In this episode of the Epigenetics Podcast, we caught up with Catherine Jensen Peña from Princeton University to talk about her work on early life stress and its effects on behavior.

The Laboratory of Catherine Peña focuses on how early life experiences are encoded and maintained into adulthood, with a long-lasting impact on behavior. Recent work showed, that child maltreatment and other forms of early life stress increase the lifetime risk of depression and other mood, anxiety, and drug disorders by 2-4 fold. The Peña Lab uses genome wide approaches to investigate key brain regions with a two-hit stress model.

Using RNA-Seq, the Peña Lab has shown that depression-like gene expression patterns are programmed by early life stress, similar to observations in mice exhibiting depression-like behavior after adult stress and are visible even before behavioral changes. Furthermore, latent and unique transcriptional responses to adult stress among a subset of genes is programmed by early life stress. The role of chromatin modifications in regulating these processes are investigated using state of the art technologies like Mod-Spec or ATAC-Seq.

References

Kronman, H., Torres-Berrío, A., Sidoli, S., Issler, O., Godino, A., Ramakrishnan, A., Mews, P., Lardner, C. K., Parise, E. M., Walker, D. M., van der Zee, Y. Y., Browne, C. J., Boyce, B. F., Neve, R., Garcia, B. A., Shen, L., Peña, C. J., & Nestler, E. J. (2021). Long-term behavioral and cell-type-specific molecular effects of early life stress are mediated by H3K79me2 dynamics in medium spiny neurons. Nature Neuroscience, 24(5), 667–676. https://doi.org/10.1038/s41593-021-00814-8

Peña, C. J., Smith, M., Ramakrishnan, A., Cates, H. M., Bagot, R. C., Kronman, H. G., Patel, B., Chang, A. B., Purushothaman, I., Dudley, J., Morishita, H., Shen, L., & Nestler, E. J. (2019). Early life stress alters transcriptomic patterning across reward circuitry in male and female mice. Nature Communications, 10(1), 5098. https://doi.org/10.1038/s41467-019-13085-6

Peña, C. J., Kronman, H. G., Walker, D. M., Cates, H. M., Bagot, R. C., Purushothaman, I., Issler, O., Loh, Y.-H. E., Leong, T., Kiraly, D. D., Goodman, E., Neve, R. L., Shen, L., & Nestler, E. J. (2017). Early life stress confers lifelong stress susceptibility in mice via ventral tegmental area OTX2. Science, 356(6343), 1185–1188. https://doi.org/10.1126/science.aan4491

Related Episodes

Nutriepigenetics: The Effects of Diet on Behavior (Monica Dus)

The Role of Small RNAs in Transgenerational Inheritance in C. elegans (Oded Rechavi)

Epigenetic Influence on Memory Formation and Inheritance (Isabelle Mansuy)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Ali Shilatifard from Northwestern University to talk about his work on targeting COMPASS to cure childhood leukemia.

The Shilatifard Lab studies childhood leukemia and how it can potentially be treated using epigenetic targets. The team focuses on is SET1/COMPASS, a histone H3 lysine4 methylase. Ali Shilatifard was able to purify and identify its activity, with results published in 2001 in PNAS. This protein complex is conserved from yeast to drosophila to humans.

Surprisingly, the Shilatifard Team could show that the catalytic activity of COMPASS is not necessary for viability of drosophila. Furthermore, they found that catalytic activity was not the decisive feature of the complex, but rather its role in the context of chromatin structure, in particular a protein domain that only spans 80 amino acids within the 4000 amino acid protein.

References

Miller, T., Krogan, N. J., Dover, J., Erdjument-Bromage, H., Tempst, P., Johnston, M., Greenblatt, J. F., & Shilatifard, A. (2001). COMPASS: A complex of proteins associated with a trithorax-related SET domain protein. Proceedings of the National Academy of Sciences, 98(23), 12902–12907. https://doi.org/10.1073/pnas.231473398

Lin, C., Garruss, A. S., Luo, Z., Guo, F., & Shilatifard, A. (2013). The RNA Pol II Elongation Factor Ell3 Marks Enhancers in ES Cells and Primes Future Gene Activation. Cell, 152(1–2), 144–156. https://doi.org/10.1016/j.cell.2012.12.015

