Martin-Trillo Mar, Lázaro Ana, Poethig R Scott, Gómez-Mena Concepción, Piñeiro Manuel A, Martinez-Zapater Jose M, Jarillo Jose A
Departamento de Genética Molecular de Plantas, Centro Nacional de Biotecnología, C/ Darwin 3, Madrid 28049, Spain.
Development. 2006 Apr;133(7):1241-52. doi: 10.1242/dev.02301. Epub 2006 Feb 22.
We have characterized Arabidopsis esd1 mutations, which cause early flowering independently of photoperiod, moderate increase of hypocotyl length, shortened inflorescence internodes, and altered leaf and flower development. Phenotypic analyses of double mutants with mutations at different loci of the flowering inductive pathways suggest that esd1 abolishes the FLC-mediated late flowering phenotype of plants carrying active alleles of FRI and of mutants of the autonomous pathway. We found that ESD1 is required for the expression of the FLC repressor to levels that inhibit flowering. However, the effect of esd1 in a flc-3 null genetic background and the downregulation of other members of the FLC-like/MAF gene family in esd1 mutants suggest that flowering inhibition mediated by ESD1 occurs through both FLC-and FLC-like gene-dependent pathways. The ESD1 locus was identified through a map-based cloning approach. ESD1 encodes ARP6, a homolog of the actin-related protein family that shares moderate sequence homology with conventional actins. Using chromatin immunoprecipitation (ChIP) experiments, we have determined that ARP6 is required for both histone acetylation and methylation of the FLC chromatin in Arabidopsis.
我们已经对拟南芥esd1突变体进行了特征分析，这些突变体导致植株在不依赖光周期的情况下提前开花，下胚轴长度适度增加，花序节间缩短，以及叶片和花的发育改变。对开花诱导途径不同位点发生突变的双突变体进行表型分析表明，esd1消除了携带FRI活性等位基因的植株以及自主途径突变体中由FLC介导的晚花表型。我们发现ESD1是FLC阻遏物表达至抑制开花水平所必需的。然而，esd1在flc - 3无效遗传背景中的作用以及esd1突变体中FLC样/MAF基因家族其他成员的下调表明，ESD1介导的开花抑制是通过FLC和FLC样基因依赖的途径发生的。ESD1基因座是通过基于图谱的克隆方法鉴定出来的。ESD1编码ARP6，它是肌动蛋白相关蛋白家族的一个同源物，与传统肌动蛋白具有中等程度的序列同源性。通过染色质免疫沉淀（ChIP）实验，我们确定ARP6是拟南芥中FLC染色质组蛋白乙酰化和甲基化所必需的。
