A Genetic Basis for Stress and Disease

The work, coordinated by Lucia Piacentini and Arianna Rinaldi at the “Charles Darwin” Department of Biology and Biotechnology at Sapienza University, suggests a genetic basis for diseases caused by strong emotional stress. The results of the study have been published on Stress, the International Journal on the Biology of Stress

The work coordinated by Lucia Piacentini and Arianna Rinaldi at the “Charles Darwin” Department of Biology and Biotechnology at Sapienza University suggests a genetic basis for diseases caused by strong emotional stress. The researchers observed that in mouse model – the most commonly used model organism in human disease research – prolonged exposure to stressful conditions can induce the uncontrolled activation of mobile genetic elements (transposons) with potentially serious health consequences. The results of this study have been published on Stress, The International Journal on the Biology of Stress.

Trasposons, also known as “jumping genes” are mobile genetic elements that move from one location in the genometo another. In the early 1950s, Barbara McClintock first suggested that transposons are capable of actively reprogramming host genetic regulatory network and fine-tuning the host response to specific environmental stress stimuli. Moreover, they certainly played an important role in the creation of genetic variability over the course of genome evolution.

However, to ensure the co-evolution with their host genome, transposons mobility must be finely regulated as an elevated transposition activity can cause genomic instability and the alteration of numerous genes with deleterious effects on organisms.

“We studied the effect of prolonged stress (2 hours a day for 5 days) on mice,” explains Lucia Piacentini. “We observed the activation of Line-1 transposons in the hippocampus, one of the areas in the brain dedicated to perception and elaboration of stressful events, while no other significant alteration was observed in other brain areas.” These results indicate that, in mice, the control of transposon expression represents an additional mechanism for physio-pathological stress response, demonstrating that their regulation is closely related to the genetic background of individuals in a specific brain region.

The study opens interesting prospects on the role of transposons in diseases and human ageing. In particular, the demonstration of differential transposon activation among different tissue cells can help us to understand why certain types of stress increase our risk of disease such as post-traumatic stress disorders of ischemic cardiopathy.

 

References:

Stress-induced Strain and Brain Region-specific Activation of LINE-1 Transposons in Adult Mice - Ugo Cappucci, Giulia Torromino, Assunta Maria Casale, Jeremy Camon, Fabrizio Capitano, Maria Berloco, Andrea Mele, Sergio Pimpinelli, Arianna Rinaldi & Lucia Piacentini, Stress, The International Journal on the Biology of Stress, Published online: 11 Jul 2018. DOI: 10.1080/10253890.2018.1485647

 

For further information

Lucia Piacentini
Dipartimento di Biologia e Biotecnologie “Charles Darwin”
lucia.piacentini@uniroma1.it

 
Friday, 03 August 2018

© Sapienza Università di Roma - Piazzale Aldo Moro 5, 00185 Roma - (+39) 06 49911 - CF 80209930587 PI 02133771002