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EPIGENETICS
 
 
RAFAL CIOSK
Cell fate determination and reprogramming in animal development and disease
During development, cells acquire distinct identities allowing the formation of wonderfully complex "biological machines" such as the human body. Occasionally, however, cells can push back the developmental clock. While in a healthy individual this is important for maintaining tissue homeostasis, uncontrolled acquisition of developmental flexibility can lead to diseases such as cancer.

The mechanisms controlling cell fate commitment are complex, and the cells that undergo cell fate reprogramming are often difficult to pinpoint. For these reasons, we are using the C. elegans germ line as a simple model to study cell fate commitment and reprogramming.

Our recent findings demonstrate a critical role for RNA regulation in maintaining cell identity, as mutations in conserved RNA-binding proteins cause (trans-) differentiation of germ cells into somatic cell types. This phenomenon, reminiscent of human tumors called teratomas, results from deregulation of the cell cycle that induces transcriptional activation of embryonic genes.

In our future research, we will continue to investigate mechanisms regulating the germ line-to-soma transition in normal development and disease. In the long term, we may identify targets whose manipulation induces cell fate reprogramming in differentiated cells. This could have an impact on the treatment of degenerative diseases such as Parkinson?s or juvenile diabetes, and cancer.
 
For further information, please contact
Administrative Assistant Isabella Bogdal
(+41 61 6976653)
 
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