Wang, L., Zhao, Z., Ozark, P. A., Fantini, D., Marshall, S. A., Rendleman, E. J., Cozzolino, K. A., Louis, N., He, X., Morgan, M. A., Takahashi, Y., Collings, C. K., Smith, E. R., Ntziachristos, P., Savas, J. N., Zou, L., Hashizume, R., Meeks, J. J., & Shilatifard, A. (2018). Resetting the epigenetic balance of Polycomb and COMPASS function at enhancers for cancer therapy. Nature Medicine, 24(6), 758–769. https://doi.org/10.1038/s41591-018-0034-6

Morgan, M. A. J., & Shilatifard, A. (2020). Reevaluating the roles of histone-modifying enzymes and their associated chromatin modifications in transcriptional regulation. Nature Genetics, 52(12), 1271–1281. https://doi.org/10.1038/s41588-020-00736-4

Related Episodes

Cancer and Epigenetics (David Jones)

Transcription and Polycomb in Inheritance and Disease (Danny Reinberg)

Epigenetic Mechanisms of Aging and Longevity (Shelley Berger)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Yael David from Memorial Sloan Kettering Cancer Center in New York to talk about her work on Effects of Non-Enzymatic Covalent Histone Modifications on Chromatin. 

The David lab studies on non-enzymatic covalent modifications of Histones, including Histone glycation and citrullination. These modifications recognize metabolites that are produced in the cell and aid as a sensor for chromatin to quickly adapt to cellular changes. These unique modifications do not have a so-called erasing enzyme, which makes them terminal, rendering these sites inaccessible for further modifications such as methylation or acetylation.  

A second area of research in the David lab is Histone H1. The lab has developed a new method to purify Histone H1, superior to the commonly used method of acid extraction which leads to degradation of Histone H1. This purification method enabled the lab to purify and characterize the functional properties of all Histone H1 variants. 

References

David, Y., Vila-Perelló, M., Verma, S., & Muir, T. W. (2015). Chemical tagging and customizing of cellular chromatin states using ultrafast trans -splicing inteins. Nature Chemistry, 7(5), 394–402. https://doi.org/10.1038/nchem.2224

David, Y., & Muir, T. W. (2017). Emerging Chemistry Strategies for Engineering Native Chromatin. Journal of the American Chemical Society, 139(27), 9090–9096. https://doi.org/10.1021/jacs.7b03430

Osunsade, A., Prescott, N. A., Hebert, J. M., Ray, D. M., Jmeian, Y., Lorenz, I. C., & David, Y. (2019). A Robust Method for the Purification and Characterization of Recombinant Human Histone H1 Variants. Biochemistry, 58(3), 171–176. https://doi.org/10.1021/acs.biochem.8b01060

Zheng, Q., Omans, N. D., Leicher, R., Osunsade, A., Agustinus, A. S., Finkin-Groner, E., D’Ambrosio, H., Liu, B., Chandarlapaty, S., Liu, S., & David, Y. (2019). Reversible histone glycation is associated with disease-related changes in chromatin architecture. Nature Communications, 10(1), 1289. https://doi.org/10.1038/s41467-019-09192-z

Zheng, Q., Osunsade, A., & David, Y. (2020). Protein arginine deiminase 4 antagonizes methylglyoxal-induced histone glycation. Nature Communications, 11(1), 3241. https://doi.org/10.1038/s41467-020-17066-y

Related Episodes

Synthetic Chromatin Epigenetics (Karmella Haynes)

Variants of Core Histones: Modulators of Chromatin Structure and Function (Sandra Hake)

Influence of Histone Variants on Chromatin Structure and Metabolism (Marcus Buschbeck)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Jason Buenrostro from Harvard University to talk about his work on developing biological tools to measure chromatin dynamics in single-cells. He explains how his lab uses these tools to study chromatin alterations in different cell types and disease states to uncover new mechanisms of gene regulation and their contribution to those diseases.

In his first years of his research career Jason Buenrostro took a risk and just added an enzyme called Transposase to cells in a cell culture. What he saw on a subsequent agarose gel astonished him. He was able to recreate a nucleosomal ladder that he knew from experiments using MNase or DNase-Seq, however, without the tedious steps of optimization. In the following years he optimized that method and data analyzation into a method known today as ATAC-Seq. In recent years he was also able to bring ATAC-Seq to the next level and developed single cell ATAC-Seq (scATAC-Seq), and combining it with RNA-Seq in a multi-omics approach.

