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

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.

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

“…39 In contrast, PG-and GG-derived cells, both in aggregation and ICM injection chimeras, appear to be sequentially eliminated from many tissues throughout gestation but are frequently found at substantial levels in the brain of later gestation and term animals. 39,45,83 In the brains of E13 and, more predominantly, E17 chimeras, AG cells contributed substantially to hypothalamus, septum and preoptic area, but less than PG or control N cells to cortex and striatum, whereas PG cells accumulated in the latter and were mostly excluded from The grey bar indicates methylation patterns expected for each parental allele based on analysis of methylation in gametes. 101 the hypothalamus.…”

Brief Report: Parthenogenetic Embryonic Stem Cells are an Effective Cell Source for Therapeutic Liver Repopulation

“…Unlike other vertebrates , mammals are not capable of parthenogenetic (PG) reproduction. Mammalian PG embryos undergo early developmental demise due to imbalanced expression of imprinted genes , and exhibit cell proliferation defects and restricted contribution to mesodermal and endodermal tissues when combined with normal embryos as chimeras . However, in both mouse and human, PG embryonic stem cells (ESCs) can be readily derived from blastocysts developing after in vitro activation of unfertilized oocytes; these cells exhibit key characteristics of pluripotent stem cells, including multilineage in vitro differentiation potential .…”