Journal articles: 'Extra-embryonic endoderm'

1

Selwood, L. "The Marsupial Blastocyst - a Study of the Blastocysts in the Hill Collection." Australian Journal of Zoology 34, no. 2 (1986): 177. http://dx.doi.org/10.1071/zo9860177.

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Blastocysts in the Hill Collection from Trichosurus vulpecula, Pefrogale penicillata, Macropus ruficollis (= M. rufogriseus), Macropus parma, Onychogalea fraenata, Bettongia gaimardi, Perameles obesula (=lsoodon obesulus), Perameles nasuta, Dasyurus viverrinus, Didelphis aurita (=D. marsupialis) and Didelphis virginiana were examined. They ranged from incomplete unilaminar blastocysts to late bilaminar blastocysts. The mode of formation of the unilaminar blastocyst appeared to be influenced by the presence or absence of the yolk mass. A unilaminar blastocyst lined by uniform protoderm cells occurred in a wide variety of marsupials. Differentiation of the unilaminar blastocyst into embryonic and extra-embryonic areas occurred at different stages of development. In macropodids and Didelphis it was found in small blastocysts soon after blastocyst completion. In dasyurids, Perameles and some other groups it was found in larger blastocysts, at least four cell generations after blastocyst completion. The first histological signs of differentiation of the unilaminar blastocyst into embryonic and extra-embryonic areas varied between different marsupials. In Didelphis, enlarged endoderm mother cells developed from the protoderm cells of one hemisphere. The protoderm cells of this hemisphere later differentiated as embryonic ectoderm and the endoderm mother cells gave rise to the primary endoderm. In D. viverrinus, bandicoots and T. vulpecula, the protoderm cells of one hemisphere differentiated simultaneously into cuboidal embryonic ectoderm and endoderm mother cells. In P. penicillata, M. ruficollis and M. parma the protoderm cells of one hemisphere proliferated to form a multilayered embryonic area which later differentiated into embryonic ectoderm and primary endoderm.

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Rossant, Janet. "Stem cells and lineage development in the mammalian blastocyst." Reproduction, Fertility and Development 19, no. 1 (2007): 111. http://dx.doi.org/10.1071/rd06125.

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The mammalian blastocyst is the source of the most pluripotent stem cells known: embryonic stem (ES) cells. However, ES cells are not totipotent; in mouse chimeras, they do not contribute to extra-embryonic cell types of the trophectoderm (TE) and primitive endoderm (PrE) lineages. Understanding the genetic pathways that control pluripotency v. extra-embryonic lineage restriction is key to understanding not only normal embryonic development, but also how to reprogramme adult cells to pluripotency. The trophectoderm and primitive endoderm lineages also provide the first signals that drive patterned differentiation of the pluripotent epiblast cells of the embryo. My laboratory has produced permanent mouse cell lines from both the TE and the PrE, termed trophoblast stem (TS) and eXtra-embryonic ENdoderm (XEN) cells. We have used these cells to explore the genetic and molecular hierarchy of lineage restriction and identify the key factors that distinguish the ES cell v. the TS or XEN cell fate. The major molecular pathways of lineage commitment defined in mouse embryos and stem cells are probably conserved across mammalian species, but more comparative studies of lineage development in embryos of non-rodent mammals will likely yield interesting differences in terms of timing and details.

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Brown, Kemar, Stephanie Legros, Jérôme Artus, Michael Xavier Doss, Raya Khanin, Anna-Katerina Hadjantonakis, and Ann Foley. "A Comparative Analysis of Extra-Embryonic Endoderm Cell Lines." PLoS ONE 5, no. 8 (August 6, 2010): e12016. http://dx.doi.org/10.1371/journal.pone.0012016.

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Murray, P., and D. Edgar. "Regulation of the differentiation and behaviour of extra-embryonic endodermal cells by basement membranes." Journal of Cell Science 114, no. 5 (March 1, 2001): 931–39. http://dx.doi.org/10.1242/jcs.114.5.931.

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Both the extracellular matrix and parathyroid hormone-related peptide (PTHrP) have been implicated in the differentiation and migration of extra-embryonic endodermal cells in the pre-implantation mammalian blastocyst. In order to define the individual roles and interactions between these factors in endodermal differentiation, we have used embryoid bodies derived from Lamc1(-/-) embryonic stem cells that lack basement membranes. The results show that in the absence of basement membranes, increased numbers of both visceral and parietal endodermal cells differentiate, but they fail to form organised epithelia. Furthermore, although parietal endodermal cells only migrate away from control embryoid bodies in the presence of PTHrP, they readily migrate from Lamc1(-/-) embryoid bodies in the absence of PTHrP, and this migration is unaffected by PTHrP. Thus, the basement membrane between epiblast and extra-embryonic endoderm is required for the proper organisation of visceral and parietal endodermal cells and also restricts their differentiation to maintain the population of primitive endodermal stem cells. Moreover, this basement membrane inhibits migration of parietal endodermal cells, the role of PTHrP being to stimulate delamination of parietal endodermal cells from the basement membrane rather than promoting migration per se.

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Mulvey, Claire M., Christian Schröter, Laurent Gatto, Duygu Dikicioglu, Isik Baris Fidaner, Andy Christoforou, Michael J. Deery, et al. "Dynamic Proteomic Profiling of Extra-Embryonic Endoderm Differentiation in Mouse Embryonic Stem Cells." STEM CELLS 33, no. 9 (June 23, 2015): 2712–25. http://dx.doi.org/10.1002/stem.2067.

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Downs, Karen M. "Is extra-embryonic endoderm a source of placental blood cells?" Experimental Hematology 89 (September 2020): 37–42. http://dx.doi.org/10.1016/j.exphem.2020.07.008.

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Rugg-Gunn, Peter. "Derivation and Culture of Extra-Embryonic Endoderm Stem Cell Lines." Cold Spring Harbor Protocols 2017, no. 1 (January 2017): pdb.prot093963. http://dx.doi.org/10.1101/pdb.prot093963.

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Ngondo, Richard Patryk, Daniel Cirera-Salinas, Jian Yu, Harry Wischnewski, Maxime Bodak, Sandrine Vandormael-Pournin, Anna Geiselmann, et al. "Argonaute 2 Is Required for Extra-embryonic Endoderm Differentiation of Mouse Embryonic Stem Cells." Stem Cell Reports 10, no. 2 (February 2018): 461–76. http://dx.doi.org/10.1016/j.stemcr.2017.12.023.

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9

Selwood, L. "Development of early cell lineages in marsupial embryos: an overview." Reproduction, Fertility and Development 6, no. 4 (1994): 507. http://dx.doi.org/10.1071/rd9940507.

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All major embryonic and extra-embryonic cell lineages are established before implantation in marsupials. In reptiles, birds, monotremes and most marsupials, the zygote is polarized, sometimes markedly so, and the cleavage pattern in relation to the polarized state provides the mechanism for the generation of positional signals. These ensure that the embryonic cell lineages develop in the centre of the developing blastoderm or blastocyst epithelium and the extra-embryonic lineages at the periphery. The evolution of the vertebrate yolky egg was accompanied by a decreasing dependence on maternal determinants and increasing dependence on positional signals to determine cell fate. It is proposed that when a less yolky egg evolved, the mechanisms for determination of cell fate in a developing epithelium were retained. It is proposed that in marsupials, positional signals are involved in the determination of cell fate of embryonic and trophectoderm cells but do so in a two-dimensional epithelium not a three-dimensional morula. The next lineage formed is the primary endoderm which separates off from the primitive ectoderm in the embryoblast and eventually lines the blastocyst cavity. Positional signals are responsible for the determination of primary endoderm in eutherian mammals, birds and probably also marsupials. Order of cell division during cleavage provides a mechanism whereby some cells in the embryoblast of marsupials have earlier and greater contact with their neighbouring cells. The mechanism for determination of primary endoderm cells in the blastocyst epithelium is examined in the Virginia opossum and the stripe-faced dunnart.

