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  • Biodiversitätsforschung  (256)
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  • 1
    Online-Ressource
    Online-Ressource
    Cellular transcripts encoded at a locus which permits retrovirus expression in mouse embryonic cells
    Elsevier BV ; 1991
    In:  Gene Vol. 101, No. 2 ( 1991-5), p. 177-183
    Details
    In: Gene, Elsevier BV, Vol. 101, No. 2 ( 1991-5), p. 177-183
    Materialart: Online-Ressource
    ISSN: 0378-1119
    URL: Article
    DOI: 10.1016/0378-1119(91)90409-5
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 1991
    ZDB Id: 1491012-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Mechanisms of gene regulation in human embryos and pluripotent stem cells
    The Company of Biologists ; 2017
    In:  Development Vol. 144, No. 24 ( 2017-12-15), p. 4496-4509
    Details
    In: Development, The Company of Biologists, Vol. 144, No. 24 ( 2017-12-15), p. 4496-4509
    Kurzfassung: Pluripotent stem cells have broad utility in biomedical research and their molecular regulation has thus garnered substantial interest. While the principles that establish and regulate pluripotency have been well defined in the mouse, it has been difficult to extrapolate these insights to the human system due to species-specific differences and the distinct developmental identities of mouse versus human embryonic stem cells. In this Review, we examine genome-wide approaches to elucidate the regulatory principles of pluripotency in human embryos and stem cells, and highlight where differences exist in the regulation of pluripotency in mice and humans. We review recent insights into the nature of human pluripotent cells in vivo, obtained by the deep sequencing of pre-implantation embryos. We also present an integrated overview of the principal layers of global gene regulation in human pluripotent stem cells. Finally, we discuss the transcriptional and epigenomic remodeling events associated with cell fate transitions into and out of human pluripotency.
    Materialart: Online-Ressource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.157404
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 2017
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Zfx mutation results in small animal size and reduced germ cell number in male and female mice
    The Company of Biologists ; 1997
    In:  Development Vol. 124, No. 11 ( 1997-06-01), p. 2275-2284
    Details
    In: Development, The Company of Biologists, Vol. 124, No. 11 ( 1997-06-01), p. 2275-2284
    Kurzfassung: The zinc-finger proteins ZFX and ZFY, encoded by genes on the mammalian X and Y chromosomes, have been spec-ulated to function in sex differentiation, spermatogenesis, and Turner syndrome. We derived Zfx mutant mice by targeted mutagenesis. Mutant mice (both males and females) were smaller, less viable, and had fewer germ cells than wild-type mice, features also found in human females with an XO karyotype (Turner syndrome). Mutant XY animals were fully masculinized, with testes and male genitalia, and were fertile, but sperm counts were reduced by one half. Homozygous mutant XX animals were fully feminized, with ovaries and female genitalia, but showed a shortage of oocytes resulting in diminished fertility and shortened reproductive lifespan, as in premature ovarian failure in humans. The number of primordial germ cells was reduced in both XX and XY mutant animals at embryonic day 11.5, prior to gonadal sex differentiation. Zfx mutant animals exhibited a growth deficit evident at embryonic day 12.5, which persisted throughout postnatal life and was not complemented by the Zfy genes. These phe-notypes provide the first direct evidence for a role ofZfx in growth and reproductive development.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.124.11.2275
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1997
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    An X-linked human collagen transgene escapes X inactivation in a subset of cells
    The Company of Biologists ; 1992
    In:  Development Vol. 116, No. 3 ( 1992-11-01), p. 687-695
    Details
    In: Development, The Company of Biologists, Vol. 116, No. 3 ( 1992-11-01), p. 687-695
    Kurzfassung: Transgenic mice carrying one complete copy of the human 1(I) collagen gene on the X chromosome (HucII mice) were used to study the effect of X inactivation on transgene expression. By chromosomal in situ hybridization, the transgene was mapped to the D/E region close to the Xce locus, which is the controlling element. Quantitative RNA analyses indicated that transgene expression in homozygous and heterozygous females was about 125% and 62%, respectively, of the level found in hemizygous males. Also, females with Searle’s translocation carrying the transgene on the inactive X chromosome (Xi) expressed about 18% transgene RNA when compared to hemizygous males. These results were consistent with the transgene being subject to but partially escaping from X inactivation. Two lines of evidence indicated that the transgene escaped X inactivation or was reactivated in a small subset of cells rather than being expressed at a lower level from the Xi in all cells, (i) None of nine single cell clones carrying the transgene on the Xi transcribed transgene RNA. In these clones the transgene was highly methylated in contrast to clones carrying the transgene on the Xa. (ii) In situ hybridization to RNA of cultured cells revealed that about 3% of uncloned cells with the transgene on the Xi expressed transgene RNA at a level comparable to that on the Xa. Our results indicate that the autosomal human collagen gene integrated on the mouse X chromosome is susceptible to X inactivation. Inactivation is, however, not complete as a subset of cells carrying the transgene on Xi expresses the transgene at a level comparable to that when carried on Xa.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.116.3.687
