An epiallele of a gene encoding a PfkB-type carbohydrate kinase affects plant architecture in maize.

Plant architecture greatly contributes to grain yield, but the epigenetic regulation of plant architecture remains elusive. Here, we identified the maize (Zea mays L.) mutant plant architecture 1 (par1), which shows reduced plant height, shorter and narrower leaves, and larger leaf angles than the wild type. Interestingly, par1 is an epiallele harboring a de novo CACTA insertion in the intron of the Par1 gene. High DNA methylation levels of the CACTA insertion are associated with strong Par1 expression and normal phenotypes. In contrast, low DNA methylation levels of this insertion are associated with weak Par1 expression and a mutant-like phenotype. The Par1 gene encodes a PfkB-type carbohydrate kinase that converts nucleosides to nucleoside monophosphates both in vitro and in vivo. Additional analyses showed that genes differentially expressed in the par1 mutant are enriched in jasmonic acid (JA) metabolism, and levels of JA metabolites were significantly higher in the mutant than in the wild type. Treatment with either nucleoside monophosphates or a synthetic inhibitor of JA biosynthesis reduced JA levels and partially rescued the mutant phenotype. In summary, we identified an epiallele of a gene encoding a PfkB-type carbohydrate kinase that might affect nucleoside monophosphate and JA levels, thus affecting maize growth.