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Gardner, R. L., S. C. Barton, and M. A. H. Surani. "Use of triple tissue blastocyst reconstitution to study the development of diploid parthenogenetic primitive ectoderm in combination with fertilization-derived trophectoderm and primitive endoderm." Genetics Research 56, no. 2-3 (October 1990): 209–22. http://dx.doi.org/10.1017/s001667230003531x.

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SummaryDiploid mouse conceptuses lacking a paternal genome can form morphologically normal but small fetuses of up to 25 somites, but they invariably fail to develop beyond mid-gestation. Such conceptuses differ from normal most notably in the poor development of extra-embryonic tissues which are largely of trophectodermal and primitive endodermal origin. However, it is not clear whether the demise of diploid parthenogenetic (P) or gynogenetic (G) conceptuses is attributable entirely to the defective development of these two tissues or whether differentiation of the primitive ectoderm, the precursor of the foetus, extra-embryonic mesoderm and amnion, is also impaired by the absence of a paternal genome. Therefore, a new blastocyst reconstitution technique was used which enabled primitive ectoderm from P blastocysts to be combined with primitive endoderm and trophectoderm from fertilization-derived (F) blastocysts. One third of the ‘triple tissue’ reconstituted blastocysts that implanted yielded foetuses. However, all foetuses recovered on the llth or 12th day of gestation were small and, with one exception, either obviously retarded or arrested in development. The exception was a living 44 somite specimen which is the most advanced P foetus yet recorded. Foetuses were invariably degenerating in conceptuses recovered on the 13th day. In contrast, at least 16% of control reconstituted blastocysts with primitive ectoderm as well as primitive endoderm and trophectoderm of F origin developed normally on the 13th day of gestation or to term. Hence, the presence of a paternal genome seems to be essential for normal differentiation of all 3 primary tissues of the mouse blastocyst.The P foetuses that developed from reconstituted blastocysts were so closely invested by their membranes that they often showed abnormal flexure of the posterior region of the body. Several also showed a deficiency of allantoic tissue. Therefore, the possibility that the defect in development of P primitive ectoderms resided in their extra-embryonic tissues was investigated by analysing a series of chimaeras produced by injecting them into intact F blastocysts. The foregoing anomalies were not discernible even when P cells made a large contribution to the extra-embryonic mesoderm or amnion plus umbilical cord. Furthermore, selection against P cells was no greater in extra-embryonic derivatives of the primitive ectoderm than in the foetus itself.

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Satou, Yutaka, Kaoru S. Imai, and Nori Satoh. "Early embryonic expression of a LIM-homeobox geneCs-lhx3is downstream of β-catenin and responsible for the endoderm differentiation inCiona savignyiembryos." Development 128, no. 18 (September 15, 2001): 3559–70. http://dx.doi.org/10.1242/dev.128.18.3559.

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In early Ciona embryos, nuclear accumulation of β-catenin is most probably the first step of endodermal cell specification. If β-catenin is mis- and/or overexpressed, presumptive notochord cells and epidermal cells change their fates into endodermal cells, whereas if β-catenin nuclear localization is downregulated by the overexpression of cadherin, the endoderm differentiation is suppressed, accompanied with the differentiation of extra epidermal cells (Imai, K., Takada, N., Satoh, N. and Satou, Y. (2000) Development127, 3009-3020). Subtractive hybridization screens of mRNAs between β-catenin overexpressed embryos and cadherin overexpressed embryos were conducted to identify potential β-catenin target genes that are responsible for endoderm differentiation in Ciona savignyi embryos. We found that a LIM-homeobox gene (Cs-lhx3), an otx homolog (Cs-otx) and an NK-2 class gene (Cs-ttf1) were among β-catenin downstream genes. In situ hybridization signals for early zygotic expression of Cs-lhx3 were evident only in the presumptive endodermal cells as early as the 32-cell stage, those of Cs-otx in the mesoendodermal cells at the 32-cell stage and those of Cs-ttf1 in the endodermal cells at the 64-cell stage. Later, Cs-lhx3 was expressed again in a set of neuronal cells in the tailbud embryo, while Cs-otx was expressed in the anterior nervous system of the embryo. Expression of all three genes was upregulated in β-catenin overexpressed embryos and downregulated in cadherin overexpressed embryos. Injection of morpholino oligonucleotides against Cs-otx did not affect the embryonic endoderm differentiation, although the formation of the central nervous system was suppressed. Injection of Cs-ttf1 morpholino oligonucleotides also failed to suppress the endoderm differentiation, although injection of its synthetic mRNAs resulted in ectopic development of endoderm differentiation marker alkaline phosphatase. By contrast, injection of Cs-lhx3 morpholino oligo suppressed the endodermal cell differentiation and this suppression was rescued by injection of Cs-lhx3 mRNA into eggs. In addition, although injection of delE-Ci-cadherin mRNA into eggs resulted in the suppression of alkaline phosphatase development, injection of delE-Ci-cadherin mRNA with Cs-lhx3 mRNA rescued the alkaline phosphatase development. These results strongly suggest that a LIM-homeobox gene Cs-lhx3 is one of the β-catenin downstream genes and that its early expression in embryonic endodermal cells is responsible for their differentiation.

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12

Adamson, Eileen D., Sidney Strickland, Miao Tu, and Brenda Kahan. "A teratocarcinoma-derived endoderm stem cell line (1H5) that can differentiate into extra-embryonic endoderm cell types." Differentiation 29, no. 1 (March 1985): 68–76. http://dx.doi.org/10.1111/j.1432-0436.1985.tb00294.x.

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13

Sobis, H., A. Verstuyf, and M. Vandeputte. "Histochemical differences in expression of X-linked glucose-6-phosphate dehydrogenase between ectoderm- and endoderm-derived embryonic and extra-embryonic tissues." Journal of Histochemistry & Cytochemistry 39, no. 5 (May 1991): 569–74. http://dx.doi.org/10.1177/39.5.2016509.

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We examined the activity of X-linked glucose-6-phosphate dehydrogenase (G6PD) in concepti of the enzyme-deficient mutant and wild-type C3H mice. By using different crosses between the G6PD-deficient homozygous, heterozygous, or wild-type females and hemizygous or wild-type males, we confirmed the inactivation of one of the two X chromosomes in female concepti by a histochemical method. With this technique, a dual (G6PD + or -) cell population could be observed in the tissue sections. We demonstrate that the paternal X chromosome is inactivated in the endoderm of parietal and visceral yolk sac and in the trophoblast, whereas in the embryo and in the yolk sac mesoderm this inactivation is random. Our results confirm biochemical observations showing that only the maternal X chromosome is expressed in all derivatives of trophectoderm and primitive endoderm, whereas derivatives of the primitive ectoderm show random X chromosome expression.

