The sudden nature of an injury demands a rapid regenerative response, which suggests the involvement of molecular mechanisms that can effect global changes in the genomic architecture of a cell—such as the result of epigenetic modifications. As you learned in Chapter 3 (see Figure 3.10), the epigenetic state of a cell refers to how accessible chromatin is for gene expression, and epigenetic changes are largely accomplished through alterations in DNA methylation and modification to histones (Xu and Huang 2014; Ikeuchi et al. 2015a). Prior to injury, epigenetic marks are in place to maintain cell differentiation while also repressing multipotency and regenerative abilities. For instance, pharmacological inhibition or loss of histone deacetylases in Arabidopsis thaliana converts differentiated leaves and shoots into embryonic-like structures (Tanaka et al. 2008). As in animals, DNA methylation often yields an opposite effect on chromatin accessibility as compared with histone acetylation. Importantly, reduced methylation due to the loss of DNA METHYLTRANSFERASE1 (MET1) has been shown to enhance shoot regeneration (Li et al. 2011).
Among the most well characterized groups of epigenetic histone modifiers are the Polycomb proteins, which play a conserved role in gene silencing across eukaryotic life (Golbabapour et al. 2013; Derkacheva and Hennig 2014; Liu et al. 2015). In A. thaliana, loss of POLYCOMB REPRESSIVE COMPLEX2 (PRC2)[i] function causes the reprogramming of differentiated root hair cells into a proliferative callus and embryonic-like structures (Figure 1; Ikeuchi et al. 2015b). PRC2 normally functions by trimethylating lysine 27 of histone H3 (H3K27me3), which serves to repress the expression of several known regulators of reprogramming and regeneration, such as WIND3, LEC2, STM, WOX5 and 11, and most important, WUS (Ikeuchi et al. 2016). Taken together, these studies demonstrate that epigenetic modifications that lead to a more euchromatic architecture (more acetylation and less methylation) are important mechanisms to promote the dedifferentiation of cells toward a more regenerative state.
[i] Loss of POLYCOMB REPRESSIVE COMPLEX2 in this report was determined by examining a double mutant for EMBRYONIC FLOWER2-3 and VERNALIZATION2-1, which are two of at least six proteins that form this repressive complex.
Derkacheva M., L. Hennig. 2014. Variations on a theme: Polycomb group proteins in plants. J Exp Bot 65(10):2769-84.
Golbabapour S., M. A. Majid, P. Hassandarvish, M. Hajrezaie, M. A. Abdulla, A. H. Hadi. 2013. Gene silencing and Polycomb group proteins: an overview of their structure, mechanisms and phylogenetics. OMICS. 17(6):283-96.
Ikeuchi M., A. Iwase, B. Rymen, H. Harashima, M. Shibata, M. Ohnuma, C. Breuer, A. K. Morao, M. de Lucas, L. De Veylder, J. Goodrich, S. M. Brady, F. Roudier, K. Sugimoto. 2015. PRC2 represses dedifferentiation of mature somatic cells in Arabidopsis. Nat Plants 1:15089.
Ikeuchi M., Y. Ogawa, A. Iwase, K. Sugimoto. 2016. Plant regeneration: cellular origins and molecular mechanisms. Development 143(9):1442-51.
Ikeuchi, M., A. Iwase, and K. Sugimoto. 2015. Control of plant cell differentiation by histone modification and DNA methylation. Curr Opin Plant Biol 28, 60–67.
Liu X., J. Yang, N. Wu, R. Song, H. Zhu. 2015. Evolution and Coevolution of PRC2 Genes in Vertebrates and Mammals. Adv Protein Chem Struct Biol 101:125-48.
Tanaka, M., A. Kikuchi, and H. Kamada. 2008. The Arabidopsis histone deacetylases HDA6 and HDA19 contribute to the repression of embryonic properties after germination. Plant Physiol 146, 149-161.
Xu, L., and H. Huang. 2014. Genetic and epigenetic controls of plant regeneration. Curr Top Dev Biol 108, 1–33.