The Lewis Lab
@peterlewislab.bsky.social
930 followers 710 following 69 posts
Chromatin biochemistry and genomics in development and cancer. UW-Madison School of Medicine and Public Health TheLewisLab.net
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peterlewislab.bsky.social
We are excited to share our new preprint demonstrating that nucleic acid interactions with SUZ12 constrain PRC2 activity, establishing a kinetic buffer essential for targeted gene silencing and revealing vulnerabilities in diffuse midline gliomas.
www.biorxiv.org/content/10.1...
Reposted by The Lewis Lab
vaclav-veverka.bsky.social
How do flexible regions of histone chaperones team up to handle histones? Together with Fred Winston’s lab
@harvardmed.bsky.social, we reveal new insights in our study just out in Mol Cell. Hats off to James Warner and Vanda Lux @iocbprague.bsky.social for their key contributions! dlvr.it/TNB145
Reposted by The Lewis Lab
hopfnerlab.bsky.social
Thrilled that our work is now finally out in Nature Comms!
rdcu.be/eG3vP

We reveal cryo-EM structures of the MRN complex bound to DNA & TRF2 - showing how DNA breaks are sensed and regulated at telomeres.
Fantastic work by first authors @yilanfan.bsky.social @filizkuybu.bsky.social & Hengjun!
Reposted by The Lewis Lab
cp-trendsgenetics.bsky.social
"Unmasked: transposable elements as drivers and targets in cancer"
by Ting Wang & colleagues

"This review synthesizes a growing body of work that positions TEs as both catalysts and antagonists of the tumor state."

Check it out!
authors.elsevier.com/sd/article/S...
Figure I. Origins of transposable element (TE)-encoded and TE-derived proteins in cancer.
Reposted by The Lewis Lab
epijenatics.bsky.social
Excited to share my postdoc work, out on bioRxiv today! Histones package DNA into nucleosomes to form the building blocks of chromatin, but how modular and programmable is this system? 1/9
Reposted by The Lewis Lab
kranzuschlab.bsky.social
How can we understand the earliest events in evolution of eukaryotic immunity? @yao-li.bsky.social reports incredible molecular fossils of complete bacterial-like operons in eukaryotes that illuminate how animal immunity was first acquired from anti-phage defense

www.biorxiv.org/content/10.1...
Reposted by The Lewis Lab
Reposted by The Lewis Lab
conwayer1.bsky.social
Delighted that our work on EZH2 dominant negativity in Weaver syndrome is now out in Genes & Development!

This exciting work on chromatinopathies 🧬 was in collab with @adrianbracken.bsky.social and spearheaded by Orla Deevy.

@ucddublin.bsky.social @ucd-sbbs.bsky.social

www.ucd.ie/newsandopini...
UCD co-lead breakthrough discovering genetic mechanism driving Weaver syndrome
www.ucd.ie
Reposted by The Lewis Lab
ambystoma22.bsky.social
New paper on the role of H3K4me3 at enhancers! We (led by Haoming Yu) used dCas9 epigenome editing to add H3K4me3 to intergenic enhancers. This was (1) sufficient to turn up transcription at open, active regions and (2) has no effect on target gene transcription. genesdev.cshlp.org/content/earl...
H3K4me3 amplifies transcription at intergenic active regulatory elements
A biweekly scientific journal publishing high-quality research in molecular biology and genetics, cancer biology, biochemistry, and related fields
genesdev.cshlp.org
Reposted by The Lewis Lab
amazouzi.bsky.social
I am thrilled to share with you my first co-corresponding author Nature paper with Jos Jonkers. This project was led by the extraordinary @sarahmoser.bsky.social . Congratulations, and thank you to all the authors, @nkinl.bsky.social , and @oncodeinstitute.bsky.social for their support.
Reposted by The Lewis Lab
tingwu-lab.bsky.social
What better way to launch our new account with the publication of @jmstein.bsky.social latest paper from the lab! 🧪 Check out the 🧵 below to learn more about tkPAINT and how we use it to image proteins, DNA, and RNA in the nucleus using DNA-PAINT.
jmstein.bsky.social
(1/n) DNA-PAINT imaging inside the nucleus at single antibody resolution using TIRF? Ultrathin sectioning makes it happen!

Grateful to share my postdoctoral work introducing “tomographic & kinetically-enhanced DNA-PAINT” or in brief: tkPAINT. Out in @pnas.org!
doi.org/10.1073/pnas...
👇🧵
Reposted by The Lewis Lab
peterlewislab.bsky.social
By contrast, removing the SUZ12 NBD yields an RNA-poor PRC2 that spreads H3K27me3 broadly in the genome, creating a massive low-level methylation background that decoys PRC1 away from its canonical targets- a global shift in mark abundance that doesn’t happen in the BRG1 setting.
peterlewislab.bsky.social
great question- in the Crabtree lab work BRG1 loss causes rapid PRC1/2 redistribution from high-occupancy domains to BAF-opposed sites without major change in bulk H3K27me3.
Reposted by The Lewis Lab
akankshathawani.bsky.social
Vertebrate retrotransposons are the future of gene therapy. But how do they insert their genes? 🔥🔥

Thrilled to share our new work now published with Kathy Collins, @nogaleslab.bsky.social @berkeleymcb.bsky.social where we investigate this with #cryoEM & biochemistry in 🧪 and cells! #RNAsky #TEsky
peterlewislab.bsky.social
VEFS: the NBD is gone. RNA binding is rare (small red bubble). Most PRC2 is RNA-free, catalytically active, and binds both CpG and non-CpG sites.
 Result: diffuse H3K27me3 that dilutes PRC1 away from its normal targets, disrupting gene silencing.
Read more in our preprint: tinyurl.com/4yrwftrn