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Kunath, T. "Imprinted X-inactivation in extra-embryonic endoderm cell lines from mouse blastocysts." Development 132, no. 7 (February 23, 2005): 1649–61. http://dx.doi.org/10.1242/dev.01715.

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Tremblay, Kimberly D., N. Ray Dunn, and Elizabeth J. Robertson. "Mouse embryos lacking Smad1 signals display defects in extra-embryonic tissues and germ cell formation." Development 128, no. 18 (September 15, 2001): 3609–21. http://dx.doi.org/10.1242/dev.128.18.3609.

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The Smad proteins are important intracellular mediators of the transforming growth factor β (TGFβ) family of secreted growth factors. Smad1 is an effector of signals provided by the bone morphogenetic protein (BMP) sub-group of TGFβ molecules. To understand the role of Smad1 in mouse development, we have generated a Smad1 loss-of-function allele using homologous recombination in ES cells. Smad1−/− embryos die by 10.5 dpc because they fail to connect to the placenta. Mutant embryos are first recognizable by 7.0 dpc, owing to a characteristic localized outpocketing of the visceral endoderm at the posterior embryonic/extra-embryonic junction, accompanied by a dramatic twisting of the epiblast and nascent mesoderm. Chimera analysis reveals that these two defects are attributable to a requirement for Smad1 in the extra-embryonic tissues. By 7.5 dpc, Smad1-deficient embryos show a marked impairment in allantois formation. By contrast, the chorion overproliferates, is erratically folded within the extra-embryonic space and is impeded in proximal migration. BMP signals are known to be essential for the specification and proliferation of primordial germ cells. We find a drastic reduction of primordial germ cells in Smad1-deficient embryos, suggesting an essential role for Smad1-dependent signals in primordial germ cell specification. Surprisingly, despite the key involvement of BMP signaling in tissues of the embryo proper, Smad1-deficient embryos develop remarkably normally. An examination of the expression domains of Smad1, Smad5 and Smad8 in early mouse embryos show that, while Smad1 is uniquely expressed in the visceral endoderm at 6.5 dpc, in other tissues Smad1 is co-expressed with Smad5 and/or Smad8. Collectively, these data have uncovered a unique function for Smad1 signaling in coordinating the growth of extra-embryonic structures necessary to support development within the uterine environment.

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Julio, M. K. d., M. J. Alvarez, A. Galli, J. Chu, S. M. Price, A. Califano, and M. M. Shen. "Regulation of extra-embryonic endoderm stem cell differentiation by Nodal and Cripto signaling." Journal of Cell Science 124, no. 18 (September 13, 2011): e1-e1. http://dx.doi.org/10.1242/jcs.098848.

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Fléchon, Jacques-E., Bernadette Fléchon, Jeril Degrouard, and Michel Guillomot. "Cellular features of the extra-embryonic endoderm during elongation in the ovine conceptus." genesis 45, no. 11 (2007): 709–15. http://dx.doi.org/10.1002/dvg.20347.

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Julio, M. K. d., M. J. Alvarez, A. Galli, J. Chu, S. M. Price, A. Califano, and M. M. Shen. "Regulation of extra-embryonic endoderm stem cell differentiation by Nodal and Cripto signaling." Development 138, no. 18 (August 23, 2011): 3885–95. http://dx.doi.org/10.1242/dev.065656.

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Anderson, Kathryn G. V., William B. Hamilton, Fabian V. Roske, Ajuna Azad, Teresa E. Knudsen, Maurice A. Canham, Lesley M. Forrester, and Joshua M. Brickman. "Insulin fine-tunes self-renewal pathways governing naive pluripotency and extra-embryonic endoderm." Nature Cell Biology 19, no. 10 (September 25, 2017): 1164–77. http://dx.doi.org/10.1038/ncb3617.

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Imai, K., N. Takada, N. Satoh, and Y. Satou. "(beta)-catenin mediates the specification of endoderm cells in ascidian embryos." Development 127, no. 14 (July 15, 2000): 3009–20. http://dx.doi.org/10.1242/dev.127.14.3009.

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In the present study, we addressed the role of (beta)-catenin in the specification of embryonic cells of the ascidians Ciona intestinalis and C. savignyi and obtained the following results: (1) During cleavages, (beta)-catenin accumulated in the nuclei of vegetal blastomeres, suggesting that it plays a role in the specification of endoderm. (2) Mis- and/or overexpression of (beta)-catenin induced the development of an endoderm-specific alkaline phosphatase (AP) in presumptive notochord cells and epidermis cells without affecting differentiation of primary lineage muscle cells. (3) Downregulation of (beta)-catenin induced by the overexpression of cadherin resulted in the suppression of endoderm cell differentiation. This suppression was compensated for by the differentiation of extra epidermis cells. (4) Specification of notochord cells did not take place in the absence of endoderm differentiation. Both the overexpression of (beta)-catenin in presumptive notochord cells and the downregulation of (beta)-catenin in presumptive endoderm cells led to the suppression of Brachyury gene expression, resulting in the failure of notochord specification. These results suggest that the accumulation of (beta)-catenin in the nuclei of endoderm progenitor cells is the first step in the process of ascidian endoderm specification.

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Schlupf, Judith, and Herbert Steinbeisser. "IGF antagonizes the Wnt/β-Catenin pathway and promotes differentiation of extra-embryonic endoderm." Differentiation 87, no. 5 (June 2014): 209–19. http://dx.doi.org/10.1016/j.diff.2014.07.003.

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Detilleux, P. G., N. F. Cheville, and B. L. Deyoe. "Pathogenesis of Brucella abortus in Chicken Embryos." Veterinary Pathology 25, no. 2 (March 1988): 138–46. http://dx.doi.org/10.1177/030098588802500206.

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Chicken embryos inoculated with Brucella abortus at 6, 10, and 12 days of incubation were examined by light and electron microscopy. B. abortus was identified by avidin-biolin immunoperoxidase and immunogold techniques. Death occurred from 2 to 5 days post-inoculation, depending on age of the embryo and route of inoculation. B. abortus was recovered from all infected eggs. Brucellae had spread throughout all tissues and localized preferentially within cells of mesodermal derivation. Organ distribution and degree of bacterial replication varied with age of the embryo at lime of inoculation. In 6-day-old embryos, B. abortus localized preferentially in endoderm and mesoderm of yolk sac wall, extra- and intraembryonic serosal epithelia, and glomeruli of the mesonephros. In 10- and 12-day-old embryos. B. abortus spread to all tissues; renal glomeruli, liver, spleen, and heart were most severely infected. Intracellular B. abortus was within the rough endoplasmic reticulum of mesenchymal, mesothelial, yolk endodermal, and hepatic cells. In mononuclear phagocytes, endothelial cells, and granulocytes, bacteria were within membrane-bound vacuoles. Intracellular replication of B. abortus in embryonic tissues, especially yolk endoderm, closely resembled that in experimental infections of trophoblasts.

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Smyth, Neil, H. Seda Vatansever, Patricia Murray, Michael Meyer, Christian Frie, Mats Paulsson, and David Edgar. "Absence of Basement Membranes after Targeting the LAMC1 Gene Results in Embryonic Lethality Due to Failure of Endoderm Differentiation." Journal of Cell Biology 144, no. 1 (January 11, 1999): 151–60. http://dx.doi.org/10.1083/jcb.144.1.151.

