背景：在成年哺乳动物脑中某些区域一生都会有神经元生成，包括在“室管膜下区”(SVZ)——在这个地方，神经前体细胞和固有星形细胞之间的相互作用会生成“成神经细胞”。
研究结论：在这项研究中，Anne Ferguson-Smith及其同事发现了同一个发育基因（即Dlk1）在神经前体细胞和星形细胞中的不同作用。该基因的基因产物（Notch ligand DLK1）有两个异构体(isoform)。其中一个是由星形细胞分泌的“诱导性生态位因子”，另一个是与膜结合在一起，神经干细胞本身需要它来对所分泌的DLK1做出反应。
随年龄的增长，印记(imprinting)发生了选择性变化，并在小鼠每种细胞类型中调控Dlk1的作用，从而调控神经的生成。干细胞环境中基因组印记的调控为后生调控（遗传外）增添了一个以前没有被认识到的元素。
生物探索推荐英文摘要
Postnatal loss of Dlk1 imprinting in stem cells and niche astrocytes regulates neurogenesis
Abstract：The gene for the atypical NOTCH ligand delta-like homologue 1 (Dlk1) encodes membrane-bound and secreted isoforms that function in several developmental processes in vitro and in vivo. Dlk1, a member of a cluster of imprinted genes, is expressed from the paternally inherited chromosome. Here we show that mice that are deficient in Dlk1have defects in postnatal neurogenesis in the subventricular zone: a developmental continuum that results in depletion of mature neurons in the olfactory bulb. We show that DLK1is secreted by niche astrocytes, whereas its membrane-bound isoform is present in neural stem cells (NSCs) and is required for the inductive effect of secreted DLK1 on self-renewal. Notably, we find that there is a requirement for Dlk1 to be expressed from both maternally and paternally inherited chromosomes. Selective absence of Dlk1 imprinting in both NSCs and niche astrocytes is associated with postnatal acquisition of DNA methylation at the germ-line-derived imprinting control region. The results emphasize molecular relationships between NSCs and the niche astrocyte cells of the microenvironment, identifying a signalling system encoded by a single gene that functions coordinately in both cell types. The modulation of genomic imprinting in a stem-cell environment adds a new level of epigenetic regulation to the establishment and maintenance of the niche, raising wider questions about the adaptability, function and evolution of imprinting in specific developmental contexts.
