Distribution of parthenogenetic cells in the mouse brain and their influence on brain development and behavior.

Allen, Nicholas Denby; Logan, Kay; Lally, G.; Drage, Deborah; Norris, M. L.; Keverne, Eric B.

doi:10.1073/pnas.92.23.10782

Cited by 106 publications

(72 citation statements)

References 17 publications

(16 reference statements)

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“…A negative RT-PCR result for the two paternally expressed imprinted genes together with a positive result for UBE3A and H19 in hPESs is consistent with a parthenogenesis origin for the hPES cell lines. Failure of development to term of parthenogenetic embryos was thought to be a consequence of having a uniparental genome [30], and although parthenogenetic stem cells were suggested to have limited differentiation potential due to the lack of paternal imprinting [30,31], modification of specifically imprinted genes was reported to help extend full organismal development and increase the differentiation ability of the ESCs and thus initial oocytes developed into blastocysts. Two ESC lines were obtained.…”

Section: Discussionmentioning

confidence: 99%

Derivation of human embryonic stem cell lines from parthenogenetic blastocysts

Mai

Li³

et al. 2007

Cell Res

192

138

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Parthenogenesis is one of the main, and most useful, methods to derive embryonic stem cells (ESCs), which may be an important source of histocompatible cells and tissues for cell therapy. Here we describe the derivation and characterization of two ESC lines (hPES-1 and hPES-2) from in vitro developed blastocysts following parthenogenetic activation of human oocytes. Typical ESC morphology was seen, and the expression of ESC markers was as expected for alkaline phosphatase, octamer-binding transcription factor 4, stage-specific embryonic antigen 3, stage-specific embryonic antigen 4, TRA-1-60, and TRA-1-81, and there was absence of expression of negative markers such as stage-specific embryonic antigen 1. Expression of genes specific for different embryonic germ layers was detected from the embryoid bodies (EBs) of both hESC lines, suggesting their differentiation potential in vitro. However, in vivo, only hPES-1 formed teratoma consisting of all three embryonic germ layers (hPES-2 did not). Interestingly, after continuous proliferation for more than 100 passages, hPES-1 cells still maintained a normal 46 XX karyotype; hPES-2 displayed abnormalities such as chromosome translocation after long term passages. Short Tandem Repeat (STR) results demonstrated that the hPES lines were genetic matches with the egg donors, and gene imprinting data confirmed the parthenogenetic origin of these ES cells. Genome-wide SNP analysis showed a pattern typical of parthenogenesis. All of these results demonstrated the feasibility to isolate and establish human parthenogenetic ESC lines, which provides an important tool for studying epigenetic effects in ESCs as well as for future therapeutic interventions in a clinical setting.

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Section: Discussionmentioning

confidence: 99%

Derivation of human embryonic stem cell lines from parthenogenetic blastocysts

Mai

Li³

et al. 2007

Cell Res

192

138

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“…Even though parthenogenetic embryos die shortly after implantation, their cells are capable of participating in normal development of chimeras when aggregated with fertilized embryos (Fundele et al 1989, Nagy et al 1989, Allen et al 1995, Boediono et al 1999. Parthenogenetic cells were detected in some organs and tissues of adult chimeras.…”

Section: Somatic Cell Nuclear Transfer In Rabbitsmentioning

confidence: 99%

Rabbit somatic cell cloning: effects of donor cell type, histone acetylation status and chimeric embryo complementation