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The LAMC1 gene coding for the laminin γ1 subunit was targeted by homologous recombination in mouse embryonic stem cells. Mice heterozygous for the mutation had a normal phenotype and were fertile, whereas homozygous mutant embryos did not survive beyond day 5.5 post coitum. These embryos lacked basement membranes and although the blastocysts had expanded, primitive endoderm cells remained in the inner cell mass, and the parietal yolk sac did not develop. Cultured embryonic stem cells appeared normal after targeting both LAMC1 genes, but the embryoid bodies derived from them also lacked basement membranes, having disorganized extracellular deposits of the basement membrane proteins collagen IV and perlecan, and the cells failed to differentiate into stable myotubes. Secretion of the linking protein nidogen and a truncated laminin α1 subunit did occur, but these were not deposited in the extracellular matrix. These results show that the laminin γ1 subunit is necessary for laminin assembly and that laminin is in turn essential for the organization of other basement membrane components in vivo and in vitro. Surprisingly, basement membranes are not necessary for the formation of the first epithelium to develop during embryogenesis, but first become required for extra embryonic endoderm differentiation.

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Cho, L. T. Y., S. E. Wamaitha, I. J. Tsai, J. Artus, R. I. Sherwood, R. A. Pedersen, A. K. Hadjantonakis, and K. K. Niakan. "Conversion from mouse embryonic to extra-embryonic endoderm stem cells reveals distinct differentiation capacities of pluripotent stem cell states." Development 139, no. 16 (July 12, 2012): 2866–77. http://dx.doi.org/10.1242/dev.078519.

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Rodriguez, T. A. "Induction and migration of the anterior visceral endoderm is regulated by the extra-embryonic ectoderm." Development 132, no. 11 (June 1, 2005): 2513–20. http://dx.doi.org/10.1242/dev.01847.

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Gardner, R. L., T. J. Davies, and M. S. Carey. "Effect of delayed implantation on differentiation of the extra-embryonic endoderm in the mouse blastocyst." Placenta 9, no. 4 (July 1988): 343–59. http://dx.doi.org/10.1016/0143-4004(88)90048-3.

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Duncan, S. A. "Generation of embryos directly from embryonic stem cells by tetraploid embryo complementation reveals a role for GATA factors in organogenesis." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1534–36. http://dx.doi.org/10.1042/bst0331534.

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Gene targeting in ES (embryonic stem) cells has been used extensively to study the role of proteins during embryonic development. In the traditional procedure, this requires the generation of chimaeric mice by introducing ES cells into blastocysts and allowing them to develop to term. Once chimaeric mice are produced, they are bred into a recipient mouse strain to establish germline transmission of the allele of interest. Although this approach has been used very successfully, the breeding cycles involved are time consuming. In addition, genes that are essential for organogenesis often have roles in the formation of extra-embryonic tissues that are essential for early stages of post-implantation development. For example, mice lacking the GATA transcription factors, GATA4 or GATA6, arrest during gastrulation due to an essential role for these factors in differentiation of extra-embryonic endoderm. This lethality has frustrated the study of these factors during the development of organs such as the liver and heart. Extraembryonic defects can, however, be circumvented by generating clonal mouse embryos directly from ES cells by tetraploid complementation. Here, we describe the usefulness and efficacy of this approach using GATA factors as an example.

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Yoshimizu, T., M. Obinata, and Y. Matsui. "Stage-specific tissue and cell interactions play key roles in mouse germ cell specification." Development 128, no. 4 (February 15, 2001): 481–90. http://dx.doi.org/10.1242/dev.128.4.481.

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Primordial germ cells (PGCs) in mice have been recognized histologically as alkaline phosphatase (AP) activity-positive cells at 7.2 days post coitum (dpc) in the extra-embryonic mesoderm. However, mechanisms regulating PGC formation are unknown, and an appropriate in vitro system to study the mechanisms has not been established. Therefore, we have developed a primary culture of explanted embryos at pre- and early-streak stages, and have studied roles of cell and/or tissue interactions in PGC formation. The emergence of PGCs from 5.5 dpc epiblasts was observed only when they were co-cultured with extra-embryonic ectoderm, which may induce the conditions required for PGC formation within epiblasts. From 6.0 dpc onwards, PGCs emerged from whole epiblasts as did a fragment of proximal epiblast that corresponds to the area containing presumptive PGC precursors without neighboring extra-embryonic ectoderm and visceral endoderm. Dissociated epiblasts at these stages, however, did not give rise to PGCs, indicating that interactions among a cluster of a specific number of proximal epiblast cells is needed for PGC differentiation. In contrast, we observed that dissociated epiblast cells from a 6.5-b (6.5+15-16 hours) to 6.75 dpc embryo that had undergone gastrulation gave rise to PGCs. Our results demonstrate that stage-dependent tissue and cell interactions play key roles in PGC determination.

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Soma, Miki, Momoe Iha, Sho Sato, Yuki Mori, Kano Kasuga, Ikuo Kojima, and Masayuki Kobayashi. "Factors Affecting the Expression of Differentiation Marker Genes for the Primitive Endoderm Lineage in a Mouse Extra-Embryonic Endoderm Stem Cell Line, XEN26 Cells." Biotechnology & Biotechnological Equipment 25, no. 4 (January 2011): 2679–82. http://dx.doi.org/10.5504/bbeq.2011.0094.

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Artus, J., J. J. Panthier, and A. K. Hadjantonakis. "A role for PDGF signaling in expansion of the extra-embryonic endoderm lineage of the mouse blastocyst." Development 137, no. 20 (September 8, 2010): 3361–72. http://dx.doi.org/10.1242/dev.050864.

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Damert, Annette, Lucile Miquerol, Marina Gertsenstein, Werner Risau, and Andras Nagy. "Insufficient VEGFA activity in yolk sac endoderm compromises haematopoietic and endothelial differentiation." Development 129, no. 8 (April 15, 2002): 1881–92. http://dx.doi.org/10.1242/dev.129.8.1881.

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Vascular endothelial growth factor A (VEGFA) plays a pivotal role in the first steps of endothelial and haematopoietic development in the yolk sac, as well as in the establishment of the cardiovascular system of the embryo. At the onset of gastrulation, VEGFA is primarily expressed in the yolk sac visceral endoderm and in the yolk sac mesothelium. We report the generation and analysis of a Vegf hypomorphic allele, Vegflo. Animals heterozygous for the targeted mutation are viable. Homozygous embryos, however, die at 9.0 dpc because of severe abnormalities in the yolk sac vasculature and deficiencies in the development of the dorsal aortae. We find that providing ‘Vegf wild-type’ visceral endoderm to the hypomorphic embryos restores normal blood and endothelial differentiation in the yolk sac, but does not rescue the phenotype in the embryo proper. In the opposite situation, however, when Vegf hypomorphic visceral endoderm is provided to a wild-type embryo, the ‘Vegf wild-type’ yolk sac mesoderm is not sufficient to support proper vessel formation and haematopoietic differentiation in this extra-embryonic membrane. These findings demonstrate that VEGFA expression in the visceral endoderm is absolutely required for the normal expansion and organisation of both the endothelial and haematopoietic lineages in the early sites of vessel and blood formation. However, normal VEGFA expression in the yolk sac mesoderm alone is not sufficient for supporting the proper development of the early vascular and haematopoietic system.

