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First, the parental imprints which must be erased and reset during gametogenesis, reflecting the sex of the individual, and must be maintained in somatic cells after fertilization [13] have been examined only in derived embryonic germ cells [8].
Functional characteristics and gene expression patterns are then faithfully maintained in somatic cell lineages over a lifetime.
Most imprinted domains are associated with differentially DNA methylated regions (DMRs) that originate in the gametes, and are maintained in somatic tissues after fertilization.
To date, all known human imprinted DMRs are stably maintained in somatic tissues, irrespective of gene expression levels, by the DNA methyltransferase activity of DNMT1 during semi-conservative DNA replication.
This induced hypermethylation is maintained in somatic cells of carriers across several generations in a t(8 20) dependent-manner however, is erased in the germ cells of the translocation carriers.
Most imprinted genes are associated with a region of differential DNA methylation that is acquired in the gametes, and maintained in somatic tissues after fertilization by the UHRF1-DNMT1 complex [ 2- 4].
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Their methylation status is thought to be maintained in all somatic lineages once acquired.
In Drosophila melanogaster, female germline stem cells (GSCs) are maintained in a somatic niche of the gonads by BMP signalling.
Thus, there is compelling evidence that sexual dimorphism in gene expression is maintained in this somatic tissue.
The normal imprinting marks are inherited from the parental gametes and are then maintained in the somatic cells of an individual.
We also observed that the methylation levels of most DMRs are maintained in adult somatic tissues and confirmed that germ-line DMRs are particularly stable with no tissue specific gain or loss of methylation.
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