Science & Career Talks

Online via Zoom, date to be announced.

Behavior and physiology in mammals are strongly influenced by the environment and by experiences, particularly in early life. While positive factors can favor proper development and a balanced mental and physical health later in life, childhood adversity and traumatic experiences can increase the risk for psychiatric, metabolic and autoimmune diseases, and cancer. Such disorders can affect exposed individuals directly but in some cases, they also impact their offspring sometimes across generations. Childhood trauma is one of the strongest risk factors for mental disorders and chronic comorbidities across families in humans, and affects about 25% of children worldwide. The biological mechanisms underlying the transmission of symptoms induced by experience from parent to offspring are thought to involve epigenetic factors but are not fully identified. This talk will present a transgenerational model of postnatal traumatic stress in mice that recapitulates trauma symptoms including increased risktaking, depressive behaviors, cognitive and social deficits. metabolic dysregulation and cardiovascular deficiencies in adulthood. The symptoms are pronounced, persist throughout life, and are transmitted to the offspring, in some cases, up to the 4th or 5th generation. Symptoms are associated with molecular changes involving RNA in germ cells, that in mice, are shown to be causally linked to symptoms expression and transmission. MiRNAs are also affected in extracellular vesicles from the reproductive tract. Comparable behavioral and metabolic alterations are observed in traumatized children and miRNAs changes in sperm of adult men, indicating conserved effects in mouse and humans. Recent work identified circulating factors as potential mediators of alterations in germ cells. Chronic injection of serum from trauma-exposed mouse males into control males recapitulates metabolic phenotypes in the offspring, suggesting information transfer from serum to germ cells. Circulating factors involving peroxisome proliferator-activated receptor (PPAR) pathways are causally linked to these effects, and pharmacological PPAR activation in vivo reproduces the metabolic dysfunctions in the offspring and grand-offspring of injected males, and affects the sperm transcriptome. Together, these results suggest an ensemble of mechanisms from the periphery to germ cells responsible for the inheritance of acquired traits.

How to attend

Information on how to attend will be available shortly.

Online via Zoom, date to be announced.

How to attend

The workshop is primarily aimed at early-career female scientists at the University. The number of participants is limited. Please register by email to exuspam prevention@uni-tuebingen.de and state

• your career level (master student (which semester), PhD student, postdoc (how many years after PhD), junior professor?),
• your department,
• topics you would like to discuss / aspects you would need advice on / personal or professional questions you have (will be passed on to Prof. Mansuy anonymously).