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Shimosato, Daisuke, Makoto Shiki, and Hitoshi Niwa. "Extra-embryonic endoderm cells derived from ES cells induced by GATA Factors acquire the character of XEN cells." BMC Developmental Biology 7, no. 1 (2007): 80. http://dx.doi.org/10.1186/1471-213x-7-80.

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Zalik, S. E., L. W. Thomson, and I. M. Ledsham. "Expression of an endogenous galactose-binding lectin in the early chick embryo." Journal of Cell Science 88, no. 4 (November 1, 1987): 483–93. http://dx.doi.org/10.1242/jcs.88.4.483.

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The gastrulating chick blastoderm contains lectin activity specific for beta-D-galactoside groups. The galactose-binding lectin isolated by affinity chromatography on rho-aminophenyl-beta-D-lactoside separates into two bands when studied by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. One of these LII has a relative molecular mass of 70 (+/− 2) X 10(3) while the other LI is a polypeptide that migrates with the dye front in 10% gels. We have prepared an antiserum against this lectin preparation and have affinity-purified antibodies against LI. When embryos at stages 3–7 were examined by immunofluorescence using the affinity-purified antibodies, lectin was expressed in cells at the lowest portions of the primitive streak as well as in cells migrating laterally from this region to form the endoderm. Lectin was also expressed by the cells of the extra-embryonic endoderm and the primordial germ cells of the proximal area opaca. In transfers of gradient gels stained with affinity-purified antibodies against LI, this lectin had an approximate molecular weight of 6.5 X 10(3). Our results indicate that this lectin is expressed in areas that are undergoing cell spreading.

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Linneberg-Agerholm, Madeleine, Yan Fung Wong, Jose Alejandro Romero Herrera, Rita S. Monteiro, Kathryn G. V. Anderson, and Joshua M. Brickman. "Naïve human pluripotent stem cells respond to Wnt, Nodal and LIF signalling to produce expandable naïve extra-embryonic endoderm." Development 146, no. 24 (November 18, 2019): dev180620. http://dx.doi.org/10.1242/dev.180620.

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Guillomot, Michel, Annick Turbe, Isabelle Hue, and Jean-Paul Renard. "Staging of ovine embryos and expression of the T-box genes Brachyury and Eomesodermin around gastrulation." Reproduction 127, no. 4 (April 2004): 491–501. http://dx.doi.org/10.1530/rep.1.00057.

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The high rates of embryonic mortalities which follow in vitro production of ruminant embryos have emphasized the need for increased knowledge of early development. It is likely that early failures in embryonic development and placenta formation involve abnormal differentiation of mesoderm. The aim of this study was to investigate the pattern of expression of two T-box genes known to control the gastrulation process, Brachyury and Eomesodermin, by whole-mount in situ hybridization. To allow a more precise comparison of both expression patterns between embryos, we describe a new staging of pre-implanted ovine embryos by gross morphology and histology from pre-gastrulation stages to the beginning of neurulation. In pre-streak embryos primitive mesoderm cells delaminated in between the primitive endoderm and the epiblast. At that stage, no expression of Brachyury or Eomesodermin could be detected in the embryos. Early expression of both T-genes was observed by the early-streak stages in epiblast cells located close to the presumptive posterior pole of the embryos. Later on, during gastrulation both genes followed a pattern of expression similar to the ones described in other mammals. These observations suggest that other genes, which remain to be identified, are responsible for extra-embryonic mesoderm differentiation in ruminant embryos.

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Zhang, Pengbo, Jian Li, Zhijia Tan, Chengyan Wang, Ting Liu, Lin Chen, Jun Yong, et al. "Short-term BMP-4 treatment initiates mesoderm induction in human embryonic stem cells." Blood 111, no. 4 (February 15, 2008): 1933–41. http://dx.doi.org/10.1182/blood-2007-02-074120.

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Human embryonic stem cells (hES cells) have unlimited self-renewal capacity and can differentiate into most, if not all, possible cell types. This unique property makes them valuable not only for investigation of early developmental processes, but also for regenerative medicine. Mesoderm-derived cardiac cells and hematopoietic cells both have the potential for various therapeutic applications. However, efficient induction of hES cell differentiation into mesoderm remains a challenge. Here, we showed that treatment of hES cells with bone morphogenetic protein-4 (BMP-4) exhibited differential effects: long-term treatment results in trophoblast and extra-embryonic endoderm differentiation, whereas short-term treatment can promote early mesoderm induction. The induction of mesoderm in hES cells occurs at a high efficiency as measured using several markers, such as Brachyury, WNT3, and MIXL1 expression. Moreover, these mesoderm progenitor cells can differentiate into cardiac and hematopoietic lineages in vitro. Further analysis showed that the mesoderm-inducing capacity of BMP-4 requires endogenous FGF and TGF-β/Nodal/activin signaling activities. Thus, our results uncover a novel role for BMP-4 in regulation of hES cell differentiation and should provide insights into the mechanism of mesoderm induction in hES cells.

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Zernicka-Goetz, Magdalena. "Patterning of the embryo: the first spatial decisions in the life of a mouse." Development 129, no. 4 (February 15, 2002): 815–29. http://dx.doi.org/10.1242/dev.129.4.815.

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Although in most species the polarity of the embryo takes its roots from the spatial patterning of the egg, mammals were viewed as an exception. This was because the anteroposterior polarity of the mouse embryo could not be seen until gastrulation, and no developmental cues were known that could define polarity at earlier stages. Why should we now re-consider this view? While mechanisms of axis formation in mammals could, in principle, be unique, the evolutionary conservation of numerous other developmental processes raises the question of why mammals would have evolved a different way or timing of organising their embryonic polarity. Indeed, recent evidence shows that well before the onset of gastrulation, the mouse embryo initiates asymmetric patterns of gene expression in its visceral endoderm. Although this extra-embryonic tissue does not contribute to the body itself, it is involved in axis formation. Other recent work has revealed that spatial distribution of cells in the visceral endoderm can be traced back to polarity present at the blastocyst stage. These insights have raised the possibility that embryonic polarity might also originate early during development of mammalian embryos. Indeed it now appears that there are at least two spatial cues that operate in the mouse egg to shape polarity of the blastocyst. One of these is at the animal pole, which is defined by the site of female meiosis, and another is associated with the position of sperm entry. In this review I discuss these recent findings, which have led to the recognition that mouse embryos initiate development of their polarity at the earliest stages of their life. This novel perspective raises questions about the nature of cellular and molecular mechanisms that could convert developmental cues in the zygote to axes of the blastocyst, and hence into polarity of the post-implantation embryo. It also brings to light the need to understand how such mechanisms could enable early mouse development to be so regulative.

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Okamoto, I., S. Tan, and N. Takagi. "X-chromosome inactivation in XX androgenetic mouse embryos surviving implantation." Development 127, no. 19 (October 1, 2000): 4137–45. http://dx.doi.org/10.1242/dev.127.19.4137.

