On 2014 Aug 05, Andrew Sharp commented:

A recent paper (PMID: 25079557) that performed DNA methylation analysis of developing embryos made some interesting observations that are potentially relevant to our findings in this paper. A quote from this paper: "...we found that SINEs and LINEs with different evolutionary ages showdifferent demethylation patterns (Fig. 4a–d and Extended Data Fig. 10d–f). For example, both LINE-1 (L1) and LINE-2 (L2) belong to the LINE family of transposable elements, with L1 being evolutionarily younger than L2 (ref. 25).The younger L1 shows a higher methylation level than L2 in oocytes, whereas they show a comparable level of methylation in sperm. More importantly, we found that during the genome-wide demethylation process, the evolutionarily younger L1 retains higher levels of residual methylation than L2. L1 was also remethylated to a higher methylation level after implantation (Fig. 4d)."

I think it is an interesting idea that this differential demethylation/remethylation might potentially explain the association of younger LINEs with the spread of X inactivation?

On 2014 Aug 05, Andrew Sharp commented:

A recent paper (PMID: 25079557) that performed DNA methylation analysis of developing embryos made some interesting observations that are potentially relevant to our findings in this paper. A quote from this paper: "...we found that SINEs and LINEs with different evolutionary ages showdifferent demethylation patterns (Fig. 4a–d and Extended Data Fig. 10d–f). For example, both LINE-1 (L1) and LINE-2 (L2) belong to the LINE family of transposable elements, with L1 being evolutionarily younger than L2 (ref. 25).The younger L1 shows a higher methylation level than L2 in oocytes, whereas they show a comparable level of methylation in sperm. More importantly, we found that during the genome-wide demethylation process, the evolutionarily younger L1 retains higher levels of residual methylation than L2. L1 was also remethylated to a higher methylation level after implantation (Fig. 4d)."

I think it is an interesting idea that this differential demethylation/remethylation might potentially explain the association of younger LINEs with the spread of X inactivation?