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1992
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 5
    Online-Ressource
    Online-Ressource
    p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF
    The Company of Biologists ; 1994
    In:  Development Vol. 120, No. 4 ( 1994-04-01), p. 1027-1033
    Details
    In: Development, The Company of Biologists, Vol. 120, No. 4 ( 1994-04-01), p. 1027-1033
    Kurzfassung: To understand the role of low-affinity neurotrophin receptor p75 in neural development, we previously generated mice carrying a null mutation in the p75 locus (Lee, K. F., Li, E., Huber, L. J., Landis, S. C., Sharpe, A. H., Chao, M. V. and Jaenisch, R. (1992) Cell 69, 737 –749). To elucidate the mechanisms leading to deficits in the peripheral nervous system in p75 mutant mice, we have employed dissociated cultures to examine the responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. We found that p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 (E15) and postnatal day 3 (P3), respectively, ages that coincide with the peak of naturally occurring cell death. Furthermore, while p75-deficient E15 DRG neurons did not change their response specificity to BDNF, NT-3, and NT-4/5, P3 SCG neurons became more responsive to NT-3 at higher concentrations (nanomolar ranges). These results may help explain the deficits in the peripheral nervous system in p75 mutant mice and provide evidence that p75 can modulate neurotrophin sensitivity in some neurons.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.120.4.1027
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1994
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 6
    Online-Ressource
    Online-Ressource
    De novo DNA cytosine methyltransferase activities in mouse embryonic stem cells
    The Company of Biologists ; 1996
    In:  Development Vol. 122, No. 10 ( 1996-10-01), p. 3195-3205
    Details
    In: Development, The Company of Biologists, Vol. 122, No. 10 ( 1996-10-01), p. 3195-3205
    Kurzfassung: It has been a controversial issue as to how many DNA cytosine methyltransferase mammalian cells have and whether de novo methylation and maintenance methylation activities are encoded by a single gene or two different genes. To address these questions, we have generated a null mutation of the only known mammalian DNA methyl-transferase gene through homologous recombination in mouse embryonic stem cells and found that the development of the homozygous embryos is arrested prior to the 8-somite stage. Surprisingly, the null mutant embryonic stem cells are viable and contain low but stable levels of methyl cytosine and methyltransferase activity, suggesting the existence of a second DNA methyltransferase in mammalian cells. Further studies indicate that de novo methylation activity is not impaired by the mutation as integrated provirus DNA in MoMuLV-infected homozygous embryonic stem cells become methylated at a similar rate as in wild-type cells. Differentiation of mutant cells results in further reduction of methyl cytosine levels, consistent with the de novo methylation activity being down regulated in differentiated cells. These results provide the first evidence that an independently encoded DNA methyl-transferase is present in mammalian cells which is capable of de novo methylating cellular and viral DNA in vivo.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.122.10.3195
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1996
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 7
    Online-Ressource
    Online-Ressource
    Incomplete reactivation of Oct4 -related genes in mouse embryos cloned from somatic nuclei
    The Company of Biologists ; 2003
    In:  Development Vol. 130, No. 8 ( 2003-04-15), p. 1673-1680
    Details
    In: Development, The Company of Biologists, Vol. 130, No. 8 ( 2003-04-15), p. 1673-1680
    Kurzfassung: The majority of cloned animals derived by nuclear transfer from somatic cell nuclei develop to the blastocyst stage but die after implantation. Mouse embryos that lack an Oct4 gene, which plays an essential role in control of developmental pluripotency, develop to the blastocyst stage and also die after implantation, because they lack pluripotent embryonic cells. Based on this similarity, we posited that cloned embryos derived from differentiated cell nuclei fail to establish a population of truly pluripotent embryonic cells because of faulty reactivation of key embryonic genes such asOct4. To explore this hypothesis, we used an in silico approach to identify a set of Oct4-related genes whose developmental expression pattern is similar to that of Oct4. When expression of Oct4and 10 Oct4-related genes was analyzed in individual cumulus cell-derived cloned blastocysts, only 62% correctly expressed all tested genes. In contrast to this incomplete reactivation of Oct4-related genes in somatic clones, ES cell-derived cloned blastocysts and normal control embryos expressed these genes normally. Notably, the contrast between expression patterns of the Oct4-related genes correlated with efficiency of embryonic development of somatic and ES cell-derived cloned blastocysts to term. These observations suggest that failure to reactivate the full spectrum of these Oct4-related genes may contribute to embryonic lethality in somatic-cell clones.
