All organisms are constantly threatened by parasites and pathogens that exploit host cellular components to proliferate. This may cause loss-of-fitness, disease, or even death. Hence, organisms have evolved mechanisms to recognize and counter such threats, relying on their ability to discriminate between self and non-self at the molecular level. Transposable elements (TEs) are mobile genetic entities that colonize and proliferate within genomes. Because they hijack the cellular machinery to increase their DNA copy number, they are commonly considered molecular parasites, with the potential to be extremely harmful due to their ability to integrate within coding genes. However, TEs also play a fundamental role in genome evolution as a source of genetic and epigenetic innovation. TEs are commonly silenced through the establishment of heterochromatin, which relies on epigenetic marks such as DNA methylation and histone modifications. Although the pathways that maintain Transcriptional Gene Silencing (TGS) in TEs in plants are well established, far less is known about the mechanisms by which new, active transposons are first detected and selectively silenced. Based on our previous research, we have now uncovered a mechanism by which the mRNA of active TEs is recognized as foreign during translation, triggering a Post-Transcriptional Gene Silencing (PTGS) small RNA response. The onset of PTGS leads to TGS to epigenetically silence all new insertions of active TEs.
Our lab is interested in the molecular mechanisms that allow the recognition of transposons and other non-self nucleic acids to initiate a silencing response at the RNA level and how the initial PTGS response is later switched into a chromatin response, leading to strong and transgenerationally stable repression of TEs and other foreign genetic elements. We also aim to gain insights into the genetic and epigenetic consequences of transposon proliferation in host genomes. Through a combination of molecular, genomic, and biochemical approaches, our goal is to better understand TE biology and opposing defense mechanisms and how such interactions shape the genome and epigenome of plants.