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3. Microglia states and nomenclature: A field at its crossroads

Author

Paolicelli, Rosa C, Sierra, Amanda, Stevens, Beth, Tremblay, Marie-Eve, Aguzzi, Adriano, Ajami, Bahareh, Amit, Ido, Audinat, Etienne, Bechmann, Ingo, Bennett, Mariko, Bennett, Frederick, Bessis, Alain, Biber, Knut, Bilbo, Staci, Blurton-Jones, Mathew, Boddeke, Erik, Brites, Dora, Brône, Bert, Brown, Guy C, Butovsky, Oleg, Carson, Monica J, Castellano, Bernardo, Colonna, Marco, Cowley, Sally A, Cunningham, Colm, Davalos, Dimitrios, De Jager, Philip L, de Strooper, Bart, Denes, Adam, Eggen, Bart JL, Eyo, Ukpong, Galea, Elena, Garel, Sonia, Ginhoux, Florent, Glass, Christopher K, Gokce, Ozgun, Gomez-Nicola, Diego, González, Berta, Gordon, Siamon, Graeber, Manuel B, Greenhalgh, Andrew D, Gressens, Pierre, Greter, Melanie, Gutmann, David H, Haass, Christian, Heneka, Michael T, Heppner, Frank L, Hong, Soyon, Hume, David A, Jung, Steffen, Kettenmann, Helmut, Kipnis, Jonathan, Koyama, Ryuta, Lemke, Greg, Lynch, Marina, Majewska, Ania, Malcangio, Marzia, Malm, Tarja, Mancuso, Renzo, Masuda, Takahiro, Matteoli, Michela, McColl, Barry W, Miron, Veronique E, Molofsky, Anna Victoria, Monje, Michelle, Mracsko, Eva, Nadjar, Agnes, Neher, Jonas J, Neniskyte, Urte, Neumann, Harald, Noda, Mami, Peng, Bo, Peri, Francesca, Perry, V Hugh, Popovich, Phillip G, Pridans, Clare, Priller, Josef, Prinz, Marco, Ragozzino, Davide, Ransohoff, Richard M, Salter, Michael W, Schaefer, Anne, Schafer, Dorothy P, Schwartz, Michal, Simons, Mikael, Smith, Cody J, Streit, Wolfgang J, Tay, Tuan Leng, Tsai, Li-Huei, Verkhratsky, Alexei, von Bernhardi, Rommy, Wake, Hiroaki, Wittamer, Valérie, Wolf, Susanne A, Wu, Long-Jun, and Wyss-Coray, Tony

Subjects
Microglia, Neurosciences, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Microglial research has advanced considerably in recent decades yet has been constrained by a rolling series of dichotomies such as "resting versus activated" and "M1 versus M2." This dualistic classification of good or bad microglia is inconsistent with the wide repertoire of microglial states and functions in development, plasticity, aging, and diseases that were elucidated in recent years. New designations continuously arising in an attempt to describe the different microglial states, notably defined using transcriptomics and proteomics, may easily lead to a misleading, although unintentional, coupling of categories and functions. To address these issues, we assembled a group of multidisciplinary experts to discuss our current understanding of microglial states as a dynamic concept and the importance of addressing microglial function. Here, we provide a conceptual framework and recommendations on the use of microglial nomenclature for researchers, reviewers, and editors, which will serve as the foundations for a future white paper.

Published
2022

6. N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer’s disease mouse model

Author

Suzzi, Stefano, Croese, Tommaso, Ravid, Adi, Gold, Or, Clark, Abbe R., Medina, Sedi, Kitsberg, Daniel, Adam, Miriam, Vernon, Katherine A., Kohnert, Eva, Shapira, Inbar, Malitsky, Sergey, Itkin, Maxim, Brandis, Alexander, Mehlman, Tevie, Salame, Tomer M., Colaiuta, Sarah P., Cahalon, Liora, Slyper, Michal, Greka, Anna, Habib, Naomi, and Schwartz, Michal

Published
2023
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10. Spinal Cord Damage

Author

Schwartz, Michal, Pfaff, Donald W., editor, Volkow, Nora D., editor, and Rubenstein, John L., editor

Published
2022
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16. SARS-CoV-2 uses a multipronged strategy to impede host protein synthesis

