To overcome this, we turned to the mammalian H3K4 methyltransferase, PRDM9. Not only does PRDM9 function brilliantly to activate gene expression, it also results in less off-target. Perhaps the orthogonality of PRDM9 means nothing to recruit /stabilise at non-targeted plant chromatin..?

All peachy right? Well there is a catch, SunTag-SDG2 also causes some off-target effects, which manifest as increased background noise in H3K4me3 ChIP-seq datasets.

Ok what about modulating something other than gene expression, like crossovers? Here, we teamed up with @hendersi.bsky.social , targeting SunTag-SDG2 to an entire centromere, finding that this unlocked recombination in surrounding regions that are normally highly suppressed. Hello plant breeding…

Next we targeted a ‘useful’ gene, namely the plant resistance gene, SNC1. We show by modifying the epigenome at this single locus, you can generate plants with enhanced resistance to pathogens. (big thanks to @jurriaanton.bsky.social group for getting us set up with this assay!)

By coupling the CRISPR/dCas9 based SunTag system with the plant H3K4me3 methyltransferase, SDG2, we show that H3K4me3 can activate the expression of a gene that is typically silent, FWA. Works super well, and honestly slightly unexpected as DNA methylation is though to be the main player for FWA...