VP16 fusion induces the multiple-knockout phenotype of redundant transcriptional repressors partly by Med25-independent mechanisms in Arabidopsis.

Abstract

Biological functions of only some plant transcriptional repressors are known owing to the lack of knockout lines or unclear phenotypes because of redundancy. Here we show that strong viral activation domain VP16 fusion to the transcriptional repressor FLOWERING LOCUS C reversed its function and caused a stronger phenotype than that of the multiple-knockout line of redundant genes, suggesting the potential of this technique to identify transcription factor function that cannot be detected in a single-knockout line. Loss-of-function of transcriptional coactivator Mediator25 did not affect VP16 activity despite their in vivo interaction, suggesting the existence of other key mechanism(s) in plants.