Unrestricted lineage differentiation of parthenogenetic ES cells

Sturm, Karin S.; Berger, Christoph; Zhou, Sheila X.; Dunwoodie, Sally L.; Tan, Seong‐Seng; Tam, Patrick

doi:10.1007/s004270050067

Cited by 17 publications

(21 citation statements)

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“…The latter were produced from intercrossing heterozygous p35 ϩ/Ϫ mice (maintained on C57BL/6J ϫ DBA background). The morulas carrying the reporter gene have normal p35 alleles (confirmed by PCR) and have the X lacZ /X lacZ or X lacZ /Y genotype (Tan et al, 1993;Sturm et al, 1997). Chimeras that contain p35 Ϫ/Ϫ cells (identified by genotyping) were selected for the study, whereas chimeras with p35 ϩ/Ϫ cells were used as controls.…”

Section: Methodsmentioning

confidence: 99%

Control of Cortical Neuron Migration and Layering: Cell and Non Cell-Autonomous Effects of p35

Hammond¹,

Tsai²,

Tan³

2004

J. Neurosci.

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The migration, arrest, and ultimately positioning of cortical neurons require signaling activity from Reelin as well as from cyclindependent kinase 5 (Cdk5). Although both molecules control neuronal positioning, they achieve their effects by quite separate molecular pathways. Cdk5 is a serine-threonine kinase, the activity of which is dependent on its activating subunits p35 and p39. Mice deficient in Cdk5, p35, or both p35 and p39 display the hallmarks of disturbed cortical development, including cortical layer inversion, neuronal disorientation, and abnormal fiber infiltration. To distinguish between the cell-and non cell-autonomous functions of p35, we constructed p35Ϫ/Ϫ chimeras using the lacZ gene as an independent marker for p35 ϩ/ϩ cells. In this shared developmental space, wild-type and mutant neurons behaved cell-autonomously with respect to layering. Wild-type cells formed a properly layered supercortex that is mirrored by an inverted mutant cortex lying underneath. However, this genotype-specific behavior was confined to the pyramidal population, and interneurons belonging to either genotype were indiscriminately distributed. However, there was also non cell-autonomous rescue of mutant neurons, and this rescue was specific only to early-born pyramidal neurons belonging to layer V. Rescued neurons reached the correct layer address and possessed appropriate neuronal morphology, orientation, and projections. Later-born neurons belonging to layers II and III were not rescued. These results demonstrate that p35 signaling can have both cell-and non cell-autonomous consequences, and their effects are not uniformly shared by cortical neurons born at different times or born at different places (projection neurons vs interneurons).

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Section: Methodsmentioning

confidence: 99%

Control of Cortical Neuron Migration and Layering: Cell and Non Cell-Autonomous Effects of p35

Hammond¹,

Tsai²,

Tan³

2004

J. Neurosci.

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“…The primers were used at a ratio of 1:2:1, respectively. Embryos were sexed by using Sry primers: Sry F (5Ј-TTCAGCCCTACAGCCACATGA-3Ј) and Sry R (5Ј-A TGTGGGTTCCTGTCCCACTG-3Ј) (63).…”

Section: Targeting Vectors and Generation Of The Cited1mentioning

confidence: 99%

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

Rodríguez¹,

Sparrow²,

Scott³

et al. 2004

Molecular and Cellular Biology

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Cited1 is a transcriptional cofactor that interacts with Smad4, estrogen receptors ␣ and ␤, TFAP2, and CBP/p300. It is expressed in a restricted manner in the embryo as well as in extraembryonic tissues during embryonic development. In this study we report the engineering of a loss-of-function Cited1 mutation in the mouse. Cited1 null mutants show growth restriction at 18.5 days postcoitum, and most of them die shortly after birth. Half the heterozygous females, i.e., those that carry a paternally inherited wild-type Cited1 allele, are similarly affected. Cited1 is normally expressed in trophectoderm-derived cells of the placenta; however, in these heterozygous females, Cited1 is not expressed in these cells. This occurs because Cited1 is located on the X chromosome, and thus the wild-type Cited1 allele is not expressed because the paternal X chromosome is preferentially inactivated. Loss of Cited1 resulted in abnormal placental development. In mutants, the spongiotrophoblast layer is irregular in shape and enlarged while the labyrinthine layer is reduced in size. In addition, the blood spaces within the labyrinthine layer are disrupted; the maternal sinusoids are considerably larger in mutants, leading to a reduction in the surface area available for nutrient exchange. We conclude that Cited1 is required in trophoblasts for normal placental development and subsequently for embryo viability.

