Some of the top-ranked differentially methylated sites in the two groups were shared, but disorder-specific alterations were also observed with DNA methylation changes in opposite directions.
Notably, some escapees were methylated in either sperm (cluster 4) or oocytes (cluster 2) and demonstrated partial methylation in gametes of the opposite gender.
Remarkably, we found that not only do the aging rates differ in these two groups by 2.6 5.1 fold but their methylation also changes over time in opposite directions.
These data suggest that there could be some common mechanism regulating DNA methylation of these two genes in opposite directions in the context of loss of function of KDM5C and gain of function of IDH1.
Our study suggests that the main methylation abnormalities at the GPC3 promoter level seems to be losses of methylation in NBs and the opposite in WTs.
For N33, MGMT, and MLH1, some associations were noted, although these were in opposite directions (increased methylation with higher red blood cell folate for N33 and decreased methylation with higher serum and colonic folate for MGMT).
As expected, GRB10, SGCE/PEG10, and MEST/MESTIT1 showed a clear parent-of-origin methylation pattern, with the methylation level of matUPD7s and patUPD7 deviating in opposite directions from the controls (Fig. 5).
Notably, methylation regulators DNMT3a and TET1 change in opposite directions.
Interestingly, the correlations between 2-h post-OGTT glucose levels and leptin DNA methylation showed opposite trends in fetal and maternal sides suggesting that both placental sides are differently affected by the mother's IGT.
