Epigenetic role for the conserved Fe-S cluster biogenesis protein AtDRE2 in Arabidopsis thaliana
Epigenetic role for the conserved Fe-S cluster biogenesis protein AtDRE2 in Arabidopsis thaliana
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DOI：
10.1073/pnas.1404058111
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发表时间：
2014-09-16
影响因子：
11.1
通讯作者：
Kinoshita, Tetsu
中科院分区：
文献类型：
--
作者：
Buzas, Diana Mihaela;Nakamura, Miyuki;Kinoshita, Tetsu
在拟南芥的受精过程中，一个母体配子，即中央细胞，形成一个类似胎盘的组织，即胚乳。DNA糖基化酶DEMETER（DME）在受精前通过中央细胞中的碱基切除修复途径切除5-甲基胞嘧啶，在胚乳谱系（EDL）中的DNA复制中产生不对称DNA甲基化和母体基因表达的模式。中央细胞中的活性DNA去甲基化对于一组基因的EDL中的转录活性是必不可少的，包括FWA（FLOWESTERN WAGENINGEN）。铁硫簇辅因子的DME结合基序是其催化活性不可或缺的。我们使用FWA-GFP报告基因来寻找EDL中FWA-GFP母体激活缺陷的突变体，并分离出酵母Dre 2/人抗凋亡因子CIAPIN 1同源物的等位基因，该等位基因编码一种以前参与细胞质Fe-S生物发生途径（CIA）的酶，我们将其命名为atdre 2 -2。我们发现AtDRE 2在中央细胞中起作用，调节DME在EDL中母系激活的基因。此外，atdre 2 -2中的FWA-GFP表达缺陷在遗传上被维持DNA甲基转移酶MET 1中的突变部分抑制;相对于WT，atdre 2 -2种子中四个DME靶点的DNA甲基化水平增加。虽然atdre 2 -2与CIA突变体共享合子种子缺陷，但它也独特地表现出dme表型特征。这些结果表明，以前未鉴定的表观遗传功能的AtDRE 2可能是独立的CIA途径。
On fertilization in Arabidopsis thaliana, one maternal gamete, the central cell, forms a placenta-like tissue, the endosperm. The DNA glycosylase DEMETER (DME) excises 5-methylcytosine via the base excision repair pathway in the central cell before fertilization, creating patterns of asymmetric DNA methylation and maternal gene expression across DNA replications in the endosperm lineage (EDL). Active DNA demethylation in the central cell is essential for transcriptional activity in the EDL of a set of genes, including FLOWERING WAGENINGEN (FWA). A DME-binding motif for iron-sulfur (Fe-S) cluster cofactors is indispensable for its catalytic activity. We used an FWA-GFP reporter to find mutants defective in maternal activation of FWA-GFP in the EDL, and isolated an allele of the yeast Dre2/ human antiapoptotic factor CIAPIN1 homolog, encoding an enzyme previously implicated in the cytosolic Fe-S biogenesis pathway (CIA), which we named atdre2-2. We found that AtDRE2 acts in the central cell to regulate genes maternally activated in the EDL by DME. Furthermore, the FWA-GFP expression defect in atdre2-2 was partially suppressed genetically by a mutation in the maintenance DNA methyltransferase MET1; the DNA methylation levels at four DME targets increased in atdre2-2 seeds relative to WT. Although atdre2-2 shares zygotic seed defects with CIA mutants, it also uniquely manifests dme phenotypic hallmarks. These results demonstrate a previously unidentified epigenetic function of AtDRE2 that may be separate from the CIA pathway.