Role of the Differentiation of Root Epidermal Cells in Nod Factor (from Rhizobium meliloti)-Induced Root-Hair Depolarization of Medicago sativa

Kurkdjian, Armen

doi:10.1104/pp.107.3.783

Cited by 75 publications

(45 citation statements)

References 22 publications

(21 reference statements)

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“…Early responses of root hairs of alfalfa to Nod factors are cytosolic pH changes (Felle et al, 1996) and membrane depolarizations (Ehrhardt et al, 1992;Felle et al, 1995;Kurkdjian, 1995). A more delayed response of alfalfa root hairs, appearing 10 min after Nod factor application, is the intracellular calcium spiking (Ehrhardt et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The role of ion fluxes in Nod factor signalling in Medicago sativa

et al. 1998

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SummaryUsing ion-selective microelectrodes, the basis of Nod factor-induced changes in the plasma membrane potential was analysed by measuring the extracellular free concentrations of Ca 2⍣ , K ⍣ , H ⍣ and Cl -in the root hair zone of alfalfa. After addition of the Rhizobium meliloti Nod factor NodRm-IV(C16:2,S) at a concentration of 0.1 µM, a decrease in [Ca 2⍣ ] was observed first, which was followed after a few seconds by an increase of [Cl -], by an alkalinization, and then by a delayed increase of [K ⍣ ], all of which were transient changes. Simultaneously with the appearance of Cl -ions in the root hair zone, a decrease in cytosolic [Cl -] was measured. It was concluded that the depolarization was caused by temporary short-circuiting of the proton pump through the rapid release of Cl -ions along their steep electrochemical gradient. Since under resting conditions the driving force for K ⍣ ions was inwardly directed, their release was delayed until their driving force was inverted. This indicates that K ⍣ serves as a charge balance that eventually stops depolarization and initiates repolarization. Since the decrease in [Ca 2⍣ ] was observed seconds before the increase in [Cl -] and the depolarization, it is argued that Ca 2⍣ entering into the cell does not cause the depolarization directly, but might initiate it by triggering the activation of an anion channel that then releases the chloride ions. The observations that the Ca 2⍣ ionophore A23187 mimicks the Nod factor response, and that the Ca 2⍣ channel antagonist nifedipine inhibits this response, support the idea that Ca 2⍣ plays a primary role in the transduction of the Nod signal in alfalfa.

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Section: Introductionmentioning

confidence: 99%

The role of ion fluxes in Nod factor signalling in Medicago sativa

et al. 1998

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“…Membrane depolarization and ion fluxes (22)(23)(24)(25)(26) occur in alfalfa root hairs within 1-5 minutes after NF application (21). Three to six minutes later, periodic oscillation of the cytoplasmic calcium levels, or calcium spiking, begins (27).…”

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Genetic analysis of calcium spiking responses in nodulation mutants of Medicago truncatula

Wais

Galera

Oldroyd

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

256

239

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The symbiotic interaction between Medicago truncatula and Sinorhizobium meliloti results in the formation of nitrogen-fixing nodules on the roots of the host plant. The early stages of nodule formation are induced by bacteria via lipochitooligosaccharide signals known as Nod factors (NFs). These NFs are structurally specific for bacterium-host pairs and are sufficient to cause a range of early responses involved in the host developmental program. Early events in the signal transduction of NFs are not well defined. We have previously reported that Medicago sativa root hairs exposed to NF display sharp oscillations of cytoplasmic calcium ion concentration (calcium spiking). To assess the possible role of calcium spiking in the nodulation response, we analyzed M. truncatula mutants in five complementation groups. Each of the plant mutants is completely Nod؊ and is blocked at early stages of the symbiosis. We defined two genes, DMI1 and DMI2, required in common for early steps of infection and nodulation and for calcium spiking. Another mutant, altered in the DMI3 gene, has a similar mutant phenotype to dmi1 and dmi2 mutants but displays normal calcium spiking. The calcium behavior thus implies that the DMI3 gene acts either downstream of calcium spiking or downstream of a common branch point for the calcium response and the later nodulation responses. Two additional mutants, altered in the NSP and HCL genes, which show root hair branching in response to NF, are normal for calcium spiking. This system provides an opportunity to use genetics to study ligand-stimulated calcium spiking as a signal transduction event.

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“…Nod factors are responsible for the induction of a series of responses in the host, such as depolarization of the root hair plasma membrane (Ehrhardt et al, 1992;Felle et al, 1995;Kurkdjian, 1995), alkalinization of root hair cells (Felle et al, 1996), oscillation of the free cytoplasmic calcium concentration in root hairs (Ehrhardt et al, 1996), induction of root hair deformation (Lerouge et al, 1990;Spaink et al, 1991;Heidstra et al, 1994), induction of early nodulin (ENOD) genes (Horvath et al, 1993;Journet et al, 1994), and mitotic reactivation of cortical cells (Spaink et al, 1991). The latter is the beginning of the formation of primordia which, upon infection by rhizobia, develop into root nodules.…”

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confidence: 99%

Sym2 of Pea Is Involved in a Nodulation Factor-Perception Mechanism That Controls the Infection Process in the Epidermis

et al. 1997

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Since the induction of the early nodulin gene FNODl2 in the epidermis and the formation of a nodule primordium in the inner cortex were not affected, we conclude that more than one Nod factor-perception mechanism is active. Furthermore, we show that symp-mediated control of infection-thread growth was affected by the bacterial nodulation gene nodO.Rhizobium bacteria have the ability to induce a developmental process in the root of leguminous plants that results in the formation of a new organ, the root nodule. These new organs create the environment in which the bacteria fix nitrogen to ammonia, which can subsequently be utilized by the plant.The symbiotic interaction of Rhizobium sp. bacteria and leguminous plants is set in motion by the exchange of signal molecules. Plant-excreted flavonoids induce the expression of bacterial nodulation (nod) genes, which are responsible for the synthesis of specific lipochitin oligosaccharides, named Nod factors (Lerouge et al., 1990;Spaink et al., 1991). Nod factors consist of a tetra-or pentameric N-acetylglucosamine backbone with a fatty acyl chain at the nonreducing terminal sugar moiety. Substituents at the terminal sugar residues and the structure of the acyl chain determine the differences in biological activity and host specificity (for review, see Carlson et al., 1994).The role of Nod factor structure in host specificity is exemplified as follows: alfalfa (Medicago sativa) belongs to the cross-inoculation group that can be nodulated by Rhi- zobium meliloti, which produces Nod factors with a sulfate group at the reducing sugar (Lerouge et al., 1990). In contrast, pea (Pisum sativum) is nodulated by Rhizobium leguminosarum bv viciae, which produces Nod factors that lack a substitution at that position (Spaink et al., 1991). When the host-specificity genes nodH, nodP, and nodQ, which are responsible for the sulfation of the Nod factors in R. meliloti, are introduced into R. leguminosarum bv viciae these bacteria can now induce noninfected, nodule-like structures on alfalfa but concomitantly lose their ability to nodulate pea and vetch (Faucher et al

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Role of the Differentiation of Root Epidermal Cells in Nod Factor (from Rhizobium meliloti)-Induced Root-Hair Depolarization of Medicago sativa

Cited by 75 publications

References 22 publications

The role of ion fluxes in Nod factor signalling in Medicago sativa

The role of ion fluxes in Nod factor signalling in Medicago sativa

Genetic analysis of calcium spiking responses in nodulation mutants of Medicago truncatula

Sym2 of Pea Is Involved in a Nodulation Factor-Perception Mechanism That Controls the Infection Process in the Epidermis

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