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Alessandra Agresti, Ph.D. - "Inside out: the double life of nucleosomes"

In vivo Chromatin and transcription Group, Division of Genetics and Cell biology, San Raffaele Scientific Institute, Milan, Italy
When Dec 05, 2017
from 12:00 PM to 01:15 PM
Where Tigem, Auditorium "Vesuvius"
Contact Name
Contact Phone 081-19230659
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Contrary to what written in textbook, the amount of histones – and therefore of nucleosomes – is not a fixed parameter but a tunable one that cells exploit to adapt or respond to the external environment. We now hypothesize that histones leave the nucleus and double up as signaling factors.
Nucleosome reduction is detectable in macrophages exposed to stress signals where it facilitates the transcriptional response of inflammatory genes. Along the same line, cells progressing toward senescence reduce their nucleosome content and a similar decrease is found in cells that are genetically ablated for HMGB1 (High Mobility Group Box 1 protein).
On the contrary, the chromatin of ES cells acquires nucleosomes as differentiation progresses, suggesting that the difference in histone content can be considered as a new hallmark of pluripotency, in addition to and besides histone modifications.
Finally, histones are found in the serum of sepsis patients and their high concentration exacerbate systemic inflammation.
Many questions arise: are histones just passively released by dying cells? Or, are they also actively secreted by inflammatory cells?
Our results indicate that activated macrophages reduce their nucleosome content and concomitantly release microvesicles/exosomes (MV/E) loaded with histones. Are the two events functionally correlated? Do they represent a specialized form of intercellular communication, including to, from and between immune cells? We are trying to provide answers to these questions. 

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