Sentence examples for rat germ cell from inspiring English sources

DBP-induced rat germ cell aggregation was evident at E21.5 but largely resolved by PND4, findings we confirmed quantitatively.

Here, we have investigated the spatiotemporal relationship between 5mC, 5hmC, 5fC and 5caC specifically during late (e14.5 e21.5) male fetal rat germ cell development by immunofluorescence using previously validated antibodies [ 13, 14, 41- 44].

We have investigated expression of GPER in mouse and rat germ cells at differential maturative stages.

The re-establishment of 5mC in male rat germ cells appears to begin at e19.5.

In accord, long-term apoptotic cell death process has been reported in adult rat germ cells exposed in utero to flutamide and vinclozolin [ 37, 38].

Thus, the stable presence of 5hmC, 5fC and 5caC in rat germ cells between e14.5 and e16.5, and in testicular somatic cells throughout late gestation, may indicate potential functionality of these modifications during germ cell development.

There was no/little detectable 5mC in germ cells between e14.5 and e18.5, suggesting that, as in mice, rat germ cells are hypomethylated relative to surrounding somatic cells by e14.5.

Our study, showing the stable persistence of 5hmC in fetal rat germ cells until e16.5, suggests that the removal of 5mC through conversion to 5hmC might also occur in the rat.

A few days later (e19.5), no rat germ cells expressed OCT4, but all continued to express VASA (Fig.  5); the loss of OCT4 immunoexpression appeared to be synchronous in all germ cells in every cord over this relatively narrow time period.

We did not observe enrichment of 5hmC in rat germ cells relative to the surrounding somatic cells between e14.5 and e16.5, and this may indicate that this occurs before e14.5 in the rat and that 5hmC levels have already begun to decline by this time, as in the mouse [ 13, 42].

Our demonstration of the absence of 5hmC, 5fC and 5caC in rat germ cells during the re-establishment of DNA methylation between e19.5 and e21.5 further supports the hypothesis that these variants form part of the initial demethylation pathway in the male germline [ 29].