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19. Stem Cell Proliferation Is Kept in Check by the Chromatin Regulators Kismet/CHD7/CHD8 and Trr/MLL3/4

Author

Gervais, Louis, primary, van den Beek, Marius, additional, Josserand, Manon, additional, Sallé, Jérémy, additional, Stefanutti, Marine, additional, Perdigoto, Carolina N., additional, Skorski, Patricia, additional, Mazouni, Khallil, additional, Marshall, Owen J., additional, Brand, Andrea H., additional, Schweisguth, François, additional, and Bardin, Allison J., additional

Published
2019
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20. Applying mechanical forces on Drosophilatissues in vivousing the StretchCo, a 3D-printable device

Author

Gracia, Mélanie, Lefèvre, Bénédicte M., Güell Alonso, Raquel, Cachoux, Victoire, Balakireva, Maria, Guirao, Boris, Cuvelier, Damien, Bardin, Allison J., and Bellaïche, Yohanns

Abstract

Applying mechanical forces to tissues helps to understand morphogenesis and homeostasis. Additionally, recording the dynamics of living tissues under mechanical constraints is needed to explore tissue biomechanics. Here, we present a protocol to 3D-print a StretchCo device and use it to apply uniaxial mechanical stress on the Drosophilapupal dorsal thorax epithelium. We describe steps for 3D printing, polydimethylsiloxane (PDMS) strip cutting, and glue preparation. We detail procedures for PDMS strip mounting, tissue compaction, and live imaging upon force application. For additional details on the use and execution of this protocol, please refer to Cachoux et al. (2023)1from which the StretchCo machine has been derived.

Published
2024
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21. Spen limits intestinal stem cell self-renewal

Author

Andriatsilavo, Maheva, primary, Stefanutti, Marine, additional, Siudeja, Katarzyna, additional, Perdigoto, Carolina N., additional, Boumard, Benjamin, additional, Gervais, Louis, additional, Gillet-Markowska, Alexandre, additional, Al Zouabi, Lara, additional, Schweisguth, François, additional, and Bardin, Allison J., additional

Published
2018
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22. Evolution and genomic signatures of spontaneous somatic mutation in Drosophilaintestinal stem cells

Author

Riddiford, Nick, Siudeja, Katarzyna, van den Beek, Marius, Boumard, Benjamin, and Bardin, Allison J.

Abstract

Spontaneous mutations can alter tissue dynamics and lead to cancer initiation. Although large-scale sequencing projects have illuminated processes that influence somatic mutation and subsequent tumor evolution, the mutational dynamics operating in the very early stages of cancer development are currently not well understood. To explore mutational processes in the early stages of cancer evolution, we exploited neoplasia arising spontaneously in the Drosophilaintestine. Analysing whole-genome sequencing data with a dedicated bioinformatic pipeline, we found neoplasia formation to be driven largely through the inactivation of Notchby structural variants, many of which involve highly complex genomic rearrangements. The genome-wide mutational burden in neoplasia was found to be similar to that of several human cancers. Finally, we identified genomic features associated with spontaneous mutation, and defined the evolutionary dynamics and mutational landscape operating within intestinal neoplasia over the short lifespan of the adult fly. Our findings provide unique insight into mutational dynamics operating over a short timescale in the genetic model system, Drosophila melanogaster.

Published
2021
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24. Molecular underpinnings and environmental drivers of loss of heterozygosity in Drosophilaintestinal stem cells

Author

Al Zouabi, Lara, Stefanutti, Marine, Roumeliotis, Spyridon, Le Meur, Gwenn, Boumard, Benjamin, Riddiford, Nick, Rubanova, Natalia, Bohec, Mylène, Gervais, Louis, Servant, Nicolas, and Bardin, Allison J.

Abstract

During development and aging, genome mutation leading to loss of heterozygosity (LOH) can uncover recessive phenotypes within tissue compartments. This phenomenon occurs in normal human tissues and is prevalent in pathological genetic conditions and cancers. While studies in yeast have defined DNA repair mechanisms that can promote LOH, the predominant pathways and environmental triggers in somatic tissues of multicellular organisms are not well understood. Here, we investigate mechanisms underlying LOH in intestinal stem cells in Drosophila. Infection with the pathogenic bacteria, Erwinia carotovora carotovora 15, but not Pseudomonas entomophila, increases LOH frequency. Using whole genome sequencing of somatic LOH events, we demonstrate that they arise primarily via mitotic recombination. Molecular features and genetic evidence argue against a break-induced replication mechanism and instead support cross-over via double Holliday junction-based repair. This study provides a mechanistic understanding of mitotic recombination, an important mediator of LOH, and its effects on stem cells in vivo.

