Loss of genomic imprinting in Drosophila clones

Genome ◽  
2006 ◽  
Vol 49 (8) ◽  
pp. 1043-1046 ◽  
Author(s):  
Andrew J Haigh ◽  
Vett K Lloyd
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Imprinting ◽  
X Chromosome ◽  
Chromatin Structure ◽  
Nuclear Transfer ◽  
Paternal Allele ◽  
Monoallelic Expression ◽  
C Elegans ◽  
Human Cancers ◽  
Parent Of Origin

Genomic imprinting is a process that genetically distinguishes maternal and paternal genomes, and can result in parent-of-origin-dependent monoallelic expression of a gene that is dependent on the parent of origin. As such, an otherwise functional maternally inherited allele may be silenced so that the gene is expressed exclusively from the paternal allele, or vice versa. Once thought to be restricted to mammals, genomic imprinting has been documented in angiosperm plants (J.L. Kermicle. 1970. Genetics, 66: 69–85), zebrafish (C.C. Martin and R. McGowan. 1995. Genet. Res. 65: 21–28), insects, and C. elegans (C.J. Bean, C.E. Schaner, and W.G. Kelly. 2004. Nat. Genet. 36: 100–105.). In each case, it appears to rely on differential chromatin structure. Aberrant imprinting has been implicated in various human cancers and has been detected in a number of cloned mammals, potentially limiting the usefulness of somatic nuclear transfer. Here we show that genomic imprinting associated with a mini-X chromosome is lost in Drosophila melanogaster clones.Key words: cloning, Drosophila, genomic imprinting, nuclear transfer.

An N-Ethyl-N-Nitrosourea Mutagenesis Screen for Epigenetic Mutations in the Mouse

Genetics ◽  
2003 ◽  
Vol 164 (4) ◽  
pp. 1481-1494
Author(s):  
Ivona Percec ◽  
Joanne L Thorvaldsen ◽  
Robert M Plenge ◽  
Christopher J Krapp ◽  
Joseph H Nadeau ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
X Chromosome ◽  
X Inactivation ◽  
Monoallelic Expression ◽  
Chromosome 15 ◽  
Chromosome 5 ◽  
Chromosome 10 ◽  
Mutagenesis Screen ◽  
Distal Chromosome ◽  
Males And Females

Abstract The mammalian epigenetic phenomena of X inactivation and genomic imprinting are incompletely understood. X inactivation equalizes X-linked expression between males and females by silencing genes on one X chromosome during female embryogenesis. Genomic imprinting functionally distinguishes the parental genomes, resulting in parent-specific monoallelic expression of particular genes. N-ethyl-N-nitrosourea (ENU) mutagenesis was used in the mouse to screen for mutations in novel factors involved in X inactivation. Previously, we reported mutant pedigrees identified through this screen that segregate aberrant X-inactivation phenotypes and we mapped the mutation in one pedigree to chromosome 15. We now have mapped two additional mutations to the distal chromosome 5 and the proximal chromosome 10 in a second pedigree and show that each of the mutations is sufficient to induce the mutant phenotype. We further show that the roles of these factors are specific to embryonic X inactivation as neither genomic imprinting of multiple genes nor imprinted X inactivation is perturbed. Finally, we used mice bearing selected X-linked alleles that regulate X chromosome choice to demonstrate that the phenotypes of all three mutations are consistent with models in which the mutations have affected molecules involved specifically in the choice or the initiation of X inactivation.

scholarly journals DNA demethylase ROS1 negatively regulates the imprinting of DOGL4 and seed dormancy in Arabidopsis thaliana

2018 ◽  
Vol 115 (42) ◽  
pp. E9962-E9970 ◽  
Author(s):  
Haifeng Zhu ◽  
Wenxiang Xie ◽  
Dachao Xu ◽  
Daisuke Miki ◽  
Kai Tang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Seed Dormancy ◽  
Genomic Imprinting ◽  
Dna Demethylation ◽  
Paternal Allele ◽  
Maternal Allele ◽  
Imprinted Gene ◽  
Differential Gene ◽  
Parent Of Origin ◽  
Dna Demethylase

