The Spen Family Protein FPA Controls Alternative Cleavage and Polyadenylation of RNA
The Spen Family Protein FPA Controls Alternative Cleavage and Polyadenylation of RNA
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DOI：
10.1016/j.devcel.2009.12.009
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发表时间：
2010-02-16
影响因子：
11.8
通讯作者：
Simpson, Gordon G.
中科院分区：
文献类型：
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作者：
Hornyik, Csaba;Terzi, Lionel C.;Simpson, Gordon G.
spen家族蛋白FPA是开花时间控制所必需的，并且与RNA沉默有关。FPA执行这些功能的机制尚不清楚。我们报告了FPA在控制mRNA 3'末端形成中的活性鉴定。我们表明，FPA功能冗余FCA，另一种RNA结合蛋白，控制开花和RNA沉默，控制表达的替代聚腺苷酸化反义RNA在基因座编码的花阻遏物FLC。此外，我们发现，在上游RNA聚合酶II依赖基因的缺陷3'端的形成解释了明显的fpa突变体中的AtSN 1 retroelement的去阻遏。转录通读解释了fpa突变体中AtSN1处DNA甲基化和siRNA丰度没有变化，这可能解释了与染色质修饰无关的表观遗传转变的其他例子。
The spen family protein FPA is required for flowering time control and has been implicated in RNA silencing. The mechanism by which FPA carries out these functions is unknown. We report the identification of an activity for FPA in controlling mRNA 3' end formation. We show that FPA functions redundantly with FCA, another RNA binding protein that controls flowering and RNA silencing, to control the expression of alternatively polyadenylated antisense RNAs at the locus encoding the floral repressor FLC. In addition, we show that defective 3' end formation at an upstream RNA polymerase II-dependent gene explains the apparent derepression of the AtSN1 retroelement in fpa mutants. Transcript readthrough accounts for the absence of changes in DNA methylation and siRNA abundance at AtSN1 in fpa mutants, and this may explain other examples of epigenetic transitions not associated with chromatin modification.