Fitz Gerald Jonathan Nesbit, Hui Poh Shi, Berger Frédéric
Temasek Life Sciences Laboratory, 1 Research Link, National University of Singapore, Singapore.
Development. 2009 Oct;136(20):3399-404. doi: 10.1242/dev.036921.
During embryogenesis, Polycomb group (PcG) complexes deposit silencing histone modifications and target homeotic genes, which regulate the patterning of other transcription factors. This transcriptional network further maintains cell fate. However, genome-wide identification of histone modifications has suggested that PcG complexes might regulate genes other than those encoding transcription factors. In Arabidopsis, we show that PcG activity directly targets the actin regulator formin ARABIDOPSIS FORMIN HOMOLOGUE 5 (AtFH5). PcG activity silences the paternal allele of AtFH5, restricting its expression to the maternal allele. AtFH5 thus appears to be a new, maternally expressed imprinted gene. We further demonstrate that AtFH5 is responsible for morphological defects caused by the loss of PcG activity in the seed.
在胚胎发育过程中,多梳蛋白家族(PcG)复合物沉积沉默组蛋白修饰并靶向同源异型基因,这些基因调控其他转录因子的模式形成。这个转录网络进一步维持细胞命运。然而,全基因组范围的组蛋白修饰鉴定表明,PcG复合物可能调控除编码转录因子的基因之外的其他基因。在拟南芥中,我们发现PcG活性直接靶向肌动蛋白调节因子formin同源物拟南芥formin同源物5(AtFH5)。PcG活性使AtFH5的父本等位基因沉默,将其表达限制在母本等位基因。因此,AtFH5似乎是一个新的母本表达的印记基因。我们进一步证明,AtFH5是种子中PcG活性丧失导致的形态缺陷的原因。