Future Seminars
Seminar Colour Guide:
| Seminar given by an external postdoc | |
| External Faculty Speaker | Friday, 6 September 2019, 11:00Polycomb, Inheritance and DiseaseDanny Reinberg, Department of Biochemistry and Molecular Pharmacology, NYU School of Medicine, New York, NY, USA, USAHost: Nicolas DescostesCNR Seminar Room, EMBL Rome Abstract: Epigenetics encompasses changes in gene expression profiles that occur without alterations in the genomic DNA sequence of a cell. This arises from the dynamic processes that structure regions of chromosomal DNA through a range of compaction in eukaryotes. The altered pattern of gene expression is pivotal to cellular differentiation and development and is inherited by daughter cells thereby maintaining the integrity, specifications, and functions for a given cell type. Aberrancies in this epigenetic process give rise to perturbations that are also inherited and disruptive to normal cellular properties. |
| Science and Society | Friday, 27 September 2019, 11:00Why do Humans Harm and Kill Each Other? A Psychological Perspective on the Causes of Aggression and ViolenceBarbara Krahé , University of Potsdam, Potsdam, GermanyHost: Halldór Stefánsson CNR Seminar Room, EMBL Rome Abstract: Aggression (defined as behavior intended to harm) and violence (behavior intended to cause severe physical harm) are ubiquitous in human societies around the world. They cause immeasurable harm and suffering to individuals, groups, and communities and also create high material costs to societies. Therefore, understanding why humans engage in these forms of destructive behavior is a challenge for scientific research that has immediate applied consequences in a wide range of societal domains.Aggression and violence are complex behaviors in which potential causes at the individual, interpersonal, group, and societal level come together, requiring a multidisciplinary approach for their understanding. Psychology, and social psychology in particular, is one of the key disciplines in this concerted search for understanding. In this talk, I will present an overview of psychological theorizing and empirical findings addressing four major questions: - How can we explain why humans show aggressive behavior and what are the processes that lead from an aggression-eliciting stimulus to an aggressive response? - Do humans differ in their propensity to engage in aggressive behavior? - What are critical factors in the situation or the social environment that make aggressive behavior more likely? - What can be done to prevent or reduce aggression? The talk will conclude by outlining a multidisciplinary agenda for future research on the causes of aggression and violence. |
| EMBL Distinguished Visitor Lecture | Friday, 4 October 2019, 10:00Synapses lost and found: developmental critical periods and Alzheimer's Disease Carla Shatz, Stanford University, Stanford, California, USAHost: Cornelius GrossCNR Seminar Room, EMBL Rome Abstract: How are connections wired up during brain development? Wiring occurs sequentially, first by forming a basic scaffold of connectivity according to strict molecular guidance cues and then the exact details of each circuit emerge by pruning and sculpting synapses. The process determining which synaptic connections remain and which are pruned is also genetically specified but in this case requires brain function. Prenatally, the brain generates its own internal neural activity patterns to jump-start the sculpting process. After birth as sensory systems such as vision mature, experience of the external world takes over to influence brain wiring during developmental critical periods. Neural activity and sensory experience regulate expression of sets of genes including several previously thought to act only in the immune system. These activity-regulated genes- including Major Histocompatibility Class I family members and Paired immunoglobulin-like receptor B- are required in neurons for synapse pruning and plasticity. Unexpectedly, they may also contribute to excessive synapse pruning in Alzheimer s disease. Thus, the baby's brain is not a miniature of the adult, but rather is a dynamically changing structure in which neural activity and experience ultimately select and stabilize essential details of neural circuitry that make each of us different from one another. |
| External Faculty Speaker | |
| EMBL Distinguished Visitor Lecture | |
| EMBL - Sapienza Lecture | Friday, 8 November 2019, 11:00The genetics of autism from risk to resilienceThomas Bourgeron, Institut Pasteur, Paris, FranceHost: Cornelius Gross / Andrea MeleSapienza Università di Roma - Aula Odeion - Museo dell'Arte Classica - P.le Aldo Moro, 5 - Roma, EMBL Rome Abstract: The genetic architecture of autism can be different from one individual to the other. It is framed by a complex combination of common and rare variants. Our previous studies pointed at one biological pathway associated with autism related to the synapse. Among the causative genes, synaptic cell adhesion molecules (neuroligins and neurexins) and scaffolding proteins (SHANK) are crucial for synapse formation/maintenance as well as correct balance between inhibitory and excitatory synaptic currents. These findings significantly advanced our knowledge on the possible causes of autism. However, they also (unintentionally) contributed to the emergence of a simplistic conception of autism as a binary trait: mutated vs. non-mutated or affected vs. non-affected. This simplification neglects the large phenotypic heterogeneity of autism, whose genetic architecture like most complex traits cannot be reduced to a single gene. In this presentation, I will discuss our recent results coming from human studies in large populations and genetic isolates as well as mouse studies that shed new light on the inheritance of autism and some of the underlying mechanisms. Finally, I will illustrate how we are currently studying Resilience to understand why some carriers of deleterious mutations seem to be protected (The Resilients) while others are severely affected. |
| External Faculty Speaker | Tuesday, 12 November 2019, 11:00Phosphorylation of histone H3 threonine 11 by the Tda1 kinase under nutritional stress requires the AMPK and CK2 kinasesJerry Workman, Stowers Institute for Medical Research, Kansas City, Missouri, USAHost: Mathieu BoulardCNR Seminar Room, EMBL Rome Abstract: Nutritional stress signaling in budding yeast includes phosphorylation of histone H3T11 (H3pT11).To understand upsteam signaling of H3pT11, we dissected kinases involved in this process. We found that H3pT11 requires both AMPK and CK2 kinases. However, these kinase do not directly phosphorylate H3T11 but instead directly phosphorylate the Tda1 kinase. Tda1 is a yeast AMPK interacting kinase that phosphorylates H3T11 in vitro and in vivo. Phosphorylation of Tda1 is required for its proper histone kinase activity and its protein stability. The Tda1 kinase thus integrates signals of multiple upstream kinases to regulate H3T11 phosphorylation upon nutrient stress. |
| Seminar given by an external postdoc | |
| EMBL - Sapienza Lecture | Thursday, 21 November 2019, 11:00Chromatin topology and its function in the regulation of gene expression: a view from 3DEileen Furlong, EMBL , Genome Biology Unit, Heidelberg, GermanyHost: Cornelius Gross / Irene BozzoniSapienza Università di Roma - Aula Odeion - Museo dell'Arte Classica - P.le Aldo Moro, 5 - Roma, EMBL Rome |
| External Faculty Speaker | |
| EMBL - Sapienza Lecture | |
| EMBL Distinguished Visitor Lecture |