Transposable Elements (TEs) are DNA fragments that can mobilize and mutate the genome, causing hundreds of diseases and progression of certain types of cancer. To prevent new mutations, the cell ‘flags’ TE regions with chemical modifications such as methylation of DNA (in plants and mammals), and histone H3 lysine 9 residues (conserved from yeast to humans). These modifications mark TE regions for long-term ‘constitutive heterochromatin’ transcriptional silencing and are epigenetically passed to daughter cells after division to prevent reactivation.
In the model plant Arabidopsis, de novo RdDM of new TEs occurs in three distinct stages – initiation, establishment and maintenance. Multiple studies have addressed how heterochromatin is epigenetically maintained, but little is known about how cells initially detect and silence newly inserted TEs without prior chromatin marks. By using TE transgene systems developed in the Slotkin laboratory, I am investigating the molecular players underlying de novo initiation of TE silencing in Arabidopsis. This project is funded by the Simons Foundation (through Life Sciences Research Foundation postdoctoral fellowship).