In this Episode we discuss how Jason Buenrostro developed ATAC-Seq in William Greenleaf's lab, how a lack of equipment shaped the ATAC-Seq protocol, and how scATAC-Seq has enabled a whole different way of looking at biological samples.

References

Buenrostro, J. D., Giresi, P. G., Zaba, L. C., Chang, H. Y., & Greenleaf, W. J. (2013). Transposition of native chromatin for fast and sensitive epigenomic profiling of open chromatin, DNA-binding proteins and nucleosome position. Nature Methods, 10(12), 1213–1218. https://doi.org/10.1038/nmeth.2688

Buenrostro, J. D., Wu, B., Litzenburger, U. M., Ruff, D., Gonzales, M. L., Snyder, M. P., Chang, H. Y., & Greenleaf, W. J. (2015). Single-cell chromatin accessibility reveals principles of regulatory variation. Nature, 523(7561), 486–490. https://doi.org/10.1038/nature14590

Buenrostro, J. D., Corces, M. R., Lareau, C. A., Wu, B., Schep, A. N., Aryee, M. J., Majeti, R., Chang, H. Y., & Greenleaf, W. J. (2018). Integrated Single-Cell Analysis Maps the Continuous Regulatory Landscape of Human Hematopoietic Differentiation. Cell, 173(6), 1535-1548.e16. https://doi.org/10.1016/j.cell.2018.03.074

Lareau, C. A., Duarte, F. M., Chew, J. G., Kartha, V. K., Burkett, Z. D., Kohlway, A. S., Pokholok, D., Aryee, M. J., Steemers, F. J., Lebofsky, R., & Buenrostro, J. D. (2019). Droplet-based combinatorial indexing for massive-scale single-cell chromatin accessibility. Nature Biotechnology, 37(8), 916–924. https://doi.org/10.1038/s41587-019-0147-6

Related Episodes

Chromatin Profiling: From ChIP to CUT&RUN, CUT&Tag and CUTAC (Steven Henikoff)

Hi-C and Three-Dimensional Genome Sequencing (Erez Lieberman Aiden)

Multiple Challenges in ChIP (Adam Blattler)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Karmella Haynes from Emory University to talk about her work on synthetic chromatin epigenetics.

The Haynes lab focuses on the design of synthetic chromatin sensor proteins. The first one of this kind, the Polycomb Transcription Factor (PcTF), was published in 2011. It senses H3K27me3 and recruits effector proteins to the sites of this modification. This sensor can be brought into cancer cells to activate hundreds of silenced genes. The lab now focuses on characterizing the effects of these sensor proteins genome wide, and seeks to find a way to deliver those sensor into cancer cells, without affecting healthy cells.

In this Episode we discuss how Karmella Haynes got into the field of Epigenetics, how she designed the PcTF sensor proteins, and the way she came to learn how important the right control experiments are. In the end we also discuss her activities to promote diversity and inclusion in science.

References

Haynes, K. A., & Silver, P. A. (2011). Synthetic Reversal of Epigenetic Silencing. Journal of Biological Chemistry, 286(31), 27176–27182. https://doi.org/10.1074/jbc.C111.229567

Haynes, K. A., Ceroni, F., Flicker, D., Younger, A., & Silver, P. A. (2012). A Sensitive Switch for Visualizing Natural Gene Silencing in Single Cells. ACS Synthetic Biology, 1(3), 99–106. https://doi.org/10.1021/sb3000035

Daer, R. M., Cutts, J. P., Brafman, D. A., & Haynes, K. A. (2017). The Impact of Chromatin Dynamics on Cas9-Mediated Genome Editing in Human Cells. ACS Synthetic Biology, 6(3), 428–438. https://doi.org/10.1021/acssynbio.5b00299

Tekel, S. J., & Haynes, K. A. (2017). Molecular structures guide the engineering of chromatin. Nucleic Acids Research, 45(13), 7555–7570. https://doi.org/10.1093/nar/gkx531

Tekel, S. J., Vargas, D. A., Song, L., LaBaer, J., Caplan, M. R., & Haynes, K. A. (2018). Tandem Histone-Binding Domains Enhance the Activity of a Synthetic Chromatin Effector. ACS Synthetic Biology, 7(3), 842–852. https://doi.org/10.1021/acssynbio.7b00281

Related Episodes

Transcription and Polycomb in Inheritance and Disease (Danny Reinberg)

Cancer and Epigenetics (David Jones)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Enrico Glaab from the University of Luxemburg to talk about his work on the development of integrative machine learning tools for neurodegenerative diseases.