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“…67 From chimera studies some evidence had evolved on the capacity of uniparental cells for hematopoiesis. Contribution of uniparental cells to the peripheral blood of postnatal chimeras, which for a longer period requires the activity of functional HSCs, has been described for postnatal AG and PG ES cell chimeras 24,36 and, more controversially, for PG aggregation chimeras, where contribution 45 as well as absence 44 have been observed. In the only human PG chimera reported to date, contribution of PG cells to peripheral blood was observed to an age of more than three years, indicating PG origin of HSC.…”

Section: Adult Repopulating Hscs Generated From Uniparental Es Cellsmentioning

confidence: 99%

“…44,[47][48][49] Although various properties, particularly the phenotype of ES cell chimeras generated with AG ES cells 24,35,50 indicate that genomic imprinting is similar in uniparental ES cells compared to primary embryonic cells such as those derived from cleavage stage embryos or the ICM of uniparental blastocysts, some phenotypic differences exist between PG ES cell chimeras and PG aggregation chimeras. 35,47 PG ES cell chimeras do not exhibit growth deficits observed with PG aggregation chimeras, 35 and the exclusion of PG cells to liver or muscle, 44,45 has not been similarly observed with PG ES cells, 36 indicating differences in the developmental potential of these cells that could be associated with epigenetic changes resulting from ES cell derivation and culture. [51][52][53] …”

Section: Developmental Potential Of Uniparental Cells In Chimerasmentioning

confidence: 99%

“…Genomic imprinting appears not be relevant for the formation of ES cells, but abnormal expression of imprinted genes influences the differentiation potential of ES cells. 33,34 While uniparental ES cells have been termed pluripotent due to their contribution to various tissues upon blastocyst injection, 24,35,36 their contribution in chimeras causes abnormal phenotypes, particularly for AG ES cells. Attempts at the formation of entirely PG ES cell-derived fetuses by tetraploid complementation resulted in developmental failure similar to PG conceptuses.…”

Section: Mammalian Uniparental Embryos: Origin and Developmentmentioning

confidence: 99%

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In vivo and in vitro differentiation of uniparental embryonic stem cells into hematopoietic and neural cell types

Eckardt

Dinger²,

Kurosaka

et al. 2008

Organogenesis

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The biological role of genomic imprinting in adult tissue is central to the consideration of transplanting uniparental embryonic stem (ES) cell-derived tissues. We have recently shown that both maternal (parthenogenetic/gynogenetic) and paternal (androgenetic) uniparental ES cells can differentiate, both in vivo in chimeras and in vitro, into adult-repopulating hematopoietic stem and progenitor cells. This suggests that, at least in some tissues, the presence of two maternal or two paternal genomes does not interfere with stem cell function and tissue homeostasis in the adult. Here, we consider implications of the contribution of uniparental cells to hematopoiesis and to development of other organ systems, notably neural tissue for which consequences of genomic imprinting are associated with a known bias in development and behavioral disorders. Our findings so far indicate that there is little or no limit to the differentiation potential of uniparental ES cells outside the normal developmental paradigm. As a potentially donor MHC-matching source of tissue, uniparental transplants may provide not only a clinical resource but also a unique tool to investigate aspects of genomic imprinting in adults.

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Unrestricted lineage differentiation of parthenogenetic ES cells

Cited by 17 publications

References 0 publications

Control of Cortical Neuron Migration and Layering: Cell and Non Cell-Autonomous Effects of p35

Control of Cortical Neuron Migration and Layering: Cell and Non Cell-Autonomous Effects of p35

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

In vivo and in vitro differentiation of uniparental embryonic stem cells into hematopoietic and neural cell types

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