Compromized Fertility Disrupts Peg1 but Not Snrpn and Peg3 Imprinted Methylation Acquisition in Mouse Oocytes.
Bibliographic record
Abstract
Genomic imprinting is a dynamic process that tightly regulates monoallelic gene expression based on parental origin. DNA methylation, an epigenetic modification that represses expression, is differentially acquired at imprinted loci during gametogenesis. This differential methylation is maintained in the subsequent embryo. In females, DNA methylation has been shown to arise during oogenesis in correlation with oocyte diameter. Here, we are the first to show the progression of this acquisition at the individual oocyte level. Given its plasticity, genomic imprinting is susceptible to disruption by environmental factors. This includes assisted reproductive technologies, although subfertility/infertility may also contribute to this epigenetic instability. During imprint acquisition, oocytes and their surrounding follicular cells communicate via hormonal and junctional mechanisms. In this study, we used two genetic models, estrogen receptor beta 1 subunit (Esr2) and connexin 37 (Gja4), that perturb these pathways to examine their effects on DNA methylation acquisition in individual oocytes. Three genes, Snrpn, Peg3 and Peg1, were chosen for this analysis based on their differential rates of imprinted methylation acquisition during oogenesis. We observed normal imprinted acquisition in both the Esr2 and Gja4 mutant oocytes at Snrpn and Peg3, as well as at Peg1 in Esr2 mutant oocytes. By comparison, Gja4-null oocytes exhibited aberrant imprinted acquisition at the Peg1 locus. This is significant as Peg1 acquires its imprinted methylation later in oogenesis than the other two genes. We propose that loss of oocyte-to-granulosa cell communication results in developmentally compromised oocytes that lead to loss or delayed imprint acquisition in late acquiring genes. Additional studies will be required to fully understand genomic imprinting regulation in gametes and embryos, as well as the impact of subfertility/infertility on children conceived via assisted reproduction.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".