RT @guberrocal: Our article is out in its final form. D. melanogaster even-skipped enhancers control transcription….

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RT @MSKCancerCenter: 🚨New in @Nature from the Tuomas Tammela Lab: how aging suppresses tumorigenesis and stemness in the lung by promoting….

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RT @aachinger: Please RT! 🧬🧬.I am looking for a #postdoc fellow to lead a new project in 3D chromatin organisation and transcriptional regu….

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Finally, thanks for reading and thanks also to our reviewers for their constructive comments! ⏰ @VictorChangInst @UNSWBABS.

6/ Interestingly, we also find similar patterns in cancer cell evolution, where late RT enhancers tend to be more recently evolved with increased mutations. This suggests to us that this connection is likely a time-invariant feature of genome evolution.

5/ We find new human enhancers are generally under weak selection and enriched for eQTLs.Enhancers also have more tissue-specific functions at DNA late replicating regions. Notably, many developmental TFs bind AT-rich motifs which are enriched at late RT regions in mammals.

4/ Late replicating domains, often linked to heterochromatin, show higher mutation rates, providing a fertile ground for new enhancer formation. Using a sequence model, we test whether these mutations could disrupt TF binding and cause enhancer turnover.