Research ArticleEpigenetics

Arabidopsis ATXR2 deposits H3K36me3 at the promoters of LBD genes to facilitate cellular dedifferentiation

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Sci. Signal.  28 Nov 2017:
Vol. 10, Issue 507, eaan0316
DOI: 10.1126/scisignal.aan0316

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Epigenetic control of dedifferentiation

Some plant cells can dedifferentiate to form a mass of pluripotent cells called callus. This not only occurs at wound sites but can also be induced by specific laboratory culture conditions. Lee et al. found that the histone lysine methyltransferase ATXR2 promoted cellular dedifferentiation during callus formation in Arabidopsis thaliana by stimulating the expression of LBD genes, which encode transcription factors that promote cell cycle progression. ATXR2 localized to LBD promoters, stimulated the accumulation of lysine-methylated histones at these promoters, and was recruited to the promoters by the transcription factors ARF7 and ARF19. Epigenetic regulation is a key mechanism controlling cell potency and differentiation in both plants and animals, and these findings contribute to understanding the remarkable developmental plasticity of plant cells.

Abstract

Cellular dedifferentiation, the transition of differentiated somatic cells to pluripotent stem cells, ensures developmental plasticity and contributes to wound healing in plants. Wounding induces cells to form a mass of unorganized pluripotent cells called callus at the wound site. Explanted cells can also form callus tissues in vitro. Reversible cellular differentiation-dedifferentiation processes in higher eukaryotes are controlled mainly by chromatin modifications. We demonstrate that ARABIDOPSIS TRITHORAX-RELATED 2 (ATXR2), a histone lysine methyltransferase that promotes the accumulation of histone H3 proteins that are trimethylated on lysine 36 (H3K36me3) during callus formation, promotes early stages of cellular dedifferentiation through activation of LATERAL ORGAN BOUNDARIES DOMAIN (LBD) genes. The LBD genes of Arabidopsis thaliana are activated during cellular dedifferentiation to enhance the formation of callus. Leaf explants from Arabidopsis atxr2 mutants exhibited a reduced ability to form callus and a substantial reduction in LBD gene expression. ATXR2 bound to the promoters of LBD genes and was required for the deposition of H3K36me3 at these promoters. ATXR2 was recruited to LBD promoters by the transcription factors AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19. Leaf explants from arf7-1arf19-2 double mutants were defective in callus formation and showed reduced H3K36me3 accumulation at LBD promoters. Genetic analysis provided further support that ARF7 and ARF19 were required for the ability of ATXR2 to promote the expression of LBD genes. These observations indicate that the ATXR2-ARF-LBD axis is key for the epigenetic regulation of callus formation in Arabidopsis.

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