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Researcher

Prof. dr. P. (Peter) Verrijzer

Principal investigator

  • Department
  • Developmental Biology
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About Prof. dr. P. (Peter) Verrijzer

Introduction

Peter Verrijzer studied mathematical biology and biochemistry at Utrecht University, the Netherlands. He obtained his PhD (1992) from the same university for his research on POU transcription factors with Peter van der Vliet. During his postdoc in the group of Robert Tjian at UC Berkeley he started to study gene regulation in animal cells. In 1996 he joined the Imperial Cancer Research Fund in London (currently part of the Crick Institute) as a group leader, and began his work on the role of chromatin and epigenetics in development and cell proliferation control. In 1999 he became full professor of Molecular and Cell Biology at the Leiden University Medical Center. In 2004, he moved to the Erasmus University Medical Center, where he headed the department of Biochemistry until 2025. Verrijzer's lab aims to understand the mechanisms of gene regulation that underpin development and disease. The main focus of his present research is the role of chromatin regulation in (neuro)development, and the coupling between cellular metabolism and epigenetics.

Publications

Selected Publications

van der Knaap J and Verrijzer CP (2025) Moonlighting Enzymes at the Interface between Metabolism and Epigenetics. Annu Rev Biochem 94: 279-303. doi: 10.1146/annurev-biochem-030122-044718.

Wolf van der Meer J, Larue A, van der Knaap J, Chalkley GE, Sijm A, Beikmohammadi L, Kozhevnikova EN, van der Vaart A, Tilly B, Bezstarosti K, Dekkers DHW, Doff WAS, van de Wetering-Tieleman J, Lanko K, Barakat TS, Allertz T, van Haren J, Demmers JAA, AtlasiY and Verrijzer CP (2025) Hao-Fountain syndrome protein USP7 controls neuronal differentiation via BCOR-ncPRC1.1. Genes Dev. 39: 401-422. doi: 10.1101/gad.352272.124.

de Potter B, Raas MWD, Seidl MF, Verrijzer CP and B Snel (2023) Uncoupled evolution of the Polycomb system and deep origin of non-canonical PRC1. Commun Biol 6: 1144. doi: 10.1038/s42003-023-05501-x.

Sijm A, Yaser Atlasi Y, van der Knaap JA, Wolf van der Meer J, Chalkley GE, Karel Bezstarosti K, Dekkers DHW, Doff WAS, Zeliha Ozgur Z, van Ijcken WFJ, Demmers JAA and Verrijzer CP (2022) USP7 regulates the ncPRC1 Polycomb axis to stimulate genomic H2AK119ub1 deposition uncoupled from H3K27me3. Science Advances 8: eabq7598. doi: 10.1126/sciadv.abq7598

Tilly BC, Chalkley GE, van der Knaap JA, Moshkin YM, Kan TW, Dekkers DHW, Demmers JAA and Verrijzer CP (2021) In vivo Analysis Reveals that ATP-hydrolysis Couples Remodeling to SWI/SNF Release from Chromatin. eLife 10: e69424. doi: 10.7554/eLife.69424

Bracken AP, Brien GL and Verrijzer CP (2019) Dangerous Liaisons: Interplay between SWI/SNF, NuRD and Polycomb in Chromatin Regulation and Cancer. Genes Dev 33: 936-959

Mohd-Sarip M, Teeuwssen M, Bot AG, De Herdt MJ, Willems SM, Baatenburg de Jong RJ, Looijenga LHJL, Zatreanu D, Bezstarosti K, Job van Riet, Edwin Oole, Wilfred F.J. van Ijcken, Harmen J. G. van de Werken, Demmers JA, Fodde R and Verrijzer CP (2017). DOC1-dependent recruitment of NURD reveals antagonism with SWI/SNF during epithelial-mesenchymal transition in oral cancer cells. Cell Reports 20: 61-75

van der Knaap JA and Verrijzer CP (2016) Undercover: gene control by metabolites and metabolic enzymes. Genes Dev 30: 2345-2369

Doyen CM, Chalkley GE, Voets O, Bezstarosti K, Demmers JAA, Moshkin YM, and Verrijzer CP (2015) A testis-specific chaperone and the chromatin remodeler ISWI mediate repackaging of the paternal genome. Cell Reports 13: 1310-1318

Reddy BA, van der Knaap JA, Bot AGM, Mohd-Sarip A, Dekkers DHW, Timmermans MA, Martens JWM, Demmers JAA and Verrijzer CP (2014) Nucleotide Biosynthetic Enzyme GMP Synthase is a TRIM21-Controlled Relay of p53 Stabilization. Mol Cell 53: 458-470

Research

We investigate the molecular mechanisms of developmental gene control with a focus on epigenetics and its connection to metabolism. In particular, we are interested in the balanced activities of trithorax group activators and the Polycomb repressors during (neuro)development and oncogenesis. We use a multi-disciplinary approach, integrating genomics, proteomics, developmental genetics, advanced imaging, biochemistry and cell biology. Taking advantage of evolutionary conservation, central pathways are studied in human (stem)cells and in the genetically tractable fruit fly.

Current Projects

The main focus of our current research is on:

1.    The role of the Polycomb system in human neurodevelopmental disorders, such as the Hao-fountain syndrome.
2.   The relationship between epigenetics and cellular state. E.g., we study the cross-talk between proteostasis and chromatin ubiquitylation, and its consequences for gene regulation.
3.   We aim to connect main metabolic signaling pathways, including AMPK signaling, to transcription control programs. We are particularly interested in the transcriptional consequences of cancer-associated metabolic adaptations.

How can intrinsically disordered domains (IDRs) in transcription factors confer specific biological information? E.g., we study how IDRs in the tumor suppressor p53 determines chromatin-binding site selection.