Author

Finkel, Yaara, Gluck, Avi, Nachshon, Aharon, Winkler, Roni, Fisher, Tal, Rozman, Batsheva, Mizrahi, Orel, Lubelsky, Yoav, Zuckerman, Binyamin, Slobodin, Boris, Yahalom-Ronen, Yfat, Tamir, Hadas, Ulitsky, Igor, Israely, Tomer, Paran, Nir, Schwartz, Michal, and Stern-Ginossar, Noam

Subjects
Messenger RNA -- Physiological aspects, Protein biosynthesis -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The coronavirus SARS-CoV-2 is the cause of the ongoing pandemic of COVID-19.sup.1. Coronaviruses have developed a variety of mechanisms to repress host mRNA translation to allow the translation of viral mRNA, and concomitantly block the cellular innate immune response.sup.2,3. Although several different proteins of SARS-CoV-2 have previously been implicated in shutting off host expression.sup.4-7, a comprehensive picture of the effects of SARS-CoV-2 infection on cellular gene expression is lacking. Here we combine RNA sequencing, ribosome profiling and metabolic labelling of newly synthesized RNA to comprehensively define the mechanisms that are used by SARS-CoV-2 to shut off cellular protein synthesis. We show that infection leads to a global reduction in translation, but that viral transcripts are not preferentially translated. Instead, we find that infection leads to the accelerated degradation of cytosolic cellular mRNAs, which facilitates viral takeover of the mRNA pool in infected cells. We reveal that the translation of transcripts that are induced in response to infection (including innate immune genes) is impaired. We demonstrate this impairment is probably mediated by inhibition of nuclear mRNA export, which prevents newly transcribed cellular mRNA from accessing ribosomes. Overall, our results uncover a multipronged strategy that is used by SARS-CoV-2 to take over the translation machinery and to suppress host defences. RNA sequencing, ribosome profiling and metabolic labelling of newly synthesized RNA reveal the strategy used by SARS-CoV-2 to shut off cellular protein synthesis in the host and allow the translation of viral transcripts., Author(s): Yaara Finkel [sup.1] , Avi Gluck [sup.1] , Aharon Nachshon [sup.1] , Roni Winkler [sup.1] , Tal Fisher [sup.1] , Batsheva Rozman [sup.1] , Orel Mizrahi [sup.1] , Yoav [...]

Published
2021
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19. The coding capacity of SARS-CoV-2

Author

Finkel, Yaara, Mizrahi, Orel, Nachshon, Aharon, Weingarten-Gabbay, Shira, Morgenstern, David, Yahalom-Ronen, Yfat, Tamir, Hadas, Achdout, Hagit, Stein, Dana, Israeli, Ofir, Beth-Din, Adi, Melamed, Sharon, Weiss, Shay, Israely, Tomer, Paran, Nir, Schwartz, Michal, and Stern-Ginossar, Noam

Published
2021
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23. Required enhancer–matrin-3 network interactions for a homeodomain transcription program

Author

Skowronska-Krawczyk, Dorota, Ma, Qi, Schwartz, Michal, Scully, Kathleen, Li, Wenbo, Liu, Zhijie, Taylor, Havilah, Tollkuhn, Jessica, Ohgi, Kenneth A, Notani, Dimple, Kohwi, Yoshinori, Kohwi-Shigematsu, Terumi, and Rosenfeld, Michael G

Subjects
Nuclear and Plasma Physics, Biological Sciences, Physical Sciences, Biotechnology, Genetics, Animals, Cells, Cultured, Enhancer Elements, Genetic, Gene Expression Regulation, Developmental, Homeodomain Proteins, Humans, Matrix Attachment Region Binding Proteins, Mice, Nuclear Matrix-Associated Proteins, Pituitary Gland, Protein Binding, RNA-Binding Proteins, Transcription Factor Pit-1, Transcription, Genetic, beta Catenin, General Science & Technology
Abstract

