Aydan Bulut-Karslıoğlu

The paper identifies mTOR's role in regulating developmental gene promoters in pluripotent mouse embryonic stem cells through interaction with PRC1 and RNA Polymerase II pausing.

This paper develops a hypoxia-mediated mouse embryo model to study neural patterning and shows hypoxia enhances anterior neural cell identity through HIF1a and TGFβ modulation.

The paper identifies early metabolic imbalances as drivers of phenotypic variation in stembryos and shows how metabolic interventions can correct aberrant morphology and lineage bias.

The paper shows that microRNA activity is essential for early mouse embryos to transition into diapause, with miRNAs regulating gene expression and linking mTOR activity to miRNA biogenesis.

This study shows that human blastoids and pluripotent stem cells can enter a dormant state via mTOR inhibition, with distinct temporal dynamics compared to mice.

The paper shows hypoxia induces an early primitive streak signature in ES cells, enhancing gastruloid elongation and lineage representation through Hif1-mediated transcriptional changes.

The paper identifies lipid metabolism as a key factor in developmental pausing, showing that enhancing fatty acid oxidation extends embryo survival during mTOR inhibition.

This study identifies Chd1's role in repairing DNA breaks in embryonic stem cells, showing its importance in maintaining hypertranscription during development.

The paper shows that translation directly regulates chromatin state and transcription in ES cells, with reduced translation causing rapid chromatin changes.