Aditya Sethi

@adityasethi.bsky.social

(he/him) Postdoc at the Genome Replication Lab at Institute of Cancer Research London https://costerlab.com/ | 🏳️‍🌈

DNA replication globally disrupts the epigenome. But does this create a chromatin-access opportunity for TF binding to facilitate cell identity change? Now 𝐫𝐞𝐩𝐥𝐢-𝐀𝐓𝐀𝐂-𝐬𝐞𝐪 shows 𝘥𝘦 𝘯𝘰𝘷𝘰 chromatin opening & TF binding occurs specifically post-replication, in cellular differentiation & reprogramming!

Post-replicative chromatin accessibility predicts cell fate change

Knudsen and colleagues use repli-ATAC-seq to compare replicated and unreplicated chromatin in two models of cell identity change. They find that lineage-specific elements are accessible earlier in rep...

cell.com

Excited to share our review where we propose models for how DNA secondary structures destabilise the replication fork and lead to ssDNA gaps — it’s comprehensive but genuinely a thought-provoking piece. Hope it’s useful to the community. @costerlab.bsky.social www.sciencedirect.com/science/arti...

How DNA secondary structures drive replication fork instability

DNA secondary structures, such as hairpins, cruciforms, triplexes, G-quadruplexes and iMotifs, are common, dynamic features that replication forks rou…

sciencedirect.com

Our review is out! A lot of hard work but completely worth it, especially with the best colleagues (and friends)! Hope you enjoy reading it

María Fernández-Casañas@emefece.bsky.social · 9mo ago

Our @costerlab.bsky.social review is out! It’s a great read on the impact of DNA secondary structures on eukaryotic replication fork progression - a totally unbiased opinion, of course! www.sciencedirect.com/science/arti... @adityasethi.bsky.social @billiedelpino.bsky.social

𝐇𝐨𝐰 𝐝𝐨 𝐜𝐞𝐥𝐥𝐬 𝐫𝐞𝐦𝐞𝐦𝐛𝐞𝐫 𝐰𝐡𝐨 𝐭𝐡𝐞𝐲 𝐚𝐫𝐞 𝐚𝐟𝐭𝐞𝐫 𝐃𝐍𝐀 𝐫𝐞𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧? Our new study “Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability” is out in 𝘚𝘤𝘪𝘦𝘯𝘤𝘦 𝘈𝘥𝘷𝘢𝘯𝘤𝘦𝘴. Led by @lleonie.bsky.social @biranalva.bsky.social 🧵 More below👇

Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability

Losing parental histones during DNA replication fork passage challenges differentiation competence and cell viability.

tinyurl.com

The 90/10 rule of scientific discovery: 90% of your results come from 10% of your explorations, but it's not possible to know in advance what specific explorations those will be.

Exciting news!🌟 Together with Alexander van Oudenaarden, @jervdberg.bsky.social and @lleonie.bsky.social, we’ve been awarded a €2M NNF Synergy grant. We're thrilled to collaborate🤝 and to develop cutting-edge single-cell and single-molecule methods for replication and chromatin research! 🚀

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Hubrecht Institute@hubrechtinstitute.bsky.social · 2y ago

How reliably is the epigenome passed from one cell to its daughter cells? Alexander van Oudenaarden @jervdberg.bsky.social @grothlab.bsky.social @lleonie.bsky.social received @novo-nordisk.bsky.social grant to study this question ➡️new strategies to prevent disease & combat aging tinyurl.com/yh925b9u

Check out our recent work uncovering an unexpected role of the replicative helicase CMG in influencing cell fate decisions in vivo! We also show that it promotes differential expression of the highly conserved cell death gene egl-1 in cells fated to die!

UCL Research Department of Cell & Developmental Biology@ucl-cdb.bsky.social · 2y ago

Our researchers, in a paper just published in Nature Comms, offer new insights into how different #cell types are generated during animal development, which in future could help to solve some #autoimmunity, #cancer and #developmental abnormalities. doi.org/10.1038/s414... @uclofficial.bsky.social

Diagrammatic illustration of the description in the paper's text, showing that, using the nematode C. elegans as a model, the authors focused on asymmetrically dividing mother cells, where one daughter cell dies (‘cell death’ fate) while the other daughter cell survives (‘cell survival’ fate). This presented them with an excellent paradigm to explore how cell fate decisions (death v survival) are made during asymmetric cell division.
 
They found that, when they reduced the function of CMG, the dying daughter cells wrongly acquired the fates of their sister cells and instead survived