Genomic imprinting is a form of epigenetic regulation resulting in differential gene expression that reflects the parent of origin. In plants, imprinted gene expression predominantly occurs in the seed endosperm. Maternal-specific DNA demethylation by the DNA demethylase DME frequently underlies genomic imprinting in endosperm. Whether other more ubiquitously expressed DNA demethylases regulate imprinting is unknown. Here, we found that the DNA demethylase ROS1 regulates the imprinting of DOGL4. DOGL4 is expressed from the maternal allele in endosperm and displays preferential methylation and suppression of the paternal allele. We found that ROS1 negatively regulates imprinting by demethylating the paternal allele, preventing its hypermethylation and complete silencing. Furthermore, we found that DOGL4 negatively affects seed dormancy and response to the phytohormone abscisic acid and that ROS1 controls these processes by regulating DOGL4. Our results reveal roles for ROS1 in mitigating imprinted gene expression and regulating seed dormancy.

Erasing genomic imprinting memory in mouse clone embryos produced from day 11.5 primordial germ cells

Development ◽  
2002 ◽  
Vol 129 (8) ◽  
pp. 1807-1817 ◽  
Author(s):  
Jiyoung Lee ◽  
Kimiko Inoue ◽  
Ryuichi Ono ◽  
Narumi Ogonuki ◽  
Takashi Kohda ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Genomic Imprinting ◽  
Nuclear Transfer ◽  
Monoallelic Expression ◽  
Parental Origin ◽  
Imprinted Genes ◽  
Specific Expression ◽  
Male And Female ◽  
Imprinted Gene ◽  
Methylation Patterns

Genomic imprinting is an epigenetic mechanism that causes functional differences between paternal and maternal genomes, and plays an essential role in mammalian development. Stage-specific changes in the DNA methylation patterns of imprinted genes suggest that their imprints are erased some time during the primordial germ cell (PGC) stage, before their gametic patterns are re-established during gametogenesis according to the sex of individuals. To define the exact timing and pattern of the erasure process, we have analyzed parental-origin-specific expression of imprinted genes and DNA methylation patterns of differentially methylated regions (DMRs) in embryos, each derived from a single day 11.5 to day 13.5 PGC by nuclear transfer. Cloned embryos produced from day 12.5 to day 13.5 PGCs showed growth retardation and early embryonic lethality around day 9.5. Imprinted genes lost their parental-origin-specific expression patterns completely and became biallelic or silenced. We confirmed that clones derived from both male and female PGCs gave the same result, demonstrating the existence of a common default state of genomic imprinting to male and female germlines. When we produced clone embryos from day 11.5 PGCs, their development was significantly improved, allowing them to survive until at least the day 11.5 embryonic stage. Interestingly, several intermediate states of genomic imprinting between somatic cell states and the default states were seen in these embryos. Loss of the monoallelic expression of imprinted genes proceeded in a step-wise manner coordinated specifically for each imprinted gene. DNA demethylation of the DMRs of the imprinted genes in exact accordance with the loss of their imprinted monoallelic expression was also observed. Analysis of DNA methylation in day 10.5 to day 12.5 PGCs demonstrated that PGC clones represented the DNA methylation status of donor PGCs well. These findings provide strong evidence that the erasure process of genomic imprinting memory proceeds in the day 10.5 to day 11.5 PGCs, with the timing precisely controlled for each imprinted gene. The nuclear transfer technique enabled us to analyze the imprinting status of each PGC and clearly demonstrated a close relationship between expression and DNA methylation patterns and the ability of imprinted genes to support development.

scholarly journals Repression of Hybrid Dysgenesis in Drosophila melanogaster by Combinations of Telomeric P-Element Reporters and Naturally Occurring P Elements

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1857-1866 ◽  
Author(s):  
Stéphane Ronsseray ◽  
Laurent Marin ◽  
Monique Lehmann ◽  
Dominique Anxolabéhère
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Chromatin Structure ◽  
Hybrid Dysgenesis ◽  
P Element ◽  
Pericentromeric Heterochromatin ◽  
Combination Effect ◽  
P Elements ◽  
Naturally Occurring ◽  
Nuclear Location

