasmic (generally organelle) and nuclear genomes may be relatively common and could potentially have major fitness consequences. As in the case of within-genome epistasis, this cytonuclear epistasis can favor the evolutionary coadaptation of high-fitness combinations of nuclear and cytoplasmic alleles. Because cytoplasmic factors are generally uniparentally inherited, the cytoplasmic genome is inherited along with only one of the nuclear haplotypes, and therefore, coadaptation is expected to evolve through the interaction of these coinherited (usually maternally inherited) genomes. Here I show that, as a result of this coinheritance of the two genomes, cytonuclear epistasis can favor the evolution of genomic imprinting such that, when the cytoplasmic factor is maternally inherited, selection favors maternal expression of the nuclear locus and when the factor is paternally inherited selection favors paternal expression. Genomic imprinting evolves in this model because it leads to a pattern of gene expression in the nuclear haplotype that is coadapted with (i.e., adaptively coordinated with) gene expression in the coinherited cytoplasmic genome. [source]

Parent-of-origin, imprinting, mitochondrial, and X-linked effects in traits related to alcohol dependence: Presentation Group 18 of Genetic Analysis Workshop 14

GENETIC EPIDEMIOLOGY, Issue S1 2005
Konstantin Strauch
Abstract The participants of Presentation Group 18 of Genetic Analysis Workshop 14 analyzed the Collaborative Study on the Genetics of Alcoholism data set to investigate sex-specific effects for phenotypes related to alcohol dependence. In particular, the participants looked at imprinting (which is also known as parent-of-origin effect), differences between recombination fractions for the two sexes, and mitochondrial and X-chromosomal effects. Five of the seven groups employed newly developed or existing methods that take imprinting into account when testing for linkage, or test for imprinting itself. Single-marker and multipoint analyses were performed for microsatellite as well as single-nucleotide polymorphism markers, and several groups used a sex-specific genetic map in addition to a sex-averaged map. Evidence for paternal imprinting (i.e., maternal expression) was consistently obtained by at least two groups at genetic regions on chromosomes 10, 12, and 21 that possibly harbor genes responsible for alcoholism. Evidence for maternal imprinting (which is equivalent to paternal expression) was consistently found at a locus on chromosome 11. Two groups applied extensions of variance components analysis that model a mitochondrial or X-chromosomal effect to latent class variables and electrophysiological traits employed in the diagnosis of alcoholism. The analysis, without using genetic markers, revealed mitochondrial or X-chromosomal effects for several of these traits. Accounting for sex-specific environmental variances appeared to be crucial for the identification of an X-chromosomal factor. In linkage analysis using marker data, modeling a mitochondrial variance component increased the linkage signals obtained for autosomal loci. Genet. Epidemiol. 29(Suppl. 1):S125,S132, 2005. © 2005 Wiley-Liss, Inc. [source]

Zinc Supplementation at the Time of Ethanol Exposure Ameliorates Teratogenicity in Mice

ALCOHOLISM, Issue 1 2003
Luke C. Carey
Background: We have previously demonstrated that ethanol teratogenicity in mice is related to the maternal expression of metallothionein (MT), a zinc (Zn)-binding protein. Ethanol induces maternal liver MT, which causes plasma Zn concentrations to decrease as Zn moves into the liver. During pregnancy it is suggested that this change decreases fetal Zn supply and contributes to abnormal development. Here we investigated whether maternal Zn supplementation at the time of ethanol exposure reduces teratogenicity. Methods: Mice were injected with 25% ethanol (0.015 ml/g intraperitoneally at 0 and 4 hr) and ZnSO4 (2.5 ,gZn/g subcutaneously at 0 hr) and were killed over 16 hr to ascertain changes in plasma Zn. Plasma Zn concentrations peaked at 2 hr, where levels were 5-fold normal and then returned toward normal over 14 hr. Pregnant mice were treated in a similar manner on gestation day 8 with saline, saline + Zn, ethanol + Zn, or ethanol alone, and fetal abnormalities were assessed on gestation day 18. Results: External abnormalities were most prevalent in offspring from dams treated with ethanol. Zn treatment at the time of ethanol exposure reduced the incidence of fetal abnormalities to basal levels. Litters from dams treated with ethanol + Zn contained more fetuses and fewer fetal resorption sites compared with those from ethanol-treated dams. Conclusions: These findings demonstrate that Zn supplementation at the time of ethanol exposure significantly negates the deleterious effects of ethanol on the fetus. [source]

Molecular characteristics of the porcine DLK1 and MEG3 genes

ANIMAL GENETICS, Issue 2 2008
X. P. Li
Summary Imprinted genes play important roles in embryo survival and postnatal growth regulation. The DLK1 and MEG3 (previously GTL2) genes are linked and reciprocally imprinted in several mammals, but their imprinting status is still unknown in pigs. In this study, we report polymorphisms, imprinting status and QTL analyses of the porcine DLK1 and MEG3 genes. Muscle and adipose DNA and RNA samples from 30-day-old animals generated with reciprocal crosses between the Korean native pig (KNP) and Yorkshire breeds were used to analyse DLK1 and MEG3 variation and expression. The samples exhibited paternal expression of DLK1 and maternal expression of MEG3 in pigs. These results indicated that the imprinting status of the DLK1 and MEG3 genes is conserved across mammalian species. By linkage analyses, we assigned the DLK1 and MEG3 genes to the telomeric region of SSC7. By QTL analyses, we confirmed a significant polar overdominance (POD) effect in DLK1, which was previously detected for several growth traits in pigs. However, no significant POD effect was found with the MEG3 locus. [source]

Genomic imprinting in the development and evolution of psychotic spectrum conditions

BIOLOGICAL REVIEWS, Issue 4 2008
Bernard Crespi
Abstract I review and evaluate genetic and genomic evidence salient to the hypothesis that the development and evolution of psychotic spectrum conditions have been mediated in part by alterations of imprinted genes expressed in the brain. Evidence from the genetics and genomics of schizophrenia, bipolar disorder, major depression, Prader-Willi syndrome, Klinefelter syndrome, and other neurogenetic conditions support the hypothesis that the etiologies of psychotic spectrum conditions commonly involve genetic and epigenetic imbalances in the effects of imprinted genes, with a bias towards increased relative effects from imprinted genes with maternal expression or other genes favouring maternal interests. By contrast, autistic spectrum conditions, including Kanner autism, Asperger syndrome, Rett syndrome, Turner syndrome, Angelman syndrome, and Beckwith-Wiedemann syndrome, commonly engender increased relative effects from paternally expressed imprinted genes, or reduced effects from genes favouring maternal interests. Imprinted-gene effects on the etiologies of autistic and psychotic spectrum conditions parallel the diametric effects of imprinted genes in placental and foetal development, in that psychotic spectrum conditions tend to be associated with undergrowth and relatively-slow brain development, whereas some autistic spectrum conditions involve brain and body overgrowth, especially in foetal development and early childhood. An important role for imprinted genes in the etiologies of psychotic and autistic spectrum conditions is consistent with neurodevelopmental models of these disorders, and with predictions from the conflict theory of genomic imprinting. [source]