Yang

Hao²,

Keßler³

et al. 2007

Reproduction

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The epigenetic status of a donor nucleus has an important effect on the developmental potential of embryos produced by somatic cell nuclear transfer (SCNT). In this study, we transferred cultured rabbit cumulus cells (RCC) and fetal fibroblasts (RFF) from genetically marked rabbits (Alicia/Basilea) into metaphase II oocytes and analyzed the levels of histone H3-lysine 9-lysine 14 acetylation (acH3K9/14) in donor cells and cloned embryos. We also assessed the correlation between the histone acetylation status of donor cells and cloned embryos and their developmental potential. To test whether alteration of the histone acetylation status affects development of cloned embryos, we treated donor cells with sodium butyrate (NaBu), a histone deacetylase inhibitor. Further, we tried to improve cloning efficiency by chimeric complementation of cloned embryos with blastomeres from in vivo fertilized or parthenogenetic embryos. The levels of acH3K9/14 were higher in RCCs than in RFFs (P!0.05). Although the type of donor cells did not affect development to blastocyst, after transfer into recipients, RCC cloned embryos induced a higher initial pregnancy rate as compared to RFF cloned embryos (40 vs 20%). However, almost all pregnancies with either type of cloned embryos were lost by the middle of gestation and only one fully developed, live RCC-derived rabbit was obtained. Treatment of RFFs with NaBu significantly increased the level of acH3K9/14 and the proportion of nuclear transfer embryos developing to blastocyst (49 vs 33% with non-treated RFF, P!0.05). The distribution of acH3K9/14 in either group of cloned embryos did not resemble that in in vivo fertilized embryos suggesting that reprogramming of this epigenetic mark is aberrant in cloned rabbit embryos and cannot be corrected by treatment of donor cells with NaBu. Aggregation of embryos cloned from NaBu-treated RFFs with blastomeres from in vivo derived embryos improved development to blastocyst, but no cloned offspring were obtained. Two live cloned rabbits were produced from this donor cell type only after aggregation of cloned embryos with a parthenogenetic blastomere. Our study demonstrates that the levels of histone acetylation in donor cells and cloned embryos correlate with their developmental potential and may be a useful epigenetic mark to predict efficiency of SCNT in rabbits.

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“…The study of imprinted-gene effects in brain development was pioneered by Keverne, whose studies of chimeric mice showed differential contribution of paternally-expressed imprinted genes to development of limbic brain regions (especially the hypothalamus), and maternally-expressed genes to development of the neocortex (Allen et al 1995;Keverne et al 1996;Keverne 2001a,b). Functional and evolutionary hypotheses for the effects of brain-expressed imprinted genes have been described in detail; these include diverse effects on affect, cognition, attention, feeding behavior, and other central brain functions (Isles et al 2006;Wilkinson et al 2007;Champagne et al 2009), some of which apparently influence resource-related interactions between mothers and offspring.…”

Section: Genomic Imprinting In the Brainmentioning

confidence: 99%

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

Crespi

2011

Brain, Behavior and Epigenetics

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I describe and evaluate the hypothesis that effects from parent-offspring conflict and genomic imprinting on human neurodevelopment and behavior are central to evolved systems of mother-child attachment. The psychological constructs of Bowlby's attachment theory provide phenomenological descriptions of how attachment orchestrates affective-cognitive development, and patterns of imprinted gene expression and co-expression provide evidence of epigenetic and evolutionary underpinnings to human growth and neurodevelopment. Social-environmental perturbations to the development of normally-secure attachment, and alterations to evolved systems of parent-offspring conflict and imprinted-gene effects, are expected to lead to specific forms of maladaptation, manifest in psychiatric conditions affecting social-brain development. In particular, under-development of the social brain in autism may be mediated in part by mechanisms that lead to physically enhanced yet psychologically under-developed attachment to the mother, and affective-psychotic conditions, such as schizophrenia and depression, may be mediated in part by forms of insecure attachment and by increased relative effects of the maternal brain, both directly from mothers and via imprinted-gene effects in offspring. These hypotheses are concordant with findings from epidemiology, attachment theory, psychiatry, and genetic and epigenetic analyses of risk factors for autism and affective-psychotic conditions, they make novel predictions for explaining the causes of psychosis in Prader-Willi syndrome and idiopathic schizophrenia, and they suggest avenues for therapeutic interventions based on normalizing alterations to epigenetic networks and targeting public-health interventions towards reduction of perturbations to the development of secure attachment in early childhood and individuation during adolescence.

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Distribution of parthenogenetic cells in the mouse brain and their influence on brain development and behavior.

Cited by 106 publications

References 17 publications

Derivation of human embryonic stem cell lines from parthenogenetic blastocysts

Derivation of human embryonic stem cell lines from parthenogenetic blastocysts

Rabbit somatic cell cloning: effects of donor cell type, histone acetylation status and chimeric embryo complementation

The Strategies of the Genes: Genomic Conflicts, Attachment Theory, and Development of the Social Brain

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