Aug. 4, 2011 Researchers from the Centre for Genomic Regulation (CRG in Spanish) have discovered that ultraviolet light affects the function of the protein EWS, the mutation of which is responsible for Ewing's sarcoma. The results, published in the journal Molecular Cell, indicate that the EWS protein has a protective effect on DNA.
The genetic circuits altered in cancer processes include the activation or inhibition of various genes and proteins. In the case of Ewing's sarcoma, EWS protein alterations induce changes in the expression of various genes, thus affecting the ability to detect and correct DNA damage.
The genetic material contains all of the information necessary for the proper functioning of cells. This material may become damaged but the cell has sophisticated mechanisms to detect and repair this damage. When the genetic material in our cells is exposed to ultraviolet light one of the strands of the DNA molecule may break. The work presented by the CRG researchers describes the effects of ultraviolet radiation on the Ewing's Sarcoma protein and its role in the response to genetic damage. "We now know that EWS plays a crucial role in cell maintenance and contributes to the response to genetic damage. Alterations in this response, such as those which occur in Ewing's sarcoma, make the cells more susceptible to DNA damage, which may contribute to the development of a tumor," explains Juan Valcárcel, group leader at the CRG and principal investigator of the study.
The group's findings indicate that during normal response to DNA damage, the EWS protein stops being joined to the genes it regulates and relocates to structures located within the cell nucleus known as nucleoli. This relocation results in changes in the expression of the genes regulated by EWS, and these changes are important for an appropriate response to DNA damage.
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- Maria Paola Paronetto, Belén Miñana, Juan Valcárcel. The Ewing Sarcoma Protein Regulates DNA Damage-Induced Alternative Splicing. Molecular Cell, 2011; 43 (3): 353 DOI: 10.1016/j.molcel.2011.05.035
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