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Epigenetic-driven Synergistic and Antagonistic regulation on Transposable Elements Carried Out by HDA6 and LDL1/2 [WGBS]

ABSTRACT: Histone deacetylases (HDAs) are evolutionally conserved enzymes and often form a multiprotein complex with histone Lysine-Specific Demethylase 1 (LSD1) to play central roles in epigenetic silencing in yeast and animals. In Arabidopsis, either HDA6 or LSD1-LIKE 1 and 2 (LDL1/2) are known to silence transposable element (TE), but their joint effect remains unexplored. Here, we revealed the individual and joint effects of HDA6 and LDL1/2 carefully by examining the transcriptomes, the genome wide distribution of H3Ac, H3K4me2, and DNA methylation in wildtype and mutants (hda6, ldl1/2 and hda6/ldl1/2). We found that HDA6 silenced 517 TEs by itself, LDL1/2 silenced 2 TEs alone and HDA6 silenced 15 TEs in cooperation with LDL1/2; suggesting that HDA6 has a stronger impact on TE silencing than LDL1/2; the effect of HDA6 is mostly independent of LDL1/2 whereas most LDL1/2 effect requires HDA6. Also, we observed that the expression of TE showed clear synergistic (enhanced de-repression in hda6/ldl1/2) and antagonistic (lower de-repression in hda6/ldl1/2) effects at different sets of TEs. Further analysis showed that the TEs targeted by either of the two effects exhibited totally different epigenome patterns.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE216787 | GEO | 2024/11/06

REPOSITORIES: GEO

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Epigenetic-driven Synergistic and Antagonistic regulation on Transposable Elements Carried Out by HDA6 and LDL1/2 [ncRNA-Seq]

Project description:Histone deacetylases (HDAs) are evolutionally conserved enzymes and often form a multiprotein complex with histone Lysine-Specific Demethylase 1 (LSD1) to play central roles in epigenetic silencing in yeast and animals. In Arabidopsis, either HDA6 or LSD1-LIKE 1 and 2 (LDL1/2) are known to silence transposable element (TE), but their joint effect remains unexplored. Here, we revealed the individual and joint effects of HDA6 and LDL1/2 carefully by examining the transcriptomes, the genome wide distribution of H3Ac, H3K4me2, and DNA methylation in wildtype and mutants (hda6, ldl1/2 and hda6/ldl1/2). We found that HDA6 silenced 517 TEs by itself, LDL1/2 silenced 2 TEs alone and HDA6 silenced 15 TEs in cooperation with LDL1/2; suggesting that HDA6 has a stronger impact on TE silencing than LDL1/2; the effect of HDA6 is mostly independent of LDL1/2 whereas most LDL1/2 effect requires HDA6. Also, we observed that the expression of TE showed clear synergistic (enhanced de-repression in hda6/ldl1/2) and antagonistic (lower de-repression in hda6/ldl1/2) effects at different sets of TEs. Further analysis showed that the TEs targeted by either of the two effects exhibited totally different epigenome patterns.

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