Abstract In Drosophila melanogaster, hybrid dysgenesis occurs in the germline of flies produced by crosses between females lacking P elements and males carrying 25–55 P elements. We have previously shown that a complete maternally inherited repression of P transposition in the germline (P cytotype) can be elicited by only two autonomous P elements located at the X chromosome telomere (cytological site 1A). We have tested whether P transgenes at 1A, unable to code for a P-repressor, may contribute to the repression of P elements. Females carrying a P-lacZ transgene at 1A [“P-lacZ(1A)”], crossed with P males, do not repress dysgenic sterility in their progeny. However, these P-lacZ(1A) insertions, maternally or paternally inherited, contribute to P-element repression when they are combined with other regulatory P elements. This combination effect is not seen when the P-lacZ transgene is located in pericentromeric heterochromatin or in euchromatin; however a P-w,ry transgene located at the 3R chromosome telomere exhibits the combination effect. The combination effect with the P-lacZ(1A) transgene is impaired by a mutant Su(var)205 allele known to impair the repression ability of the autonomous P elements at 1A. We hypothesized that the combination effect is due to modification of the chromatin structure or nuclear location of genomic P elements.

scholarly journals Lack of parent-of-origin effects in Nasonia jewel wasp: A replication and extension study

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252457
Author(s):  
Kimberly C. Olney ◽  
Joshua D. Gibson ◽  
Heini M. Natri ◽  
Avery Underwood ◽  
Juergen Gadau ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Sequence Data ◽  
Original Data ◽  
Paternal Allele ◽  
Analysis Strategy ◽  
Parent Of Origin ◽  
Origin Effects ◽  
New Processing ◽  
Diploid Cells ◽  
Origin Effect

In diploid cells, the paternal and maternal alleles are, on average, equally expressed. There are exceptions from this: a small number of genes express the maternal or paternal allele copy exclusively. This phenomenon, known as genomic imprinting, is common among eutherian mammals and some plant species; however, genomic imprinting in species with haplodiploid sex determination is not well characterized. Previous work reported no parent-of-origin effects in the hybrids of closely related haplodiploid Nasonia vitripennis and Nasonia giraulti jewel wasps, suggesting a lack of epigenetic reprogramming during embryogenesis in these species. Here, we replicate the gene expression dataset and observations using different individuals and sequencing technology, as well as reproduce these findings using the previously published RNA sequence data following our data analysis strategy. The major difference from the previous dataset is that they used an introgression strain as one of the parents and we found several loci that resisted introgression in that strain. Our results from both datasets demonstrate a species-of-origin effect, rather than a parent-of-origin effect. We present a reproducible workflow that others may use for replicating the results. Overall, we reproduced the original report of no parent-of-origin effects in the haplodiploid Nasonia using the original data with our new processing and analysis pipeline and replicated these results with our newly generated data.

scholarly journals Genomic Imprinting and Position-Effect Variegation in Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1503-1516 ◽  
Author(s):  
Vett K Lloyd ◽  
Don A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Imprinting ◽  
X Chromosome ◽  
Position Effect ◽  
Specific Effect ◽  
Position Effect Variegation ◽  
Mitotic Instability ◽  
Effect Variegation ◽  
Allele Specific ◽  
The Individual

Abstract Genomic imprinting is a phenomenon in which the expression of a gene or chromosomal region depends on the sex of the individual transmitting it. The term imprinting was first coined to describe parent-specific chromosome behavior in the dipteran insect Sciara and has since been described in many organisms, including other insects, plants, fish, and mammals. In this article we describe a mini-X chromosome in Drosophila melanogaster that shows genomic imprinting of at least three closely linked genes. The imprinting of these genes is observed as mosaic silencing when the genes are transmitted by the male parent, in contrast to essentially wild-type expression when the same genes are maternally transmitted. We show that the imprint is due to the sex of the parent rather than to a conventional maternal effect, differential mitotic instability of the mini-X chromosome, or an allele-specific effect. Finally, we have examined the effects of classical modifiers of position-effect variegation on the maintenance and the establishment of the imprint. Factors that modify position-effect variegation alter the somatic expression but not the establishment of the imprint. This suggests that chromatin structure is important in maintenance of the imprint, but a separate mechanism may be responsible for its initiation.

scholarly journals Parent-of-Origin Effects on mRNA Expression in Drosophila melanogaster Not Caused by Genomic Imprinting

Genetics ◽  
2006 ◽  
Vol 173 (3) ◽  
pp. 1817-1821 ◽  
Author(s):  
Patricia J. Wittkopp ◽  
Belinda K. Haerum ◽  
Andrew G. Clark
Keyword(s):  
Drosophila Melanogaster ◽  
Mrna Expression ◽  
Genomic Imprinting ◽  
Parent Of Origin ◽  
Origin Effects

scholarly journals Lack of parent-of-origin effects in Nasonia jewel wasp: a replication and extension study

