In the article, Penmetsa et al say:

Development of the Rhizobium-legume symbiosis is controlled by the host plant, although the underlying mechanisms have remained obscure. A mutant in the annual legume Medicago truncatula exhibits an increase of more than an order of magnitude in the number of persistent rhizobial infections. Physiological and genetic analyses indicate that this same mutation confers insensitivity to the plant hormone ethylene for multiple aspects of plant development, including nodulation. These data support the hypothesis that ethylene is a component of the signaling pathway controlling rhizobial infection of legumes.

The article states:

"In contrast to pathogenic plant-microbe interactions where persistent infection is correlated with cellular dysfunction and disease, compatible rhizobia trigger morphogenesis of a nodule organ and symbiotic nitrogen fixation on their legume host plant. Despite the beneficial aspects of this symbiosis, rhizobial infection is regulated by the plant host. One mechanism for controlling infection by compatible rhizobia, referred to as feedback inhibition of nodulation, is evidenced as a transient susceptibility to rhizobial infection in root hair cells. This transient susceptibility results in a narrow zone of infection and nodule differentiation. Plant mutants defective in feedback inhibition of nodulation continue to produce nodules from newly developed root tissue. A possible second mechanism for controlling rhizobial infection involves the early arrest of rhizobial infections within the nodulation zone; in fact, only a minority of rhizobial infections persist to colonize differentiating nodule tissue. Vasse et al. observed that many such infections arrest after infection structures (infection threads) penetrate one to several cells, and plant cells containing arrested infections often display characteristics of induced host defense mechanisms.

A possible clue to the physiology underlying rhizobial infection arrest comes from the observation that inhibitors of ethylene biosynthesis, such as aminoethoxyvinyl glycine (AVG), cause an increase in persistent rhizobial infections. Certain rhizobia produce rhizobitoxine, an analog of AVG, although roles in nodulation or regulation of ethylene synthesis in plants have not been demonstrated. Conversely, application of ethylene reduces nodulation in wild-type pea, and ethylene has been implicated as a second signal in the inhibition of nodulation by both light and nitrate. Thus, ethylene may provide an endogenous signal for regulation of rhizobial infection, and plant mutants with defects in production or transduction of the ethylene signal might be expected to have correspondingly altered infection phenotypes."

The authors go on to say:

"Our results support the hypothesis that ethylene is involved in controlling the persistence of rhizobial infection. Ethylene is known to control differentiation of root hair cells, the cell type infected by Rhizobium. This, endogenous ethylene may affect the persistence of rhizobial infection by controlling the formation of infectable root hair cells. Alternatively, ethylene may act as a diffusible signal for activation of mechanisms that arrest rhizobial infection. ACC is inhibitory to nodulation when applied after the initiation of rhizobial infection. Similarly, the ethylene biosynthesis inhibitor AVG can increase nodule number when applied after the initiation of infection. These observations are consistent with a model wherein endogenous ethylene acts subsequent to infection initiation and root hair differentiation.

If ethylene provides a signal for induction of infection arrest, then plant cells containing persistent Rhizobium infections either must avoid the ethylene signal or must be insensitive to the signal. Localized production of ethylene at sites of infection arrest could facilitate avoidance of ethylene by infections destined for nodule colonization. A model for cell-specific regulation of ethylene synthesis during root hair cell differentiation has been proposed in Arabidopsis. In wild- type M. truncatula, all rhizobial infections can be blocked by treatment with ACC as late as 48 hours after inoculation, indicating that infections destined for nodule conlonization are not inherently insensitive to ethylene. However, after macroscopic nodule primordial appear, nodulation is largely insensitive to exogenous ACC; thus, sustained rhizobial infections may acquire insensitivity to ethylene.

In plant-pathogen interactions, ethylene has been implicated as an endogenous cue for induction of host defense- related genes. Despite extensive correlative data, however, a causal role for ethylene in resistance to pathogens has not been established. In M. truncatula, the sickle mutation causes extensive developmental abnormalities and hyperinfection by Rhizobium, which indicates that skl1encodes a function common to both plant development and control of rhizobial infection."