Cold Spring Harbor, N.Y. Much like cancer cells, plant cells grown for a long time outside of their normal milieu, in culture dishes, have highly unstable genomes. Changes in gene activity, or how genes are "expressed," help cells cope with challenging culture conditions but inadvertently also leave genes prone to mis-regulation by transposons -- bits of DNA that can jump around in the genome, inserting themselves into random genetic locations, often disrupting normal gene function and regulation.
Such genomic chaos, found in cancer and other diseases, is normally prevented by a host of mechanisms that scientists call epigenetic: they modify the expression of genes, although not by causing mutations in the sequence of the genome's DNA "letters."
How transposons (sometimes called mobile genetic elements) escape these controls is one of the questions driving the research of Professor Robert Martienssen -- a pioneer of plant epigenetics -- at Cold Spring Harbor Laboratory (CSHL). By undertaking the ambitious task of mapping the changing epigenetic landscape of continuously dividing plant cells, Martienssen's team has succeeded in capturing in detail epigenetic alterations and the molecular players that allow transposons to run amok. Their findings are described in a paper published in the December 9th issue of PLoS Biology.
Shifting RNA patterns
The numerous and diverse transposons present within the plant genome are normally rendered inactive by a series of complicated steps masterminded by small molecules of RNA, called small interfering RNA (siRNA). They perform this feat in a phenomenon known as RNA interference (RNAi). The discovery that modifications of heterochromatin -- densely packed, genetically "inactive" regions of DNA -- are targeted by RNAi was made by Martienssen's team in yeast cells and heralded as one of the leading scientific breakthroughs of 2002.
Martienssen's team now has found t
|Contact: Hema Bashyam|
Cold Spring Harbor Laboratory