    Materialart: Online-Ressource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.00366
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 2003
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 8
    Online-Ressource
    Online-Ressource
    Meiotic sex chromosome inactivation in male mice with targeted disruptions of Xist
    The Company of Biologists ; 2002
    In:  Journal of Cell Science Vol. 115, No. 21 ( 2002-11-01), p. 4097-4105
    Details
    In: Journal of Cell Science, The Company of Biologists, Vol. 115, No. 21 ( 2002-11-01), p. 4097-4105
    Kurzfassung: X chromosome inactivation occurs twice during the life cycle of placental mammals. In normal females, one X chromosome in each cell is inactivated early in embryogenesis, while in the male, the X chromosome is inactivated together with the Y chromosome in spermatogenic cells shortly before or during early meiotic prophase. Inactivation of one X chromosome in somatic cells of females serves to equalise X-linked gene dosage between males and females, but the role of male meiotic sex chromosome inactivation (MSCI) is unknown. The inactive X-chromosome of somatic cells and male meiotic cells share similar properties such as late replication and enrichment for histone macroH2A1.2,suggesting a common mechanism of inactivation. This possibility is supported by the fact that Xist RNA that mediates somatic X-inactivation is expressed in the testis of male mice and humans. In the present study we show that both Xist RNA and Tsix RNA, an antisense RNA that controls Xist function in the soma, are expressed in the testis in a germ-cell-dependent manner. However, our finding that MSCI and sex-body formation are unaltered in mice with targeted mutations of Xist that prevent somatic X inactivation suggests that somatic X-inactivation and MSCI occur by fundamentally different mechanisms.
    Materialart: Online-Ressource
    ISSN: 1477-9137 , 0021-9533
    URL: Article
    DOI: 10.1242/jcs.00111
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 2002
    ZDB Id: 219171-4
    ZDB Id: 1483099-1
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 9
    Online-Ressource
    Online-Ressource
    Alpha 3 beta 1 integrin has a crucial role in kidney and lung organogenesis
    The Company of Biologists ; 1996
    In:  Development Vol. 122, No. 11 ( 1996-11-01), p. 3537-3547
    Details
    In: Development, The Company of Biologists, Vol. 122, No. 11 ( 1996-11-01), p. 3537-3547
    Kurzfassung: A mutation was targeted to the murine α3 integrin gene. Homozygous mutant mice survived to birth, but died during the neonatal period. The mutation caused abnormal kidney and lung development. Mutant kidneys displayed decreased branching of the medullary collecting ducts, although the number of nephrons was not altered. Proximal tubules exhibited two distinct subsets of abnormalities, with the epithelial cells either containing excess lysosomes or becoming microcystic. In addition, glomerular development was markedly affected. In mutant kidneys, the extent of branching of glomerular capillary loops was decreased, with capillary lumina being wider than normal. The glomerular basement membrane was disorganized and glomerular podocytes were unable to form mature foot processes. Branching of the bronchi in lungs of mutant mice was also decreased and the large bronchi extended to the periphery. These results indicate a role for integrin receptors in basement membrane organization and branching morphogenesis.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.122.11.3537
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1996
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 10
    Online-Ressource
    Online-Ressource
    Phenotypic rescue of mutant brown melanocytes by a retrovirus carrying a wild-type tyrosinase-related protein gene
    The Company of Biologists ; 1990
    In:  Development Vol. 110, No. 2 ( 1990-10-01), p. 471-475
    Details
    In: Development, The Company of Biologists, Vol. 110, No. 2 ( 1990-10-01), p. 471-475
    Kurzfassung: A mouse cDNA for the developmentally controlled, melanocyte-specific protein, tyrosinase-related protein 1 (TRP-1), was previously cloned and reported to show genetic linkage with the coat-colour locus brown (b) on mouse chromosome 4. The cDNA has been inserted into a retroviral vector derived from Moloney murine leukaemia virus, under the control of the human histone H4 promoter. This vector was used to infect melanocytes of the immortal line melan-b, which are homozygous for the b mutation and which display light brown pigmentation in culture. Infected cultures containing between 0.2 and 2 copies of provirus per cell displayed an altered phenotype: 20-50 % of cells now had the black to dark brown colour characteristic of cultured wild-type (Black, B/B) mouse melanocytes. Thus the TRP-1 gene complements the brown mutation. We conclude that TRP-1 is the product of the wild-type-b-locus.
    Materialart: Online-Ressource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.110.2.471
    Sprache: Englisch
    Verlag: The Company of Biologists
    Publikationsdatum: 1990
    ZDB Id: 2007916-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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