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Using genetic and cytogenetic markers, we assessed early development and X-chromosome inactivation (X-inactivation) in XX mouse androgenones produced by pronuclear transfer. Contrary to the current view, XX androgenones are capable of surviving to embryonic day 7.5, achieving basically random X-inactivation in all tissues including those derived from the trophectoderm and primitive endoderm that are characterized by paternal X-activation in fertilized embryos. This finding supports the hypothesis that in fertilized female embryos, the maternal X chromosome remains active until the blastocyst stage because of a rigid imprint that prevents inactivation, whereas the paternal X chromosome is preferentially inactivated in extra-embryonic tissues owing to lack of such imprint. In spite of random X-inactivation in XX androgenones, FISH analyses revealed expression of stable Xist RNA from every X chromosome in XX and XY androgenonetic embryos from the four-cell to morula stage. Although the occurrence of inappropriate X-inactivation was further suggested by the finding that Xist continues ectopic expression in a proportion of cells from XX and XY androgenones at the blastocyst and the early egg cylinder stage, a replication banding study failed to provide positive evidence for inappropriate X-inactivation at E6. 5.

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Lake, J., J. Rathjen, J. Remiszewski, and P. D. Rathjen. "Reversible programming of pluripotent cell differentiation." Journal of Cell Science 113, no. 3 (February 1, 2000): 555–66. http://dx.doi.org/10.1242/jcs.113.3.555.

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We have undertaken an in vitro differentiation analysis of two related, interconvertible, pluripotent cell populations, ES and early primitive ectoderm-like (EPL) cells, which are most similar in morphology, gene expression, cytokine responsiveness and differentiation potential in vivo to ICM and early primitive ectoderm, respectively. Pluripotent cells were differentiated in vitro as aggregates (embryoid bodies) and the appearance and abundance of cell lineages were assessed by morphology and gene expression. Differentiation in EPL cell embryoid bodies recapitulated normal developmental progression in vivo, but was advanced in comparison to ES cell embryoid bodies, with the rapid establishment of late primitive ectoderm specific gene expression, and subsequent loss of pluripotent cell markers. Nascent mesoderm was formed earlier and more extensively in EPL cell embryoid bodies, and resulted in the appearance of terminally differentiated mesodermal cell types prior to and at higher levels than in ES cell embryoid bodies. Nascent mesoderm in EPL cell embryoid bodies was not specified but could be programmed to alternative fates by the addition of exogenous factors. EPL cells remained competent to form primitive endoderm even though this is not the normal fate of primitive ectoderm in vivo. The establishment of primitive ectoderm-like gene expression and inability to participate in embryogenesis following blastocyst injection is therefore not directly associated with restriction in the ability to form extra-embryonic lineages. However, the EPL cell embryoid body environment did not support differentiation of primitive endoderm to visceral endoderm, indicating the lack of an inductive signal for visceral endoderm formation deduced to originate from the pluripotent cells. Similarly, the inability of EPL cells to form neurons when differentiated as embryoid bodies was attributable to perturbation of the differentiation environment and loss of inductive signals rather than a restricted differentiation potential. Reversion of EPL cells to ES cells was accompanied by restoration of ES cell-like differentiation potential. These results demonstrate the ability of pluripotent cells to adopt developmentally distinct, stable cell states with altered differentiation potentials.

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Byrd, Noah, Sandy Becker, Peter Maye, Roopa Narasimhaiah, Benoit St-Jacques, Xiaoyan Zhang, Jill McMahon, Andrew McMahon, and Laura Grabel. "Hedgehog is required for murine yolk sac angiogenesis." Development 129, no. 2 (January 15, 2002): 361–72. http://dx.doi.org/10.1242/dev.129.2.361.

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Blood islands, the precursors of yolk sac blood vessels, contain primitive erythrocytes surrounded by a layer of endothelial cells. These structures differentiate from extra-embryonic mesodermal cells that underlie the visceral endoderm. Our previous studies have shown that Indian hedgehog (Ihh) is expressed in the visceral endoderm both in the visceral yolk sac in vivo and in embryonic stem (ES) cell-derived embryoid bodies. Differentiating embryoid bodies form blood islands, providing an in vitro model for studying vasculogenesis and hematopoiesis. A role for Ihh in yolk sac function is suggested by the observation that roughly 50% of Ihh–/– mice die at mid-gestation, potentially owing to vascular defects in the yolk sac. To address the nature of the possible vascular defects, we have examined the ability of ES cells deficient for Ihh or smoothened (Smo), which encodes a receptor component essential for all hedgehog signaling, to form blood islands in vitro. Embryoid bodies derived from these cell lines are unable to form blood islands, and express reduced levels of both PECAM1, an endothelial cell marker, and α-SMA, a vascular smooth muscle marker. RT-PCR analysis in the Ihh–/– lines shows a substantial decrease in the expression of Flk1 and Tal1, markers for the hemangioblast, the precursor of both blood and endothelial cells, as well as Flt1, an angiogenesis marker. To extend these observations, we have examined the phenotypes of embryo yolk sacs deficient for Ihh or Smo. Whereas Ihh–/– yolk sacs can form blood vessels, the vessels are fewer in number and smaller, perhaps owing to their inability to undergo vascular remodeling. Smo–/– yolk sacs arrest at an earlier stage: the endothelial tubes are packed with hematopoietic cells, and fail to undergo even the limited vascular remodeling observed in the Ihh–/– yolk sacs. Our study supports a role for hedgehog signaling in yolk sac angiogenesis.

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Phua, Dominic C. Y., Jianliang Xu, Safiah Mohamed Ali, Adrian Boey, Natalia V. Gounko, and Walter Hunziker. "ZO-1 and ZO-2 Are Required for Extra-Embryonic Endoderm Integrity, Primitive Ectoderm Survival and Normal Cavitation in Embryoid Bodies Derived from Mouse Embryonic Stem Cells." PLoS ONE 9, no. 6 (June 6, 2014): e99532. http://dx.doi.org/10.1371/journal.pone.0099532.

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Raju, Priyadharsini, Gunsmaa Nyamsuren, Manar Elkenani, Aleksandra Kata, Erdenechimeg Tsagaan, Wolfgang Engel, and Ibrahim M. Adham. "Pelota mediates gonocyte maturation and maintenance of spermatogonial stem cells in mouse testes." REPRODUCTION 149, no. 3 (March 2015): 213–21. http://dx.doi.org/10.1530/rep-14-0391.

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Pelota (Pelo) is an evolutionarily conserved gene, and its deficiency in Drosophila affects both male and female fertility. In mice, genetic ablation of Pelo leads to embryonic lethality at the early implantation stage as a result of the impaired development of extra-embryonic endoderm (ExEn). To define the consequences of Pelo deletion on male germ cells, we temporally induced deletion of the gene at both embryonic and postnatal stages. Deletion of Pelo in adult mice resulted in a complete loss of whole-germ cell lineages after 45 days of deletion. The absence of newly emerging spermatogenic cycles in mutants confirmed that spermatogonial stem cells (SSCs) were unable to maintain spermatogenesis in the absence of PELO protein. However, germ cells beyond the undifferentiated SSC stage were capable of completing spermatogenesis and producing spermatozoa, even in the absence of PELO. Following the deletion of Pelo during embryonic development, we found that although PELO is dispensable for maintaining gonocytes, it is necessary for the transition of gonocytes to SSCs. Immunohistological and protein analyses revealed the attenuation of FOXO1 transcriptional activity, which induces the expression of many SSC self-renewal genes. The decreased transcriptional activity of FOXO1 in mutant testes was due to enhanced activity of the PI3K/AKT signaling pathway, which led to phosphorylation and cytoplasmic sequestration of FOXO1. These results suggest that PELO negatively regulates the PI3K/AKT pathway and that the enhanced activity of PI3K/AKT and subsequent FOXO1 inhibition are responsible for the impaired development of SSCs in mutant testes.