The work of Dr. Enrico Glaab focuses on neurodegenerative disorders like Parkinson’s and Alzheimer’s disease. In his group his team works on the development of software tools to analyze molecular, clinical and neuroimaging data for those diseases that can be used and applied easily by scientists and deliver publication ready figures. More recently, Enrico Glaab's group got interested in the influence of Epigenetics in Parkinson's and Alzheimer's disease.

In this Episode we discuss how Enrico Glaab made the switch from wet-lab to becoming a bioinformatician and how he uses integrative machine learning tools to find approaches to not only cure but also be able to detect neurodegenerative diseases like Alzheimer's or Parkinson's early on.

References

Enrico Glaab, Reinhard Schneider (2015) RepExplore: addressing technical replicate variance in proteomics and metabolomics data analysis (Bioinformatics) DOI: 10.1093/bioinformatics/btv127

Enrico Glaab, Reinhard Schneider (2015) Comparative pathway and network analysis of brain transcriptome changes during adult aging and in Parkinson’s disease (Neurobiology of Disease) DOI: 10.1016/j.nbd.2014.11.002

Sandra Köglsberger, Maria Lorena Cordero-Maldonado, … Enrico Glaab (2017) Gender-Specific Expression of Ubiquitin-Specific Peptidase 9 Modulates Tau Expression and Phosphorylation: Possible Implications for Tauopathies (Molecular Neurobiology) DOI: 10.1007/s12035-016-0299-z

Enrico Glaab, Paul Antony, … Manuel Buttini (2019) Transcriptome profiling data reveals ubiquitin-specific peptidase 9 knockdown effects (Data in Brief) DOI: 10.1016/j.dib.2019.104130

Related Episodes

Epigenetic Influence on Memory Formation and Inheritance (Isabelle Mansuy)

CpG Islands, DNA Methylation, and Disease (Sir Adrian Bird)

Epigenetics & Glioblastoma: New Approaches to Treat Brain Cancer (Lucy Stead)

Cancer and Epigenetics (David Jones)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Diane Dickel from Lawrence Berkeley National Laboratory to talk about her work on ultraconserved enhancers and enhancer redundancy.

Diane Dickel and her co-workers study non-coding regions of the genome that harbor distant-acting transcriptional regulatory regions, called enhancers. Enhancers have been shown to be critical for normal embryonic development, implying evolutional conservation. Diane Dickel and her team try to identify and characterize enhancers at a genomic scale. Their efforts include the use of CRISPR/CAS9 to mutate enhancer sequences in order to understand sequence dependent functional relevance.

In this episode we discuss the function of ultraconserved enhancers, what ultraconservation actually means, how enhancer redundancy works and how Diane Dickel dealt with a failed PhD project.

References

Dickel, D. E., Ypsilanti, A. R., Pla, R., Zhu, Y., Barozzi, I., Mannion, B. J., Khin, Y. S., Fukuda-Yuzawa, Y., Plajzer-Frick, I., Pickle, C. S., Lee, E. A., Harrington, A. N., Pham, Q. T., Garvin, T. H., Kato, M., Osterwalder, M., Akiyama, J. A., Afzal, V., Rubenstein, J. L. R., … Visel, A. (2018). Ultraconserved Enhancers Are Required for Normal Development. Cell, 172(3), 491-499.e15. https://doi.org/10.1016/j.cell.2017.12.017

Gorkin, D. U., Barozzi, I., Zhao, Y., Zhang, Y., Huang, H., Lee, A. Y., Li, B., Chiou, J., Wildberg, A., Ding, B., Zhang, B., Wang, M., Strattan, J. S., Davidson, J. M., Qiu, Y., Afzal, V., Akiyama, J. A., Plajzer-Frick, I., Novak, C. S., … Ren, B. (2020). An atlas of dynamic chromatin landscapes in mouse fetal development. Nature, 583(7818), 744–751. https://doi.org/10.1038/s41586-020-2093-3

Snetkova, V., Ypsilanti, A. R., Akiyama, J. A., Mannion, B. J., Plajzer-Frick, I., Novak, C. S., Harrington, A. N., Pham, Q. T., Kato, M., Zhu, Y., Godoy, J., Meky, E., Hunter, R. D., Shi, M., Kvon, E. Z., Afzal, V., Tran, S., Rubenstein, J. L. R., Visel, A., … Dickel, D. E. (2021). Ultraconserved enhancer function does not require perfect sequence conservation. Nature Genetics, 53(4), 521–528. https://doi.org/10.1038/s41588-021-00812-3

Related Episodes

Identification of Functional Elements in the Genome (Bing Ren)

Epigenetic Reprogramming During Mammalian Development (Wolf Reik)

Unraveling Mechanisms of Chromosome Formation (Job Dekker)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Sandra Hake from the Justus Liebig University in Giessen to talk about her work on variants of core histones and their role as modulators of chromatin structure and function.

