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Your search keyword '"Audergon, Pauline"' showing total 4 results
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4 results on '"Audergon, Pauline"'

1. The future of integrated structural biology

Author

Schwalbe, Harald, Audergon, Pauline, Haley, Natalie, Amaro, Claudia Alen, Agirre, Jon, Baldus, Marc, Banci, Lucia, Baumeister, Wolfgang, Blackledge, Martin, Carazo, Jose Maria, Carugo, Kristina Djinovic, Celie, Patrick, Felli, Isabella, Hart, Darren J, Hauß, Thomas, Lehtiö, Lari, Lindorff-Larsen, Kresten, Márquez, José, Matagne, André, Pierattelli, Roberta, Rosato, Antonio, Sobott, Frank, Sreeramulu, Sridhar, Steyaert, Jan, Sussman, Joel L, Trantirek, Lukas, Weiss, Manfred S, Wilmanns, Matthias, Schwalbe, Harald, Audergon, Pauline, Haley, Natalie, Amaro, Claudia Alen, Agirre, Jon, Baldus, Marc, Banci, Lucia, Baumeister, Wolfgang, Blackledge, Martin, Carazo, Jose Maria, Carugo, Kristina Djinovic, Celie, Patrick, Felli, Isabella, Hart, Darren J, Hauß, Thomas, Lehtiö, Lari, Lindorff-Larsen, Kresten, Márquez, José, Matagne, André, Pierattelli, Roberta, Rosato, Antonio, Sobott, Frank, Sreeramulu, Sridhar, Steyaert, Jan, Sussman, Joel L, Trantirek, Lukas, Weiss, Manfred S, and Wilmanns, Matthias

Abstract

Instruct-ERIC, "the European Research Infrastructure Consortium for Structural biology research," is a pan-European distributed research infrastructure making high-end technologies and methods in structural biology available to users. Here, we describe the current state-of-the-art of integrated structural biology and discuss potential future scientific developments as an impulse for the scientific community, many of which are located in Europe and are associated with Instruct. We reflect on where to focus scientific and technological initiatives within the distributed Instruct research infrastructure. This review does not intend to make recommendations on funding requirements or initiatives directly, neither at the national nor the European level. However, it addresses future challenges and opportunities for the field, and foresees the need for a stronger coordination within the European and international research field of integrated structural biology to be able to respond timely to thematic topics that are often prioritized by calls for funding addressing societal needs.

Published
2024

2. Restricted epigenetic inheritance of H3K9 methylation

Author

Audergon, Pauline Nicole Clotilde Beatrice, Allshire, Robin, and Bird, Adrian

Subjects
572.8, epigenetics, H3K9me, heterochromatin, S. pombe
Abstract

In most eukaryotes methylation of histone H3 on lysine 9 (H3K9me) is the key post-translational modification required for the assembly of constitutive heterochromatin at centromeres and other chromosomal regions. H3K9me is bound by the chromodomain proteins HP1/Swi6 and the Suv39/Clr4 H3K9 methyltransferase itself suggesting that, once established, H3K9me might act as an epigenetic mark that can transmit the chromatin state independently of the initiator signal. However, it has not been demonstrated that H3K9me does indeed act as an epigenetic mark. Fission yeast represents an excellent system to address this question since S. pombe lacks DNA methylation and H3K9me is catalysed by the unique, non-essential H3K9 methyltransferase Clr4. To determine whether H3K9me carries epigenetic properties it is important to uncouple H3K9me from genomic domains that have the intrinsic ability to recruit the heterochromatin machinery. One way to solve this problem is to isolate H3K9me from its original context and investigate whether at an ectopic site H3K9me can self-propagate through cell division. To accomplish this, we tethered regulatable TetR-Clr4 fusion protein at euchromatic loci in fission yeast. This resulted in the assembly of an extensive domain of H3K9me-dependent heterochromatin that is rapidly disassembled following TetR-Clr4 release. Strikingly, the inactivation of Epe1, a putative histone demethylase, is sufficient to maintain the silent H3K9me-dependent heterochromatin at the tethering sites through mitotic and meiotic cell divisions in absence of TetR-Clr4. These results indicate that H3K9me acts as an epigenetic mark to maintain heterochromatin domains; however, a regulatory mechanism dependent on Epe1 exists to actively remove H3K9me and thus prevent heterochromatin from being transmitted when assembled at inappropriate regions of the genome.

Published
2015

3. Cohesin controls X chromosome structure remodeling and X-reactivation during mouse iPSC-reprogramming

Author

Hubrecht Institute with UMC, Generoso, Serena F., Neguembor, Maria Victoria, Hershberg, Elliot A., Sadreyev, Ruslan I., Kurimoto, Kazuki, Yabuta, Yukihiro, Ricci, Raffaele, Audergon, Pauline, Bauer, Moritz, Saitou, Mitinori, Hochedlinger, Konrad, Beliveau, Brian J., Cosma, Maria Pia, Lee, Jeannie T., Payer, Bernhard, Hubrecht Institute with UMC, Generoso, Serena F., Neguembor, Maria Victoria, Hershberg, Elliot A., Sadreyev, Ruslan I., Kurimoto, Kazuki, Yabuta, Yukihiro, Ricci, Raffaele, Audergon, Pauline, Bauer, Moritz, Saitou, Mitinori, Hochedlinger, Konrad, Beliveau, Brian J., Cosma, Maria Pia, Lee, Jeannie T., and Payer, Bernhard

Published
2023

4. Controlled X-chromosome dynamics defines meiotic potential of female mouse in vitro germ cells

Author

Hubrecht Institute with UMC, Severino, Jacqueline, Bauer, Moritz, Mattimoe, Tom, Arecco, Niccolò, Cozzuto, Luca, Lorden, Patricia, Hamada, Norio, Nosaka, Yoshiaki, Nagaoka, So I., Audergon, Pauline, Tarruell, Antonio, Heyn, Holger, Hayashi, Katsuhiko, Saitou, Mitinori, Payer, Bernhard, Hubrecht Institute with UMC, Severino, Jacqueline, Bauer, Moritz, Mattimoe, Tom, Arecco, Niccolò, Cozzuto, Luca, Lorden, Patricia, Hamada, Norio, Nosaka, Yoshiaki, Nagaoka, So I., Audergon, Pauline, Tarruell, Antonio, Heyn, Holger, Hayashi, Katsuhiko, Saitou, Mitinori, and Payer, Bernhard

Published
2022

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