PRC2 Represses Hormone-Induced Somatic Embryogenesis in Vegetative Tissue of Arabidopsis thaliana

• Published in: PLoS genetics Vol. 13; no. 1; p. e1006562
• Main Authors: Mozgová, Iva, Muñoz-Viana, Rafael, Hennig, Lars
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 17.01.2017; Public Library of Science (PLoS)
• Subjects: Arabidopsis - drug effects; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Biology and Life Sciences; Botanik; Botany; Colleges & universities; Embryonic development; Embryos; Flowers & plants; Funding; Gene expression; Gene Expression Regulation, Plant; Genetic aspects; Genomics; Indoleacetic Acids - pharmacology; Kinases; Phase transitions; Physiological aspects; Plant biology; Plant hormones; Plant Roots - growth & development; Plant Roots - metabolism; Plant Shoots - growth & development; Plant Shoots - metabolism; Plant Somatic Embryogenesis Techniques; Repressor Proteins - genetics; Repressor Proteins - metabolism; Research and Analysis Methods; Transcription factors; Sweden
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1006562

Many plant cells can be reprogrammed into a pluripotent state that allows ectopic organ development. Inducing totipotent states to stimulate somatic embryo (SE) development is, however, challenging due to insufficient understanding of molecular barriers that prevent somatic cell dedifferentiation. Here we show that Polycomb repressive complex 2 (PRC2)-activity imposes a barrier to hormone-mediated transcriptional reprogramming towards somatic embryogenesis in vegetative tissue of Arabidopsis thaliana. We identify factors that enable SE development in PRC2-depleted shoot and root tissue and demonstrate that the establishment of embryogenic potential is marked by ectopic co-activation of crucial developmental regulators that specify shoot, root and embryo identity. Using inducible activation of PRC2 in PRC2-depleted cells, we demonstrate that transient reduction of PRC2 activity is sufficient for SE formation. We suggest that modulation of PRC2 activity in plant vegetative tissue combined with targeted activation of developmental pathways will open possibilities for novel approaches to cell reprogramming.