Published
2023
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29. Aurora B and Cyclin B Have Opposite Effects on the Timing of Cytokinesis Abscission in Drosophila Germ Cells and in Vertebrate Somatic Cells

Author

Mathieu, Juliette, primary, Cauvin, Clothilde, additional, Moch, Clara, additional, Radford, Sarah J., additional, Sampaio, Paula, additional, Perdigoto, Carolina N., additional, Schweisguth, François, additional, Bardin, Allison J., additional, Sunkel, Claudio E., additional, McKim, Kim, additional, Echard, Arnaud, additional, and Huynh, Jean-René, additional

Published
2013
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32. Regulation of the mitotic exit network components Tem1 and Cde 15 in Saccharomyces cerevisiae

Author

Angelika Amon Lab., Massachusetts Institute of Technology. Dept. of Biology., Bardin, Allison J. (Allison Johanna), 1975, Angelika Amon Lab., Massachusetts Institute of Technology. Dept. of Biology., and Bardin, Allison J. (Allison Johanna), 1975

Abstract

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2003., Includes bibliographical references., The division of a single eukaryotic cell resulting in two daughter progeny is controlled by cyclin dependent kinase activity (CDK). Mitotic cyclins associated with CDK promote the segregation of genetic material ensuring that each daughter receives a complete complement of the genome. In order for exit from mitosis into G1 to occur, mitotic CDK activity must be inactivated. In the budding yeast, Saccharomyces cerevisiae, a network of proteins called the mitotic exit network is essential for mitotic CDK inactivation and, therefore, exit from mitosis. The work presented herein describes the regulation of two components of the mitotic exit network, Teml and Cdc 15. A model for activation of the mitotic exit network is proposed. The spatial separation of the GTPase Teml from its activating GEF, Ltel, until anaphase is suggested to be one signal leading to correct timing of mitotic exit. Additionally, the roles of distinct regions of the protein kinase, CdclS5, are examined. Domains necessary and sufficient for localization of CdclS5 to the spindle pole body, association with other Cdc 15 molecules, and a putative inhibitory domain are investigated. This work investigates the regulatory mechanisms controlling two essential components of the mitotic exit network., Allison J. Bardin., Ph.D.

Published
2005

33. Regulation of the mitotic exit network components Tem1 and Cde 15 in Saccharomyces cerevisiae

Author

Massachusetts Institute of Technology. Dept. of Biology., Angelika Amon Lab., Bardin, Allison J. (Allison Johanna), 1975, Massachusetts Institute of Technology. Dept. of Biology., Angelika Amon Lab., and Bardin, Allison J. (Allison Johanna), 1975

Abstract

The division of a single eukaryotic cell resulting in two daughter progeny is controlled by cyclin dependent kinase activity (CDK). Mitotic cyclins associated with CDK promote the segregation of genetic material ensuring that each daughter receives a complete complement of the genome. In order for exit from mitosis into G1 to occur, mitotic CDK activity must be inactivated. In the budding yeast, Saccharomyces cerevisiae, a network of proteins called the mitotic exit network is essential for mitotic CDK inactivation and, therefore, exit from mitosis. The work presented herein describes the regulation of two components of the mitotic exit network, Teml and Cdc 15. A model for activation of the mitotic exit network is proposed. The spatial separation of the GTPase Teml from its activating GEF, Ltel, until anaphase is suggested to be one signal leading to correct timing of mitotic exit. Additionally, the roles of distinct regions of the protein kinase, CdclS5, are examined. Domains necessary and sufficient for localization of CdclS5 to the spindle pole body, association with other Cdc 15 molecules, and a putative inhibitory domain are investigated. This work investigates the regulatory mechanisms controlling two essential components of the mitotic exit network., Allison J. Bardin., Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2003., Includes bibliographical references.

