By Sarah Adai
Department of Molecular Carcinogenesis
Over the past few decades it has become increasingly clear that epigenetic changes - heritable changes in the cell that do not result from DNA sequence alteration - may be just as important as gene mutations in cancer development. Researchers have identified a host of factors involved in epigenetic control of gene expression and development, but many of the precise mechanisms underlying this type of regulation remain unclear.
A new study by Mark Bedford, Ph.D., professor of Molecular Carcinogenesis, and colleagues published in Molecular Cell sheds light on the mechanism by which TDRD3 - a protein that "reads" epigenetic marks on chromosomal proteins - turns on certain genes.
The study establishes a link between TDRD3 and an enzyme that unwinds DNA at regions of active gene expression, and provides evidence that this partnership can prevent DNA breakage and chromosomal translocations - two of the hallmarks of cancer.
Decoding epigenetic marks
DNA is tightly packaged into chromosomes along with histone proteins. Chemical modification of these histones is one way that the cell regulates the packing and unpacking of the DNA and its associated proteins (collectively called chromatin), which in turn helps to determine whether a given gene is activated or repressed.
Several types of chemical modifications of the five major histone protein families give rise to a complex "histone code" that signals the transcriptional machinery to turn genes on or off.