The overarching goal of Sandra Hake's research group is to understand how changes in chromatin structure and composition can influence various DNA-based processes, such as gene expression, repair of DNA damage, cell cycle progression, and genome stability. Their work deals with the study of histone variants which, together with DNA, represent the building blocks of the smallest chromatin components, the nucleosomes. They also investigate whether mutations and/or post-translational histone modifications and the deregulation of histone variant networks influence the emergence of diseases, especially the emergence of tumors.

In this episode we discuss how Sandra Hake approaches the characterization and identification of novel histone variants like H3.3, H3.X and H3.Y, what it's like to work in such a small field like histone variants, and what is coming up next for the Hake lab.

References

Hake, S. B., Garcia, B. A., Duncan, E. M., Kauer, M., Dellaire, G., Shabanowitz, J., Bazett-Jones, D. P., Allis, C. D., & Hunt, D. F. (2006). Expression Patterns and Post-translational Modifications Associated with Mammalian Histone H3 Variants. Journal of Biological Chemistry, 281(1), 559–568. https://doi.org/10.1074/jbc.M509266200

Wiedemann, S. M., Mildner, S. N., Bönisch, C., Israel, L., Maiser, A., Matheisl, S., Straub, T., Merkl, R., Leonhardt, H., Kremmer, E., Schermelleh, L., & Hake, S. B. (2010). Identification and characterization of two novel primate-specific histone H3 variants, H3.X and H3.Y. Journal of Cell Biology, 190(5), 777–791. https://doi.org/10.1083/jcb.201002043

Bönisch, C., Schneider, K., Pünzeler, S., Wiedemann, S. M., Bielmeier, C., Bocola, M., Eberl, H. C., Kuegel, W., Neumann, J., Kremmer, E., Leonhardt, H., Mann, M., Michaelis, J., Schermelleh, L., & Hake, S. B. (2012). H2A.Z.2.2 is an alternatively spliced histone H2A.Z variant that causes severe nucleosome destabilization. Nucleic Acids Research, 40(13), 5951–5964. https://doi.org/10.1093/nar/gks267

Link, S., Spitzer, R. M. M., Sana, M., Torrado, M., Völker-Albert, M. C., Keilhauer, E. C., Burgold, T., Pünzeler, S., Low, J. K. K., Lindström, I., Nist, A., Regnard, C., Stiewe, T., Hendrich, B., Imhof, A., Mann, M., Mackay, J. P., Bartkuhn, M., & Hake, S. B. (2018). PWWP2A binds distinct chromatin moieties and interacts with an MTA1-specific core NuRD complex. Nature Communications, 9(1), 4300. https://doi.org/10.1038/s41467-018-06665-5

Related Episodes

Regulation of Chromatin Organization by Histone Chaperones (Geneviève Almouzni)

Influence of Histone Variants on Chromatin Structure and Metabolism (Marcus Buschbeck)

Chromatin Analysis using Mass Spectrometry (Axel Imhof)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Déborah Bourc'his from L'Institut Curie in Paris to talk about her work on the role of DNA methylation in mammalian development.

During her postdoc years Déborah Bourc'his was able to characterize DNMT3L, a protein with unknown function at that time. It turned out that this protein is the cofactor responsible for stimulating DNA methylation activity in both the male and the female germline. Later on she discovered a novel DNA methylation enzyme called DNMT3C, which was unknown because it was not properly annotated, there was no sign of expression, and it was only expressed in male fetal germ cells. Furthermore, this enzyme only evolved in rodents, as a defense against young transposons.

In this episode we discuss the story behind how Déborah Bourc'his was able to discover and characterize the DNA methylation enzymes DNMT3L and DNMT3C and their role in mammalian development.

