The long molecules of DNA that carry our genetic information are wrapped up together with proteins into a dense complex called chromatin. The structure of chromatin is dynamic and varies according to different phases of a cell ™s life, a phenomenon that is called chromatin plasticity. Chromatin structure plays a critical role in regulating our genes and research in this area has the potential to aid the understanding of biological processes and disease, including aging and cancer.
The Chromatin Plasticity Network brings together 13 academic and industrial research groups from 9 countries around the world to reveal novel mechanisms in the regulation of chromatin structure. Combining complementary approaches from disciplines as different as structural biology, mouse genetics, immunology, bioinformatics and drug design, the research partners are aiming to develop new approaches and tools to achieve a thorough understanding of chromatin plasticity, as well as to identify potential therapeutic targets for cancer and heart disease.
In this project, great emphasis is placed on training PhD students and postdoctoral researchers through collaborative exchanges, practical courses and visits within the network, contributing to the development of the next generation of European researchers.
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"We knew it was an important process for the cell, but until this study, we didn't know exactly why it was so important," Ibba said. "Other researchers have actually disrupted this process in mice, and found that it leads to neurodegenerative diseases resembling Alzheimer's and Parkinson's."
Ibba and his team face more challenges. They want to know precisely how cells correct for these mistakes, and knowing this may give them insight to neurological diseases.
"The key to efficient cell growth is to limit the level of mistakes to a tolerable amount," Ibba said. "In spite of all its checks and balances, a cell isn't perfect. Even though textbooks tell you that gene expression is flawless, this just isn't possible in real life.
"Ultimately “ and it's a long way off “ we hope to develop a way to therapeutically correct for these errors," he said. "If we understand how these diseases start, and it relates to mistakes in the mechanism we studied, then there may be a means to try and correct these mistakes."
Ibba conducted the study with Ohio State colleagues Jiqiang Ling, a graduate research associate in the Ohio State Biochemistry Program, and Herv?© Roy, a postdoctoral researcher in microbiology.
This study was supported by a grant from the National Science Foundation.
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