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Sam, Jessica, Emily J. Mercer, Ingrid Torregroza, Kelly M. Banks, and Todd Evans. "Specificity, redundancy and dosage thresholds among gata4/5/6 genes during zebrafish cardiogenesis." Biology Open 9, no. 6 (June 15, 2020): bio053611. http://dx.doi.org/10.1242/bio.053611.

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ABSTRACTThe Gata4/5/6 sub-family of zinc finger transcription factors regulate many aspects of cardiogenesis. However, critical roles in extra-embryonic endoderm also challenge comprehensive analysis during early mouse cardiogenesis, while zebrafish models have previously relied on knockdown assays. We generated targeted deletions to disrupt each gata4/5/6 gene in zebrafish and analyzed cardiac phenotypes in single, double and triple mutants. The analysis confirmed that loss of gata5 causes cardia bifida and validated functional redundancies for gata5/6 in cardiac precursor specification. Surprisingly, we discovered that gata4 is dispensable for early zebrafish development, while loss of one gata4 allele can suppress the bifid phenotype of the gata5 mutant. The gata4 mutants eventually develop an age-dependent cardiomyopathy. By combining combinations of mutant alleles, we show that cardiac specification depends primarily on an overall dosage of gata4/5/6 alleles rather than a specific gene. We also identify a specific role for gata6 in controlling ventricle morphogenesis through regulation of both the first and second heart field, while loss of both gata4/6 eliminates the ventricle. Thus, different developmental programs are dependent on total dosage, certain pairs, or specific gata4/5/6 genes during embryonic cardiogenesis.This article has an associated First Person interview with the first author of the paper.

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Popovic, Mina, Monika Bialecka, Maria Gomes Fernandes, Jasin Taelman, Margot Van Der Jeught, Petra De Sutter, Björn Heindryckx, and Susana M. Chuva De Sousa Lopes. "Human blastocyst outgrowths recapitulate primordial germ cell specification events." Molecular Human Reproduction 25, no. 9 (June 18, 2019): 519–26. http://dx.doi.org/10.1093/molehr/gaz035.

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Abstract Our current knowledge of the mechanisms leading to human primordial germ cell (PGC) specification stems solely from differentiation experiments starting from human pluripotent stem cells. However, information regarding the origin of PGCs in vivo remains obscure. Here we apply an improved system for extended in vitro culture of human embryos to investigate the presence of PGC-like cells (PGCLCs) 12 days post fertilization (dpf). Good quality blastocysts (n = 141) were plated at 6 dpf and maintained in hypoxia, in medium supplemented with Activin A until 12 dpf. We primarily reveal that 12 dpf outgrowths recapitulate human peri-implantation events and demonstrate that blastocyst quality significantly impacts both embryo viability at 12 dpf, as well as the presence of POU5F1+ cells within viable outgrowths. Moreover, detailed examination of 12 dpf blastocyst outgrowths revealed a population of POU5F1+, SOX2– and SOX17+ cells that may correspond to PGCLCs, alongside POU5F1+ epiblast-like cells and GATA6+ endoderm-like cells. Our findings suggest that, in human, PGC precursors may become specified within the epiblast and migrate either transiently to the extra-embryonic mesoderm or directly to the dorsal part of the yolk sac endoderm around 12 dpf. This is a descriptive analysis and as such the conclusion that POU5F1+ and SOX17+ cells represent bona fide PGCs can only be considered as preliminary. In the future, other PGC markers may be used to further validate the observed cell populations. Overall, our findings provide insights into the origin of the human germline and may serve as a foundation to further unravel the molecular mechanisms governing PGC specification in human.

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Ciruna, B. G., L. Schwartz, K. Harpal, T. P. Yamaguchi, and J. Rossant. "Chimeric analysis of fibroblast growth factor receptor-1 (Fgfr1) function: a role for FGFR1 in morphogenetic movement through the primitive streak." Development 124, no. 14 (July 15, 1997): 2829–41. http://dx.doi.org/10.1242/dev.124.14.2829.

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Fibroblast growth factor (FGF) signaling has been implicated in the patterning of mesoderm and neural lineages during early vertebrate development. In the mouse, FGF receptor-1 (FGFR1) is expressed in an appropriate spatial and temporal manner to be orchestrating these functions. Mouse embryos homozygous for a mutated Fgfr1 allele (fgfr1(delta tmk)) die early in development, show abnormal growth and aberrant mesodermal patterning. We have performed a chimeric analysis to further study FGFR1 function in the morphogenesis and patterning of the mesodermal germ layer at gastrulation. At E9.5, fgfr1(delta tmk)/fgfr1(delta tmk) cells showed a marked deficiency in their ability to contribute to the extra-embryonic, cephalic, heart, axial and paraxial mesoderm, and to the endoderm of chimeric embryos. Analysis at earlier stages of development revealed that fgfr1(delta tmk)/fgfr1(delta tmk) cells accumulated within the primitive streak of chimeric embryos, and consequently failed to populate the anterior mesoderm and endodermal lineages at their inception. We suggest that the primary defect associated with the fgfr1(delta tmk) mutation is a deficiency in the ability of epiblast cells to traverse the primitive streak. fgfr1(delta tmk)/fgfr1(delta tmk) cells that accumulated within the primitive streak of chimeric embryos tended to form secondary neural tubes. These secondary neural tubes were entirely fgfr1(delta tmk)/fgfr1(delta tmk) cell derived. The adoption of ectopic neural fate suggests that normal morphogenetic movement through the streak is essential not only for proper mesodermal patterning but also for correct determination of mesodermal/neurectodermal cell fates.

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Sun, Qizhi, Mohamed I. Gatie, and Gregory M. Kelly. "Serum-dependent and -independent regulation of PARP2." Biochemistry and Cell Biology 97, no. 5 (October 2019): 600–611. http://dx.doi.org/10.1139/bcb-2018-0345.

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PARP2 belongs to a family of proteins involved in cell differentiation, DNA damage repair, cellular energy expenditure, and chromatin modeling. In addition to these overlapping functions with PARP1, PARP2 participates in spermatogenesis, T-cell maturation, extra-embryonic endoderm formation, adipogenesis, lipid metabolism, and cholesterol homeostasis. Knowledge of the functions of PARP2 is far from complete, and the mechanism(s) by which the gene and protein are regulated are unknown. In this study, we found that two different mechanisms are used in vitro to regulate PARP2 levels. In the presence of serum, PARP2 is degraded through the ubiquitin–proteasome pathway; however, when serum is removed or dialyzed with a 3.5 kDa molecular cut membrane, PARP2 rapidly becomes sodium dodecyl sulphate- and urea-insoluble. Despite the presence of a putative serum response element in the PARP2 gene, transcription is not affected by serum deprivation, and PARP2 levels are restored when serum is replaced. The loss of PARP2 affects cell differentiation and gene expression linked to cholesterol and lipid metabolism. These observations highlight the critical roles that PARP2 plays under different physiological conditions, and reveal that PARP2 is tightly regulated by distinct pathways.

