Miwa Hiroki, Sun Jongho, Oldroyd Giles E D, Downie J Allan
John Innes Centre, Colney Lane, Norwich NR4 7UH, UK.
Mol Plant Microbe Interact. 2006 Aug;19(8):914-23. doi: 10.1094/MPMI-19-0914.
Nodulation (Nod)-factor signaling molecules are essential for rhizobia to initiate the nitrogen-fixing symbiotic interaction with legumes. Using a dual dye ratiometric calcium imaging technique, we have shown that 10 nM Nod factor added to roots of Lotus japonicus seedlings induces an intracellular calcium increase (calcium flux) that precedes oscillations in intracellular calcium (calcium spiking). The calcium flux was not observed with 1 or 0.1 nM Nod factor, which did induce calcium spiking. The calcium flux was variable in timing of initiation and duration and was observed in approximately half of the root hairs examined. Representatives from 11 complementation groups of symbiotically defective mutants were analyzed for the calcium flux. Mutants from four groups (sym6, ccamk, sym35, and nin) which retained calcium spiking all showed a normal calcium flux. Two classes of mutants (nfr1 and nfr5) lacked both calcium influx and calcium spiking, whereas five classes of mutants (symRK, castor, pollux, nup133, and sym24) defective for calcium spiking retained a calcium flux. There was no correlation between calcium spiking and induction of root hair deformation by Nod factor. We propose that increased bacterial numbers within infection foci in root hairs leads to accumulation of Nod factor to sufficient levels to activate the calcium flux, and this may drive infection thread growth.
结瘤(Nod)因子信号分子对于根瘤菌启动与豆科植物的固氮共生相互作用至关重要。使用双染料比率钙成像技术,我们发现添加到日本百脉根幼苗根部的10 nM Nod因子会诱导细胞内钙增加(钙通量),这先于细胞内钙振荡(钙尖峰)。1 nM或0.1 nM Nod因子未观察到钙通量,它们确实诱导了钙尖峰。钙通量在起始时间和持续时间上是可变的,并且在大约一半被检查的根毛中观察到。对来自11个共生缺陷突变体互补组的代表进行了钙通量分析。来自四组(sym6、ccamk、sym35和nin)保留钙尖峰的突变体均显示出正常的钙通量。两类突变体(nfr1和nfr5)既缺乏钙内流也缺乏钙尖峰,而五类对钙尖峰有缺陷的突变体(symRK、蓖麻、花粉管、nup133和sym24)保留了钙通量。钙尖峰与Nod因子诱导的根毛变形之间没有相关性。我们提出,根毛感染部位内细菌数量的增加导致Nod因子积累到足以激活钙通量的水平,这可能驱动感染丝生长。