Environmental change drives accelerated adaptation through stimulated copy number variation
Fig 1
Systems for stimulated copy number variation (CNV) at the ribosomal DNA (rDNA) and at a model gene.
a: Minimal elements implicated in control of rDNA recombination: transcription from bidirectional promoter E-pro and replication fork stalling at the Fob1-induced replication fork barrier (RFB). Green arrows represent noncoding RNAs IGS1-R and IGS1-F transcribed from the E-pro promoter; blue arrows show the rRNA genes (not to scale). b: Schematic representation of a general system in which a bidirectional promoter is adjacent to a replication fork stalling (RFS) site. Activation of the bidirectional promoter leads to transcription of the ORF (red arrow) and a noncoding RNA (green arrow). This system should, by analogy to the rDNA, be subject to stimulated CNV when the promoter for the indicated ORF is induced. Stalling of replication forks leads to an accumulation of S139-phosphorylated histone H2A (γH2A) (indicated by orange peaks) that can be detected by chromatin immunoprecipitation (ChIP).