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Bender R, Fundele R, Surani MA, et al. Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Rouxs Arch Dev Biol. 1995;204(7):436-443doi: 10.1007/BF00360851.
Bender, R., Fundele, R., Surani, M. A., Li, L. L., Kothary, R., Fürst, D. O., & Christ, B. (1995). Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Roux's archives of developmental biology : the official organ of the EDBO, 204(7), 436-443. https://doi.org/10.1007/BF00360851
Bender, R, et al. "Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras." Roux's archives of developmental biology : the official organ of the EDBO vol. 204,7 (1995): 436-443. doi: https://doi.org/10.1007/BF00360851
Bender R, Fundele R, Surani MA, Li LL, Kothary R, Fürst DO, Christ B. Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Rouxs Arch Dev Biol. 1995 Aug;204(7):436-443. doi: 10.1007/BF00360851. PMID: 28305863.
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Rouxs Arch Dev Biol. 1995 Aug;204(7):436-443. doi: 10.1007/BF00360851.

Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras.

Roux's archives of developmental biology : the official organ of the EDBO

R Bender, R Fundele, M A Surani, L-L Li, R Kothary, D O Fürst, B Christ

Affiliations

  1. Institut für Biologie III der Universität Freiburg, Schänzlestrasse 1, D-79104, Freiburg, Germany.
  2. Wellcome/CRC Institute of Cancer and Developmental Biology, Tennis Court Road, CB2 1QR, Cambridge.
  3. Physiological Laboratory, University of Cambridge, UK.
  4. Institut du Cancer de Montréal, 1560 rue Sherbrooke est, H2L 4MI, Montréal, Québec, Canada.
  5. Max-Planck-Institut für Biophysikalische Chemie, Am Fassberg, D-37077, Göttingen, Germany.
  6. Institut für Anatomie der Universität Freiburg, Albertstraße 17, D-79104, Freiburg, Germany.

PMID: 28305863 DOI: 10.1007/BF00360851

Abstract

Parthenogenetic cells are lost from fetal chimeras. This may be due to decreased proliferative potential. To address this question, we have made use of combined cell lineage and cell proliferation analysis. Thus, the incorporation of bromodeoxyuridine in S-phase was determined for both parthenogenetic and normal cells in several tissues of fetal day 13 and 17 chimeras. A pronounced reduction of bromodesoxyuridine incorporation by parthenogenetic cells at both developmental stages was only observed in cartilage. In brain, skeletal muscle, heart and intestinal epithelium, this reduction was either less pronounced or observed only at one of the developmental stages analysed. No difference between parthenogenetic and normal cells was observed in epidermis and ganglia. Our results show that a loss of proliferative potential of parthenogenetic cells during fetal development contributes to their rapid elimination in some tissues. The analysis of the fate of parthenogenetic cells in skeletal muscle and cartilage development demonstrated different selection mechanisms in these tissues. In skeletal muscle, parthenogenetic cells were largely excluded from the myogenic lineage proper by early post-midgestation. In primary hyaline cartilage, parthenogenetic cells persisted into adulthood but were lost from cartilages that undergo ossification during late fetal development.

Keywords: Differentiation; Mouse chimeras; Parthenogenesis; Proliferation

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