Policy makers, genetic engineers, and an engaged public can work together to create climate-resilient plants.

As climate change affects weather patterns and soil health, agricultural productivity could decrease substantially. Synthetic biology can be used to enhance climate resilience in plants and create the next generation of crops, if the public will accept it.

Transcriptional and post-transcriptional controls for tuning gene expression in plants.

Plant biotechnologists seek to modify plants through genetic reprogramming, but our ability to precisely control gene expression in plants is still limited. Here, we review transcription and translation in the model plants Arabidopsis thaliana and Nicotiana benthamiana with an eye toward control points that may be used to predictably modify gene expression. We highlight differences in gene expression requirements between these plants and other species, and discuss the ways in which our understanding of gene expression has been used to engineer plants. This review is intended to serve as a resource for plant scientists looking to achieve precise control over gene expression.

The H3.3 K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.

Histone H3.3 is frequently mutated in cancers, with the lysine 36 to methionine mutation (K36M) being a hallmark of chondroblastomas. While it is known that H3.3K36M changes the cellular epigenetic landscape, it remains unclear how it affects the dynamics of gene expression. Here, we use a synthetic reporter to measure the effect of H3.3K36M on silencing and epigenetic memory after recruitment of KRAB: a member of the largest class of human repressors, commonly used in synthetic biology, and associated with H3K9me3. We find that H3.3K36M, which decreases H3K36 methylation, leads to a decrease in epigenetic memory and promoter methylation weeks after KRAB release. We propose a new model for establishment and maintenance of epigenetic memory, where H3K36 methylation is necessary to convert H3K9me3 domains into DNA methylation for stable epigenetic memory. Our quantitative model can inform oncogenic mechanisms and guide development of epigenetic editing tools.