| Transposable elements are a dynamic component of the genome. Their regulation is key to understanding many aspects of genome biology. Here I report the genetic and molecular analysis of the initiation, establishment, and maintenance of epigenetic silencing of Mutator transposons in maize.;Previous work in this lab has uncovered a locus, Mu killer, which heritably silences Mutator transposons in maize. The maintenance of the Mutator silenced state was elucidated through the use of a mutant, mop1 (mediator of paramutation1), known to suppress paramutation. mop1 mutants reactivate silenced MuDR elements over several generations, eventually permitting the reactivated MuDR element to persist in mop1 heterozygotes. This reactivation is dependent upon the maternal genotype; reciprocal crosses indicate that heritable reactivation of MuDR only proceeds when the female parent is mop1/mop1;MuDR. Reactivation only occurs at the transposase, mudrA; mudrB, the gene involved in transposition, remains silenced in a mop1 mutant background.;Mop1 was found to be an RNA-dependent RNA polymerase 2, which is involved in the RNA silencing pathway. mop1 mutants did not prevent Mutator silencing by Mu killer, an inverted duplication of mudrA discovered previously in this lab that heritably silences Mutator elements. However, another mutant corresponding to a NAP1 ortholog, did prevent Mutator silencing by Mu killer. NAP1 is a histone chaperone, and it is thought that the NAP1 gene is involved in the establishment of the Mutator silenced state as opposed to its maintenance, as NAP1 mutants did not reactivate silenced MuDR elements.;Together, the genetic and molecular analysis of Mu killer, Mop1, and NAP1 have permitted the proposal of a Mutator silencing pathway that distinguishes between silencing initiation, establishment, and maintenance of Mutator elements, and places into context the epigenetic regulation of transposons in the genome. |
