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在短日照 7(ESD7)中编码 DNA 聚合酶 ε 的催化亚基,并通过涉及表观遗传基因沉默的机制来抑制开花。

EARLY IN SHORT DAYS 7 (ESD7) encodes the catalytic subunit of DNA polymerase epsilon and is required for flowering repression through a mechanism involving epigenetic gene silencing.

机构信息

CBGP (INIA-UPM) Departamento de Biotecnología, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Campus de Montegancedo, Madrid 28223, Spain.

出版信息

Plant J. 2010 Feb;61(4):623-36. doi: 10.1111/j.1365-313X.2009.04093.x. Epub 2009 Nov 26.

DOI:10.1111/j.1365-313X.2009.04093.x
PMID:19947980
Abstract

We have characterized a mutation affecting the Arabidopsis EARLY IN SHORT DAYS 7 (ESD7) gene encoding the catalytic subunit of DNA polymerase epsilon (epsilon), AtPOL2a. The esd7-1 mutation causes early flowering independently of photoperiod, shortened inflorescence internodes and altered leaf and root development. esd7-1 is a hypomorphic allele whereas knockout alleles displayed an embryo-lethal phenotype. The esd7 early flowering phenotype requires functional FT and SOC1 proteins and might also be related to the misregulation of AG and AG-like gene expression found in esd7. Genes involved in the modulation of chromatin structural dynamics, such as LHP1/TFL2 and EBS, which negatively regulate FT expression, were found to interact genetically with ESD7. In fact a molecular interaction between the carboxy terminus of ESD7 and TFL2 was demonstrated in vitro. Besides, fas2 mutations suppressed the esd7 early flowering phenotype and ICU2 was found to interact with ESD7. Discrete regions of the chromatin of FT and AG loci were enriched in activating epigenetic marks in the esd7-1 mutant. We concluded that ESD7 might be participating in processes involved in chromatin-mediated cellular memory.

摘要

我们对拟南芥 EARLY IN SHORT DAYS 7(ESD7)基因的一个突变进行了鉴定,该基因编码 DNA 聚合酶 epsilon(epsilon)的催化亚基,AtPOL2a。esd7-1 突变导致开花提前,独立于光周期,缩短了花序节间,改变了叶片和根系的发育。esd7-1 是一个功能降低的等位基因,而缺失突变体表现出胚胎致死表型。esd7 早花表型需要功能正常的 FT 和 SOC1 蛋白,并且可能还与 esd7 中发现的 AG 和 AG 样基因表达的失调有关。参与染色质结构动力学调节的基因,如负调控 FT 表达的 LHP1/TFL2 和 EBS,被发现与 ESD7 在遗传上相互作用。事实上,在体外证明了 ESD7 的羧基末端与 TFL2 之间存在分子相互作用。此外,fas2 突变抑制了 esd7 早花表型,并且发现 ICU2 与 ESD7 相互作用。在 esd7-1 突变体中,FT 和 AG 基因座的染色质的离散区域富含激活的表观遗传标记。我们得出结论,ESD7 可能参与了涉及染色质介导的细胞记忆的过程。

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