Institut für Pflanzengenetik, Leibniz Universität Hannover, D-30419 Hannover, Germany.
Plant Physiol. 2012 Aug;159(4):1671-85. doi: 10.1104/pp.112.195990. Epub 2012 May 31.
The formation of root nodules and arbuscular mycorrhizal (AM) roots is controlled by a common signaling pathway including the calcium/calmodulin-dependent kinase Doesn't Make Infection3 (DMI3). While nodule initiation by lipochitooligosaccharide (LCO) Nod factors is well characterized, diffusible AM fungal signals were only recently identified as sulfated and nonsulfated LCOs. Irrespective of different outcomes, the perception of symbiotic LCOs in Medicago truncatula is mediated by the LysM receptor kinase M. truncatula Nod factor perception (MtNFP). To shed light on transcriptional responses toward symbiotic LCOs and their dependence on MtNFP and Ca(2+) signaling, we performed genome-wide expression studies of wild-type, Nod-factor-perception mutant1, and dmi3 mutant roots challenged with Myc- and Nod-LCOs. We show that Myc-LCOs lead to transient, quick responses in the wild type, whereas Nod-LCOs require prolonged incubation for maximal expression activation. While Nod-LCOs are most efficient for an induction of persistent transcriptional changes, sulfated Myc-LCOs are less active, and nonsulfated Myc-LCOs display the lowest capacity to activate and sustain expression. Although all symbiotic LCOs up-regulated a common set of genes, discrete subsets were induced by individual LCOs, suggesting common and specific functions for these in presymbiotic signaling. Surprisingly, even sulfated fungal Myc-LCOs and Sinorhizobium meliloti Nod-LCOs, having very similar structures, each elicited discrete subsets of genes, while a mixture of both Myc-LCOs activated responses deviating from those induced by single treatments. Focusing on the precontact phase, we identified signaling-related and transcription factor genes specifically up-regulated by Myc-LCOs. Comparative gene expression studies in symbiotic mutants demonstrated that transcriptional reprogramming by AM fungal LCOs strictly depends on MtNFP and largely requires MtDMI3.
根瘤和丛枝菌根（AM）根的形成受一个共同的信号通路控制，包括钙/钙调蛋白依赖性激酶 Doesn't Make Infection3（DMI3）。虽然脂寡糖（LCO）结瘤因子诱导的根瘤起始已经得到很好的描述，但可扩散的 AM 真菌信号最近才被确定为硫酸化和非硫酸化的 LCO。尽管结果不同，但 Medicago truncatula 中共生 LCO 的感知是由 LysM 受体激酶 M. truncatula Nod factor perception（MtNFP）介导的。为了阐明对共生 LCO 的转录反应及其对 MtNFP 和 Ca(2+)信号的依赖性，我们对野生型、结瘤因子感知突变体 1 和 dmi3 突变体的根进行了全基因组表达研究，这些根受到 Myc-和 Nod-LCO 的挑战。我们表明，Myc-LCO 会导致野生型根的短暂、快速反应，而 Nod-LCO 需要长时间孵育才能最大程度地激活表达。虽然 Nod-LCO 对持久转录变化的诱导最有效，但硫酸化 Myc-LCO 活性较低，非硫酸化 Myc-LCO 激活和维持表达的能力最低。尽管所有共生 LCO 都上调了一组共同的基因，但单个 LCO 诱导了不同的基因子集，这表明这些基因在共生信号转导中具有共同和特定的功能。令人惊讶的是，即使是硫酸化的真菌 Myc-LCO 和 Sinorhizobium meliloti Nod-LCO，它们的结构非常相似，每个都诱导了不同的基因子集，而两种 Myc-LCO 的混合物则激活了与单一处理诱导的反应不同的反应。我们关注预接触阶段，鉴定了由 Myc-LCO 特异性上调的信号转导相关和转录因子基因。在共生突变体中的比较基因表达研究表明，AM 真菌 LCO 引起的转录重编程严格依赖于 MtNFP，并且在很大程度上需要 MtDMI3。
