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      <i>Arabidopsis</i> ATXR2 deposits H3K36me3 at the promoters of <i>LBD</i> genes to facilitate cellular dedifferentiation

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      https://www.riss.kr/link?id=A107429422

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      <P><B>Epigenetic control of dedifferentiation</B></P><P>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 <I>et al</I>. found that the histone lysine methyltransferase ATXR2 promoted cellular dedifferentiation during callus formation in <I>Arabidopsis thaliana</I> by stimulating the expression of <I>LBD</I> genes, which encode transcription factors that promote cell cycle progression. ATXR2 localized to <I>LBD</I> 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.</P><P>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 <I>LATERAL ORGAN BOUNDARIES DOMAIN</I> (<I>LBD</I>) genes. The <I>LBD</I> genes of <I>Arabidopsis thaliana</I> are activated during cellular dedifferentiation to enhance the formation of callus. Leaf explants from <I>Arabidopsis atxr2</I> mutants exhibited a reduced ability to form callus and a substantial reduction in <I>LBD</I> gene expression. ATXR2 bound to the promoters of <I>LBD</I> genes and was required for the deposition of H3K36me3 at these promoters. ATXR2 was recruited to <I>LBD</I> promoters by the transcription factors AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19. Leaf explants from <I>arf7-1arf19-2</I> double mutants were defective in callus formation and showed reduced H3K36me3 accumulation at <I>LBD</I> promoters. Genetic analysis provided further support that ARF7 and ARF19 were required for the ability of ATXR2 to promote the expression of <I>LBD</I> genes. These observations indicate that the ATXR2-ARF-LBD axis is key for the epigenetic regulation of callus formation in <I>Arabidopsis</I>.</P>
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      <P><B>Epigenetic control of dedifferentiation</B></P><P>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 labor...

      <P><B>Epigenetic control of dedifferentiation</B></P><P>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 <I>et al</I>. found that the histone lysine methyltransferase ATXR2 promoted cellular dedifferentiation during callus formation in <I>Arabidopsis thaliana</I> by stimulating the expression of <I>LBD</I> genes, which encode transcription factors that promote cell cycle progression. ATXR2 localized to <I>LBD</I> 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.</P><P>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 <I>LATERAL ORGAN BOUNDARIES DOMAIN</I> (<I>LBD</I>) genes. The <I>LBD</I> genes of <I>Arabidopsis thaliana</I> are activated during cellular dedifferentiation to enhance the formation of callus. Leaf explants from <I>Arabidopsis atxr2</I> mutants exhibited a reduced ability to form callus and a substantial reduction in <I>LBD</I> gene expression. ATXR2 bound to the promoters of <I>LBD</I> genes and was required for the deposition of H3K36me3 at these promoters. ATXR2 was recruited to <I>LBD</I> promoters by the transcription factors AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19. Leaf explants from <I>arf7-1arf19-2</I> double mutants were defective in callus formation and showed reduced H3K36me3 accumulation at <I>LBD</I> promoters. Genetic analysis provided further support that ARF7 and ARF19 were required for the ability of ATXR2 to promote the expression of <I>LBD</I> genes. These observations indicate that the ATXR2-ARF-LBD axis is key for the epigenetic regulation of callus formation in <I>Arabidopsis</I>.</P>

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