Epigenetic Silencing of Transposons in the Green Alga Chlamydomonas reinhardtii

Abstract

Transposons are mobile genetic elements that live parasitically within the genome of cellular organisms. They can affect the fitness of their hosts by influencing gene function, gene activity, genome structure, and overall DNA content. Since excessive transposon activity can result in a high mutagenic rate and genomic instability, eukaryotes have evolved epigenetic mechanisms to reduce transposition to manageable levels. The alga Chlamydomonas reinhardtii appears to have several, at least partly independent, transposon repression pathways that operate at either the transcriptional or the post-transcriptional level. Two genes have been implicated in the transcriptional silencing of transposons and single-copy transgenes: Mut9, which encodes a novel serine/ threonine protein kinase capable of phosphorylating histones H3 and H2A, and Mut11, which encodes a WD40-repeat containing protein. The Mut11 protein functions as a subunit of a histone methyltransferase complex(es) that is required for monomethylation of histone H3 lysine 4 and the maintenance of repressed euchromatic domains. These mechanisms of transcriptional gene silencing operate independently from the RNA interference (RNAi) machinery.