2021 ◽  
Author(s):  
Kimberly C. Olney ◽  
Joshua D. Gibson ◽  
Heini M. Natri ◽  
Avery Underwood ◽  
Juergen Gadau ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Sequence Data ◽  
Original Data ◽  
Paternal Allele ◽  
Analysis Strategy ◽  
Parent Of Origin ◽  
Origin Effects ◽  
New Processing ◽  
Diploid Cells ◽  
Origin Effect

AbstractIn diploid cells, the paternal and maternal alleles are, on average, equally expressed. There are exceptions from this: a small number of genes express the maternal or paternal allele copy exclusively. This phenomenon, known as genomic imprinting, is common among eutherian mammals and some plant species; however, genomic imprinting in species with haplodiploid sex determination is not well characterized. Previous work reported no parent-of-origin effects in the hybrids of closely related haplodiploid Nasonia vitripennis and Nasonia giraulti jewel wasps, suggesting a lack of epigenetic reprogramming during embryogenesis in these species. Here, we replicate the gene expression dataset and observations using different individuals and sequencing technology, as well as reproduce these findings using the previously published RNA sequence data following our data analysis strategy. The major difference from the previous dataset is that they used an introgression strain as one of the parents and we found several loci that resisted introgression in that strain. Our results from both datasets demonstrate a species-of-origin effect, rather than a parent-of-origin effect. We present a reproducible workflow that others may use for replicating the results. Overall, we reproduced the original report of no parent-of-origin effects in the haplodiploid Nasonia using the original data with our new processing and analysis pipeline and replicated these results with our newly generated data.

scholarly journals Quantitative and functional interrogation of parent-of-origin allelic expression biases in the brain

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Julio D Perez ◽  
Nimrod D Rubinstein ◽  
Daniel E Fernandez ◽  
Stephen W Santoro ◽  
Leigh A Needleman ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Gene Dosage ◽  
Transcript Level ◽  
Monoallelic Expression ◽  
Strongly Correlated ◽  
Parent Of Origin ◽  
Parental Bias ◽  
The Brain ◽  
Specific Neuron ◽  
Specific Deletion

The maternal and paternal genomes play different roles in mammalian brains as a result of genomic imprinting, an epigenetic regulation leading to differential expression of the parental alleles of some genes. Here we investigate genomic imprinting in the cerebellum using a newly developed Bayesian statistical model that provides unprecedented transcript-level resolution. We uncover 160 imprinted transcripts, including 41 novel and independently validated imprinted genes. Strikingly, many genes exhibit parentally biased—rather than monoallelic—expression, with different magnitudes according to age, organ, and brain region. Developmental changes in parental bias and overall gene expression are strongly correlated, suggesting combined roles in regulating gene dosage. Finally, brain-specific deletion of the paternal, but not maternal, allele of the paternally-biased Bcl-x, (Bcl2l1) results in loss of specific neuron types, supporting the functional significance of parental biases. These findings reveal the remarkable complexity of genomic imprinting, with important implications for understanding the normal and diseased brain.

UNIPARENTAL DISOMY: MECHANISMS AND CLINICAL CONSEQUENCES

2003 ◽  
Vol 14 (2) ◽  
pp. 155-175 ◽  
Author(s):  
LISA G SHAFFER
Keyword(s):  
Genomic Imprinting ◽  
Normal State ◽  
Diploid Number ◽  
Uniparental Disomy ◽  
Monoallelic Expression ◽  
Clinical Consequences ◽  
Epigenetic Phenomenon ◽  
Parent Of Origin

During gametogenesis in mammals, half of the parental chromosomes segregate to each gamete. Upon fertilization of two haploid gametes, the diploid number is restored (Figure 1A). Nondisjunction, malsegregation of the chromosomes during gametogenesis, can give rise to chromosomally unbalanced offspring (trisomies and monosomies) (Figure 1B). Genomic imprinting is an epigenetic phenomenon in which the activity of a gene is reversibly modified depending on the parent of origin. This leads to unequal, monoallelic expression of the maternal and paternal alleles of a diploid locus (Figure 1C). Thus, the normal state of an imprinted locus is an “imbalance”, not of chromosomes, but of the functional genetic content.

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