References

R. Duffie, S. Ajjan, … D. Bourc’his (2014) The Gpr1/Zdbf2 locus provides new paradigms for transient and dynamic genomic imprinting in mammals (Genes & Development) DOI: 10.1101/gad.232058.113

Natasha Zamudio, Joan Barau, … Déborah Bourc’his (2015) DNA methylation restrains transposons from adopting a chromatin signature permissive for meiotic recombination (Genes & Development) DOI: 10.1101/gad.257840.114](https://doi.org/10.1101/gad.257840.114)

Marius Walter, Aurélie Teissandier, … Déborah Bourc’his (2016) An epigenetic switch ensures transposon repression upon dynamic loss of DNA methylation in embryonic stem cells (eLife) DOI: 10.7554/eLife.11418](https://doi.org/10.7554/eLife.11418)

Joan Barau, Aurélie Teissandier, … Déborah Bourc’his (2016) The DNA methyltransferase DNMT3C protects male germ cells from transposon activity (Science (New York, N.Y.)) DOI: 10.1126/science.aah5143

Maxim V. C. Greenberg, Juliane Glaser, … Déborah Bourc’his (2017) Transient transcription in the early embryo sets an epigenetic state that programs postnatal growth (Nature Genetics) DOI: 10.1038/ng.3718

Roberta Ragazzini, Raquel Pérez-Palacios, … Raphaël Margueron (2019) EZHIP constrains Polycomb Repressive Complex 2 activity in germ cells (Nature Communications) DOI: 10.1038/s41467-019-11800-x

Dura, M., Teissandier, A., Armand, M., Barau, J., Bonneville, L., Weber, M., Baudrin, L. G., Lameiras, S., & Bourc’his, D. (2021). DNMT3A-dependent DNA methylation is required for spermatogonial stem cells to commit to spermatogenesis [Preprint]. Developmental Biology. https://doi.org/10.1101/2021.04.19.440465

Related Episodes

Effects of DNA Methylation on Diabetes (Charlotte Ling)

Epigenetic Reprogramming During Mammalian Development (Wolf Reik)

Effects of DNA Methylation on Chromatin Structure and Transcription (Dirk Schübeler)

CpG Islands, DNA Methylation, and Disease (Sir Adrian Bird)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]

In this episode of the Epigenetics Podcast, we caught up with Axel Imhof from the Ludwig Maximilian University of Munich in Germany to talk about his work on the identification of chromatin associated proteins using mass spectrometry.

As the head of the Proteomics Core Facility Axel Imhof collaborates with research groups around the world. In addition, in his own lab, he focuses on the assembly and composition of chromatin, how environmental metabolites influence epigenetic marks, and how chromatin factors can be used as markers for pathological states.

In this episode we discuss what has changed in the field of mass spectrometry over the years, how Axel Imhof takes advantage of collaborations, how metabolites influence chromatin, and how he is helping to bring epigenetic profiling via mass spectrometry to the clinic.

References

Bonaldi, T., Regula, J. T., & Imhof, A. (2003). The Use of Mass Spectrometry for the Analysis of Histone Modifications. In Methods in Enzymology (Vol. 377, pp. 111–130). Elsevier. https://doi.org/10.1016/S0076-6879(03)77006-2

Völker-Albert, M. C., Pusch, M. C., Fedisch, A., Schilcher, P., Schmidt, A., & Imhof, A. (2016). A Quantitative Proteomic Analysis of In Vitro Assembled Chromatin. Molecular & Cellular Proteomics, 15(3), 945–959. https://doi.org/10.1074/mcp.M115.053553

Scharf, A. N. D., Meier, K., Seitz, V., Kremmer, E., Brehm, A., & Imhof, A. (2009). Monomethylation of Lysine 20 on Histone H4 Facilitates Chromatin Maturation. Molecular and Cellular Biology, 29(1), 57–67. https://doi.org/10.1128/MCB.00989-08

Van den Ackerveken, P., Lobbens, A., Turatsinze, J.-V., Solis-Mezarino, V., Völker-Albert, M., Imhof, A., & Herzog, M. (2021). A novel proteomics approach to epigenetic profiling of circulating nucleosomes. Scientific Reports, 11(1), 7256. https://doi.org/10.1038/s41598-021-86630-3

Related Episodes

Regulation of Chromatin Organization by Histone Chaperones (Geneviève Almouzni)

Transcription and Polycomb in Inheritance and Disease (Danny Reinberg)

Contact

Active Motif on Twitter

Epigenetics Podcast on Twitter

Active Motif on LinkedIn

Active Motif on Facebook

Email: [email protected]