Joined March 2019
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Mar 24
New preprint from our lab! An H3.3 knockout does two things at once: it removes H3.3 from chromatin and destabilizes DAXX. We disentangle those functions and find that DAXX-mediated H3.3 deposition can be uncoupled from ERV silencing.
biorxiv.org/content/10.64898โฆ
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The Lewis Lab retweeted
Jun 12
Excited to share that our preprint 'RNA reinforces condensate nucleation on chromatin to amplify oncogenic transcription' is now online @MolecularCell cell.com/molecular-cell/fullโฆ @PennMedCSO @PennCancer @PennEpiInst
4 Aug 2025
(1/n) Excited to share our new preprint! We uncover that RNA actively promotes nucleation and function of pathogenic condensates, amplifying locus-specific oncogenic transcription and promoting tumorigenesis. #epigenetics #condensates #cancer #RNA biorxiv.org/content/10.1101/โฆ
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Jun 12
๐ Happy to share our review in @NatureRevGenet on the mechanisms that integrate the environment into gene responses.
nature.com/articles/s41576-0โฆ
@CarolineDeanLab @JohnInnesCentre
#environment #epigenetics #climatechange
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๐ Check out the latest paper titled ๐๐๐๐๐ค ๐ฎ๐ฆ๐ต๐ฉ๐บ๐ญ๐ต๐ณ๐ข๐ฏ๐ด๐ง๐ฆ๐ณ๐ข๐ด๐ฆ ๐ข๐ค๐ต๐ช๐ท๐ช๐ต๐บ ๐ฑ๐ณ๐ฐ๐ฎ๐ฐ๐ต๐ฆ๐ด ๐ค๐ฐ๐ณ๐ณ๐ฆ๐ค๐ต ๐ต๐ณ๐ข๐ฏ๐ด๐ค๐ณ๐ช๐ฑ๐ต๐ช๐ฐ๐ฏ ๐ช๐ฏ๐ช๐ต๐ช๐ข๐ต๐ช๐ฐ๐ฏ ๐ข๐ฏ๐ฅ ๐ต๐ฆ๐ณ๐ฎ๐ช๐ฏ๐ข๐ต๐ช๐ฐ๐ฏ, just published in the EMBO Reports @SpringerNature!
๐ฒ doi.org/10.1038/s44319-026-0โฆ
๐ฉ๐ปโ๐ฌ๐จ๐ปโ๐ฌ The publication was authored by researchers from the GLaboratory of Genome Regulation (@STOPlabPI) and the Laboratory of Developmental Epigenetics, CAT AMU: Magda Kopczyลska, Agata Stฤpieล, Michaล Gdula, and Kinga Kamieniarz-Gdula. ๐ฉ๐ปโ๐ฌ๐จ๐ปโ๐ฌThe remaining authors are Chihiro Nakayama and Prof. Takayuki Nojima from @KyushuUniv_EN in Japan.
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Allosteric activation of PRC2 is coupled to adoption of the compact state. Our new bioRxiv manuscript shows that EZH2 S21-phos, adjacent to the SANT1 domain, restrains this conformational transition and limits activation. @vignesh_k757 & Ben Garcia lab tinyurl.com/4369kmh2
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How do cells tune PRC2 allostery? We find EZH2 Ser21-phos restrains PRC2 adoption of the compact active state. Loss of this restraint promotes H3K27me3, redistributes cPRC1, and impairs differentiation. New bioRxiv with @vignesh_k757 & Ben Garcia lab! tinyurl.com/4369kmh2
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Allosteric activation of PRC2 is coupled to adoption of the compact state. Our new bioRxiv manuscript shows that EZH2 S21-phos, adjacent to the SANT1 domain, restrains this conformational transition and limits activation. @vignesh_k757 & Ben Garcia lab tinyurl.com/4369kmh2
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In a genome not so far away, the most elegant design in the galaxy was already wrapped into ~147 base pairs. #HappyNucleosomeDay, May-The-Fourth Be With You.
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The Lewis Lab retweeted
Excited to share our latest study in @NatureComms where we uncover a new mechanism of chromatin regulation that is essential in certain SWI/SNF-mutant cancers. Congrats to @HaydenMalone3 and coauthors! #SWISNF #cancer (1/8)
@stjuderesearch @stjudegraduate
nature.com/articles/s41467-0โฆ
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The Lewis Lab retweeted
Excited to share our structural insights into how microtubules differentially guide phosphorylation of kinetochore-microtubule regulators, Ndc80 and MCAK, for chromosome segregation. Heroic efforts by Yiming Niu with a fun collaboration with DeLuca lab!
science.org/doi/10.1126/sciaโฆ
Microtubules have been viewed as passive structural supports, but a study from @HironoriFunabi1 in @ScienceAdvances redefines microtubules as active regulators, helping to prevent abnormalities in the number of chromosomes, a hallmark of cancer.
๐: bit.ly/4v8miCC
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The Lewis Lab retweeted
Our latest research is now out in @NatureCellBio nature.com/articles/s41556-0โฆ
We show that nonsense-mediated mRNA decay (NMD) pathway safeguards #telomere integrity in pluripotent #stemcells
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The Lewis Lab retweeted
Apr 9
A single-nucleotide enhancer mutation overrides chromosomal sex to drive XX male development | Nature Communications nature.com/articles/s41467-0โฆ
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Apr 9
Preprint: The tumour suppressor RBM5 activates the helicase DHX15 to regulate splicing
researchsquare.com/article/rโฆ @UCLA
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The Lewis Lab retweeted
Our linker histone H1 paper is out @ScienceAdvances: science.org/doi/10.1126/sciaโฆ
@MasaAShimazoe et al. reveal that H1 acts as a liquid-like "glue" to organize chromatin in living cells. ๐ Fantastic collab with @rcollepardo, @janhuemar, Charlie Phillips and othersโhuge thanks! ๐ ยฝ
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How to make a heterochromatin by major satellite repeats transcripts?
Congrat @AleciaYHLO and Thomas Jenuwein lab for the work.
nature.com/articles/s41467-0โฆ
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The Lewis Lab retweeted
Epigenetics Update - Accessory subunits of PRC2 mimic H3K27me3 to restrict the spread of Polycomb domains bit.ly/3NmLO5Q
Edwina McGlinn & Chen Davidovich in Mol Cell
#Epigenetics #PRC2 #H3K27me3
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Perfect for cancer, immunology, and aging; epigenometech.com
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Mar 24
New preprint from our lab! An H3.3 knockout does two things at once: it removes H3.3 from chromatin and destabilizes DAXX. We disentangle those functions and find that DAXX-mediated H3.3 deposition can be uncoupled from ERV silencing.
biorxiv.org/content/10.64898โฆ
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Mar 24
Which DAXX functions are required for ERV silencing? Mutants defective in ATRX binding or H3.3 deposition restore ERV repression. By contrast, deletion of the SIM abolishes silencing. Thus, ERV repression requires the C-terminal SIM, but not ATRX binding or H3.3 deposition.
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Mar 24
These separation-of-function mutants show that H3.3 deposition can be uncoupled from ERV silencing. This supports our finding that H3.3 deposition at ERVs is dispensable for repression. Instead, repression depends on the C-terminal SIM and interaction with SUMOylated effectors.
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