Homeodomain proteins, described 30 years ago, exert essential roles in development as regulators of target gene expression; however, the molecular mechanisms underlying transcriptional activity of homeodomain factors remain poorly understood. Here investigation of a developmentally required POU-homeodomain transcription factor, Pit1 (also known as Pou1f1), has revealed that, unexpectedly, binding of Pit1-occupied enhancers to a nuclear matrin-3-rich network/architecture is a key event in effective activation of the Pit1-regulated enhancer/coding gene transcriptional program. Pit1 association with Satb1 (ref. 8) and β-catenin is required for this tethering event. A naturally occurring, dominant negative, point mutation in human PIT1(R271W), causing combined pituitary hormone deficiency, results in loss of Pit1 association with β-catenin and Satb1 and therefore the matrin-3-rich network, blocking Pit1-dependent enhancer/coding target gene activation. This defective activation can be rescued by artificial tethering of the mutant R271W Pit1 protein to the matrin-3 network, bypassing the pre-requisite association with β-catenin and Satb1 otherwise required. The matrin-3 network-tethered R271W Pit1 mutant, but not the untethered protein, restores Pit1-dependent activation of the enhancers and recruitment of co-activators, exemplified by p300, causing both enhancer RNA transcription and target gene activation. These studies have thus revealed an unanticipated homeodomain factor/β-catenin/Satb1-dependent localization of target gene regulatory enhancer regions to a subnuclear architectural structure that serves as an underlying mechanism by which an enhancer-bound homeodomain factor effectively activates developmental gene transcriptional programs.

Published
2014

30. Potential roles of gut microbiome and metabolites in modulating ALS in mice

Author

Blacher, Eran, Bashiardes, Stavros, Shapiro, Hagit, Rothschild, Daphna, Mor, Uria, Dori-Bachash, Mally, Kleimeyer, Christian, Moresi, Claudia, Harnik, Yotam, Zur, Maya, Zabari, Michal, Brik, Rotem Ben-Zeev, Kviatcovsky, Denise, Zmora, Niv, Cohen, Yotam, Bar, Noam, Levi, Izhak, Amar, Nira, Mehlman, Tevie, Brandis, Alexander, Biton, Inbal, Kuperman, Yael, Tsoory, Michael, Alfahel, Leenor, Harmelin, Alon, Schwartz, Michal, Israelson, Adrian, Arike, Liisa, Johansson, Malin E. V., Hansson, Gunnar C., Gotkine, Marc, Segal, Eran, and Elinav, Eran

Published
2019
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33. No democracy, no academia

Author

Albin, Einat, primary, Bressler, Shikma, additional, Rolls, Asya, additional, Schwartz, Michal, additional, and Shapiro, Ehud, additional

Published
2023
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46. Microglia development follows a stepwise program to regulate brain homeostasis

Author

Matcovitch-Natan, Orit, Winter, Deborah R., Guadi, Amir, Aguilar, Stephanie Vargas, Spinrad, Amit, Sarrazin, Sandrine, Ben-Yehuda, Hila, David, Eyal, González, Fabiola Zelada, Perrin, Pierre, Keren-Shaul, Hadas, Gury, Meital, Lara-Astaiso, David, Thaiss, Christoph A., Cohen, Merav, Halpern, Keren Bahar, Baruch, Kuti, Deczkowska, Aleksandra, Lorenzo-Vivas, Erika, Itzkovitz, Shalev, Elinav, Eran, Sieweke, Michael H., Schwartz, Michal, and Amit, Ido

Published
2016

48. TREM2-dependent senescent microglia conserved in aging and Alzheimer's disease

Author

Rachmian, Noa, primary, Medina, Sedi, additional, Cherqui, Ulysse, additional, Akiva, Hagay, additional, Deitch, Daniel, additional, Edilbi, Dunya, additional, Croese, Tommaso, additional, Salame, Tomer Meir, additional, Peralta Ramos, Javier Maria, additional, Cahalon, Liora, additional, Krizhanovsky, Valery, additional, and Schwartz, Michal, additional

Published
2023
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49. Targeting the immune system towards novel therapeutic avenues to fight brain aging and neurodegeneration

Author

Peralta Ramos, Javier María, Kviatcovsky, Denise, and Schwartz, Michal

Subjects
Alzheimer Disease, Immune System, General Neuroscience, Longevity, Humans, Brain
Abstract

The incidence of age-related dementia is growing with increased longevity, yet there are currently no disease-modifying therapies for these devastating disorders. Studies over the last several years have led to an evolving awareness of the role of the immune system in supporting brain maintenance and repair, displaying a diverse repertoire of functions while orchestrating the crosstalk between the periphery and the brain. Here, we provide insights into the current understanding of therapeutic targets that could be adopted to modulate immune cell fate, either systemically or locally, to defeat brain aging and neurodegeneration.

Published
2022
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