Published
2005

43. Transcriptional control of stem cell maintenance in the Drosophila intestine.

Author

Bardin, Allison J., Perdigoto, Carolina N., Southall, Tony D., Brand, Andrea H., and Schweisguth, François

Subjects
*STEM cells, *DROSOPHILA, *REPRESSION (Psychology), *PHYSIOLOGICAL control systems, *TRANSCRIPTION factors
Abstract

Adult stem cells maintain tissue homeostasis by controlling the proper balance of stem cell self-renewal and differentiation. The adult midgut of Drosophila contains multipotent intestinal stem cells (ISCs) that self-renew and produce differentiated progeny. Control of ISC identity and maintenance is poorly understood. Here we find that transcriptional repression of Notch target genes by a Hairless-Suppressor of Hairless complex is required for ISC maintenance, and identify genes of the Enhancer of split complex [E(spl)-C] as the major targets of this repression. In addition, we find that the bHLH transcription factor Daughterless is essential to maintain ISC identity and that bHLH binding sites promote ISC-specific enhancer activity. We propose that Daughterless-dependent bHLH activity is important for the ISC fate and that E(spl)-C factors inhibit this activity to promote differentiation. [ABSTRACT FROM AUTHOR]

Published
2010
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44. Stem Cell Proliferation Is Kept in Check by the Chromatin Regulators Kismet/CHD7/CHD8 and Trr/MLL3/4

Author

Gervais, Louis, Van Den Beek, Marius, Josserand, Manon, Sallé, Jérémy, Stefanutti, Marine, Perdigoto, Carolina N, Skorski, Patricia, Mazouni, Khallil, Marshall, Owen J, Brand, Andrea H, Schweisguth, François, and Bardin, Allison J

Subjects
Cbl, tissue homeostasis, EGFR, adult stem cells, Histones, Kismet/CHD7/CHD8, Animals, Drosophila Proteins, Receptors, Invertebrate Peptide, Trr/MLL3/4, Cell Proliferation, Homeodomain Proteins, Stem Cells, fungi, DNA Helicases, Epigenetic, Cell Differentiation, Histone-Lysine N-Methyltransferase, Drosophila midgut, Chromatin Assembly and Disassembly, Chromatin, 3. Good health, ErbB Receptors, Drosophila melanogaster, chromatin regulators, RNA Polymerase II, Proliferation control, Signal Transduction, Transcription Factors
Abstract

Chromatin remodeling accompanies differentiation, however, its role in self-renewal is less well understood. We report that in Drosophila, the chromatin remodeler Kismet/CHD7/CHD8 limits intestinal stem cell (ISC) number and proliferation without affecting differentiation. Stem-cell-specific whole-genome profiling of Kismet revealed its enrichment at transcriptionally active regions bound by RNA polymerase II and Brahma, its recruitment to the transcription start site of activated genes and developmental enhancers and its depletion from regions bound by Polycomb, Histone H1, and heterochromatin Protein 1. We demonstrate that the Trithorax-related/MLL3/4 chromatin modifier regulates ISC proliferation, colocalizes extensively with Kismet throughout the ISC genome, and co-regulates genes in ISCs, including Cbl, a negative regulator of Epidermal Growth Factor Receptor (EGFR). Loss of kismet or trr leads to elevated levels of EGFR protein and signaling, thereby promoting ISC self-renewal. We propose that Kismet with Trr establishes a chromatin state that limits EGFR proliferative signaling, preventing tumor-like stem cell overgrowths.

45. [The Drosophila midgut as a model to study adult stem cells].

Author

Andriatsilavo M, Gervais L, Fons C, and Bardin AJ

Subjects
Animals, Cell Proliferation, Homeostasis, Intestines cytology, Models, Animal, Receptors, Notch, Adult Stem Cells, Drosophila melanogaster cytology
Abstract

Constant renewal of cells occurs in most tissues throughout the adult lifetime and is insured by the activity of resident stem cells. Recent work has demonstrated the presence of adult stem cells in the Drosophila intestine and consequently, the Drosophila intestine has become a powerful model to understand adult stem cells in vivo. In this review, we summarize our current understanding of the mechanisms controlling cell fate decisions of the intestinal stem cells with a particular focus on the role of the Notch pathway in this process. We also summarize what is known about proliferation control of the intestinal stem cells, which is crucial to maintain tissue homeostasis during normal and environmentally stressful conditions., (© 2013 médecine/sciences – Inserm / SRMS.)

Published
2013
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