Table 1.
Summary of the functional annotation of 565 parenting-associated genes performed using the DAVID annotation tool.
| Function | GO term | Genes Count | Genes % | p-value | Fold Enrichment | FDR-adjusted p-value* |
|---|---|---|---|---|---|---|
| GTPase regulator activity | GO:0030695∼GTPase regulator activity | 26 | 6.30 | 3.68E-06 | 2.89 | .0018 |
| GO:0060589∼nucleoside-triphosphatase regulator activity | 26 | 6.30 | 5.44E-06 | 2.82 | .0014 | |
| GO:0005083∼small GTPase regulator activity | 16 | 3.87 | 0.001195 | 2.62 | .0488 | |
| ATP binding | GO:0032559∼adenyl ribonucleotide binding | 57 | 13.80 | 5.44E-05 | 1.71 | .0091 |
| GO:0005524∼ATP binding | 55 | 13.32 | 1.39E-04 | 1.67 | .0139 | |
| GO:0030554∼adenyl nucleotide binding | 58 | 14.04 | 1.19E-04 | 1.65 | .0148 | |
| GO:0001883∼purine nucleoside binding | 58 | 14.04 | 1.78E-04 | 1.62 | .0148 | |
| GO:0001882∼nucleoside binding | 58 | 14.04 | 2.13E-04 | 1.62 | .0152 | |
| Metal ion binding | GO:0046872∼metal ion binding | 119 | 28.81 | 6.38E-04 | 1.29 | .0392 |
| GO:0043169∼cation binding | 119 | 28.81 | 9.40E-04 | 1.28 | .0461 | |
| GO:0005509∼calcium ion binding | 36 | 8.72 | 0.001177 | 1.76 | .0503 | |
| Associated with the long qt syndrome** | 5 | 1.21 | 5.74E-05 | 21.48 | .0066 | |
Notes.
The FDR-adjusted p-values (≤ .05) were used as inclusion criteria to trim the overrepresented term lists. Fold enrichment of each gene group is estimated in comparison to the base set of genes in the DAVID databases (19,235 genes).
The long QT syndrome—a rare inherited heart condition related to the violation of ventricular fibrillation. The enrichment in this functional group of genes (5 of 12 known associates including two candidate genes, KCNQ1 and KCNH2) is considered an unexpected finding. We cannot speculate about the causal association between these genes and parenting. Most likely, the association was obtained because of the presence of the disease in the study cohort, known to be a population with a high risk and frequency of cardio-vascular disorders (an assumption we could not confirm due to a lack of medical records), and a possible causal relation between the syndrome and abnormal methylation of the candidate genes. This might be an issue for future investigation of the candidate-genes for the disorder.