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The maintenance of imprinted genes through the preimplantation period is essential for normal embryonic development (Surani 2001; Wu Q et al. 2004).
These proteins, like Kaiso, bind methylated DNA but can also bind a non-methylated consensus., Very recently, another zinc finger protein, ZFP57, was also shown to bind methylated DNA and to act in DNA methylation-dependent maintenance of imprinted genes.
These data point to a direct role for secondary DMRs in the regulation of imprinted gene expression, although the observation that secondary DMRs acquire differential methylation after the onset of imprinted expression has led to the hypothesis that secondary DMRs play a role in the maintenance of imprinted expression rather than its establishment [ 6- 8].
Oocyte-derived Kap1 is essential for the maintenance of imprinted DMR methylation in the single-cell embryo before it is provided at zygotic genome activation (Messerschmidt et al., 2012).
A recent study reported that RNAi knockdown of Kcnq1ot1 in embryonic (ES), trophoblast (TS) and extra-embryonic endoderm (XEN) stem cells had no effect on the maintenance of imprinted expression raising the possibility that the ncRNA product plays no role in silencing [ 26].
How the mouse paternal X retains the inactive mark is still unclear, but knockout experiments have identified genes that are essential for maintenance of imprinted XCI in the mouse placenta, namely Eed and Tsix (Kalantry and Magnuson 2006; Kalantry et al. 2006; Lee et al. 1999; Luikenhuis et al. 2001; Wang et al. 2001).
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The effect of ovulation induction on maintenance of imprinting can be expressed at three levels.
Interestingly, ORMES-5 was the only cell line that showed normal maintenance of imprinting and maternal expression of H19.
Most experiments address the effects of ovulation induction and preimplantation embryo culture on maintenance of imprinting up to mid-gestation.
(i) That on maintenance of imprinting at recruitment of an antral follicle, (ii) that expressed as a maternal early embryonic ('zygotic') cellular effect on maintenance of the imprint after gamete fusion and (iii) that expressed via the maternal tractus.
In contrast to the maintenance of imprinting observed in the 1.2 Mb duplication, we found that the 160 kb duplication was associated with lack of ICR2 imprinted methylation.
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