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Sensken, Sandra, Juergen Enczmann, Thorsten Trapp, Esmail Zanjani, Peter Wernet, and Gesine Koegler. "Pluripotent Unrestricted Somatic Stem Cells (USSC) from Cord Blood Generate Hepatocytes in Vivo, but In Vitro Convert into Immature Endodermal Precursors: The Critical Role of the Biological Niche." Blood 104, no. 11 (November 16, 2004): 3596. http://dx.doi.org/10.1182/blood.v104.11.3596.3596.

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Abstract As shown recently by our group (Koegler et al. 2004; J. Exp. Med.200: 19:1–13) transplantation of USSC in a non-injury model, the preimmune fetal sheep, resulted in more than 20% albumin-producing human parenchymal hepatic cells with absence of cell fusion. Here we examined whether we are able to trigger USSC in vitro into the an endodermal differentiation pathway applying protocols described for both embryonal as well as adult stem cell. The following matrix/growth factors/organic substances were applied: Neurobasal medium/supplement B27/bFGF with and without nicotinamid, on fibronectin, laminin or matrigel for differentiation into the pancreatic development as well as HGF, NGF, bFGF and HGF, FGF4 with or without Oncostatin M to induce liver development. 15 different USSC lines were differentiated for 1, 2, 3, 4 and 6 weeks. Primers were designed with the strategy to define stages of endodermal development on the basis of the embryonic cell development from mouse and human. Therefore the following markers were established: GATA 4, HNF-1, HNF3ß and HNF 4a to define the embryonic and visceral (extra-embryonic) endoderm, a common precursor phenotype for both liver/exocrine pancreas development. To further assess differentiation into liver cells, a-1 antitrypsin, a-fetoprotein, albumin, HGF, Cyp2B6, Cyp3A4, Gys2 and PDX-1, PAX4, ISL-1, NKx6.1, NeuroD, insulin to determine differentiation into the pancreatic development as well as epithelial markers as CK8, CK18, CK19 were analyzed by RT-PCR and subsequent hybridization using gene-specific oligonucleotide probes. USSC were tested negativ for the majority of the markers, only HGF and cytokeratin markers CK8/18 and CK19 were tested positiv. In vitro differentiation shows that USSC never expressed Neuro D, HNF1, HNF3b, PDX-1, PAX4, insulin and a-fetoprotein, but do express depending on the culture conditions common endodermal precursor markers HNF4a, GATA4 (but not HNF1 or HNF3ß) as well as albumin, Cyp2B6, Cyp3A4, Gys2 (liver development) and Nkx6.1 and ISL-1 (pancreatic development. It is very interesting to note that ISL-1, required for the formation of the dorsal mesenchym and essential for the dorsal exocrine pancreas development is strong expressed, although all other markers as PDX-1 and PAX4 were always tested negative. We have never observed the expression of a-fetoprotein, which might be explained by the kinetic of this factor (Young-Yang, Nat.Cell Biology 2004). In summary, the results show that under the vitro conditions applied, only an endodermal precursor phenotype could be established. Therefore at present co-cultivation experiments with injured hepatocytes from sheep/rat/human are performed to mimic the biological niche in vitro as shown by Young-Yang et al. Western blots with an human albumin specific antibody (moAb, clone HAS-11, Sigma) revealed that this approach resulted in an strong expression of albumin in USSC. Moreover, this co-cultivation model is useful for the identification and characterization of factors who are responsible for the biological niche in vivo.

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Young, J. C., V. L. Dias, M. Holland, and K. L. Loveland. "262. Towards derivation of primordial germ cells from murine embryonic stem cells." Reproduction, Fertility and Development 17, no. 9 (2005): 106. http://dx.doi.org/10.1071/srb05abs262.

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The process of primordial germ cell (PGC) specification begins at the earliest stages of murine embryogenesis. The mechanisms underlying this process are the strong instructive cues generated by the extra-embryonic ectoderm, which, via ligand-receptor signalling in the visceral endoderm, activate pathways in the proximal epiblast to induce the PGC phenotype. We have subjected murine embryonic stem (ES) cells to similar cues in order to drive PGC lineage specification in vitro. ES cells were differentiated as aggregates (embryoid bodies (EBs)), a process that is thought to recapitulate the early stages of embryogenesis by providing an environment conducive to the spontaneous emergence of multiple cell lineages. To date, we have shown that EBs can also support the spontaneous emergence of cells expressing PGC markers. Expression analysis was performed on EBs from 1 to 30 days in culture. PGC markers, including nanog, dazl, fragilis, stella and SSEA1, are expressed in undifferentiated ES cells, but rapidly become undetectable in EBs as the constituent ES cells undergo differentiation. The spontaneous emergence of cells expressing these markers occurred only following long-term EB culture. This indicates a lag in the signalling normally required for PGC specification. In vivo, the lack of BMP4, its receptor (ALK-2) or downstream signalling molecules (Smad 1 and 5), results in the absence of PGCs in embryos. Therefore, in order to enhance PGC specification in our in vitro system, we have added BMP4 into the culture media. Under these conditions, the emergence of cells expressing PGC markers occurs at both an apparently higher efficiency and in a shorter time period. This suggests that BMP4 response pathways are present within the EB context and, when activated, can direct PGC specification. Thus, by recapitulating an in vivo physical and biochemical environment, we are able to direct PGC lineage specification in vitro.

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Fleming, Tom P., Adam J. Watkins, Congshan Sun, Miguel A. Velazquez, Neil R. Smyth, and Judith J. Eckert. "Do little embryos make big decisions? How maternal dietary protein restriction can permanently change an embryo’s potential, affecting adult health." Reproduction, Fertility and Development 27, no. 4 (2015): 684. http://dx.doi.org/10.1071/rd14455.

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Periconceptional environment may influence embryo development, ultimately affecting adult health. Here, we review the rodent model of maternal low-protein diet specifically during the preimplantation period (Emb-LPD) with normal nutrition during subsequent gestation and postnatally. This model, studied mainly in the mouse, leads to cardiovascular, metabolic and behavioural disease in adult offspring, with females more susceptible. We evaluate the sequence of events from diet administration that may lead to adult disease. Emb-LPD changes maternal serum and/or uterine fluid metabolite composition, notably with reduced insulin and branched-chain amino acids. This is sensed by blastocysts through reduced mammalian target of rapamycin complex 1 signalling. Embryos respond by permanently changing the pattern of development of their extra-embryonic lineages, trophectoderm and primitive endoderm, to enhance maternal nutrient retrieval during subsequent gestation. These compensatory changes include stimulation in proliferation, endocytosis and cellular motility, and epigenetic mechanisms underlying them are being identified. Collectively, these responses act to protect fetal growth and likely contribute to offspring competitive fitness. However, the resulting growth adversely affects long-term health because perinatal weight positively correlates with adult disease risk. We argue that periconception environmental responses reflect developmental plasticity and ‘decisions’ made by embryos to optimise their own development, but with lasting consequences.

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Dupont, Cathérine, Cheryl Maduro, Hannah Den Braanker, Ruben Boers, Dorota Kurek, and Joost Gribnau. "Characterization of Histone Modifications Associated with Inactive X-Chromosome in Trophoblast Stem Cells, eXtra-Embryonic Endoderm Cells and in In Vitro Derived Undifferentiated and Differentiated Epiblast Like Stem Cells." PLOS ONE 11, no. 12 (December 15, 2016): e0167154. http://dx.doi.org/10.1371/journal.pone.0167154.

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Journal articles on the topic 'Extra-embryonic endoderm'

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