Genomes are dynamic entities that change over time. An important mechanism by which genomes
evolve novel functions is gene and genome duplication. However, not all cellular processes are
equally malleable by evolution through gene duplication. Studies in human genomes have revealed
that certain genes might be intolerant to duplication, leading to human disease. Similarly, we
recently discovered that many flowering plant (angiosperm) genes appear preferentially as single
copy in all angiosperm genomes sequenced. This is surprising given the duplication-rich history of
the angiosperms. The basis of this intolerance for duplication remains unknown. A popular
hypothesis is that duplication directly influences the amount of protein that gets produced and as
such disturbs key pathways in which these ‘dosage-sensitive’ genes are involved. Alternatively,
putative mutations in the duplicate copy might interfere with the essential wild-type function of the
corresponding single copy gene, as such promoting fast removal of duplicated copies from the
genome. Here, we will leverage the availability of large collections of omics data, to pinpoint key
determinants underlying intolerance to duplication. We believe that obtaining a deep understanding
in a widespread evolutionary process such as gene duplication, will have wide-ranging applications
from understanding the role of duplication in adaptation to understanding how it can impact plant
fitness.