Bacterial infection of legume root nodule primordia is tightly controlled and closely synchronised with the progressing primordial cell divisions and organ development. This coordination has long prevented the separation of the molecular mechanisms underlying these two developmental processes and has limited the identification of plant genes controlling the bacterial infection process, but not nodule organogenesis. As a consequence the genetics of infection thread development is fairly undescribed and among the genes defining this pathway, only Nap1, Pir1 and Cerberus have so far been characterised at the molecular level (Yano et al. 2009; Yokota et al. 2009). Most of the Nod-factor signal transduction pathway mutants mentioned above suffer from simultaneous absence or severe impairment of both organ formation and infection thread development. This has made the dissection of direct and indirect mutational impact on the two processes very difficult. However, combining gain of function mutations with loss of function mutations in trangenes or double, triple and quadruple mutants opened new possibilities for assessing the role of the genes inactivated by loss of function mutations (Hayashi et al. 2010; Madsen et al. 2010). The autoactive versions of CCaMK and LHK1 encoded by the snf1 or snf2 alleles, respectively, were key to this approach. Both snf mutants form spontaneous nodules independent of bacterial presence or infection (Tirichine et al. 2006, 2007). Exploiting the ability of these gain of function alleles to activate the developmental processes from downstream positions defined the backbones of two parallel pathways facilitating (1) infection thread formation and (2) root nodule organogenesis (Hayashi et al. 2010; Madsen et al. 2010). Furthermore, the approach revealed cross-signalling functions between these two pathways for some of the examined genes. It was shown that the LRR receptor kinase SYMRK, the nucleoporins NUP133 and NUP85 and the cation channels CASTOR and POLLUX, all involved in signal transduction down-stream of Nod-factor perception, were dispensable for root hair infection thread development and invasion of nodule primordia in a snf1 genetic background. Since inacti-vation of the LRR receptor kinase SYMRK, the nucleoporins and the cation channels results in absence of calcium spiking (Miwa et al. 2006), these results further indicate that calcium spiking, apart from activation of CCaMK, is dispensable for infection thread formation (Madsen et al. 2010).
On the other hand, the NFR1 and NFR5 Nod-factor receptors were required for root hair infection thread initiation, and the NAP1 and PIR1 proteins mediating actin rearrangement together with the CERBERUS ubiquitin E3 ligase were required for infection thread progression (Madsen et al. 2010). These observations support an early branching of the Nod-factor signal transduction pathway. The NIN, NSP1 and NSP2 transcriptional regulators were required for both infection thread formation and organogenesis, supporting a simultaneous or sequential role of these proteins in both of these processes. The absence of infection in cyclops snf1 double mutants (Madsen et al. 2010) along with the reported protein-protein interaction between CCaMK and CYCLOPS (Messinese et al. 2007; Yano et al. 2008), indicated a role for CYCLOPS in cross signalling between the organogenic and infection pathways (Madsen et al. 2010).
Nod-factor induced root hair deformation, Ca2+ influx and Ca2+ spiking preceding infection thread formation all require the initial NFR1 and NFR5 mediated perception event (Radutoiu et al. 2003; Miwa et al. 2006). The relation between these phenomena is however not yet fully clarified. Ca2+ spiking following application of Nod-factors is not required for root hair deformation (Miwa et al. 2006)
and the presumed Ca2+ dependent activation of CCaMK as mimicked by the snf1 mutation seems insufficient for root hair infection thread formation (Madsen et al. 2010). Separation of root hair deformation and influx was also implied by the observation that three orders of magnitude lower Nod-factor concentration was sufficient to induce root hair deformation compared with that required for the Ca2+ influx (Radutoiu et al. 2003; Miwa et al. 2006). This could suggest that the NFR receptor dependent Ca2+ influx observed in root hairs at high Nod-factor concentration may be a prerequisite for root hair infection thread formation. So far these observations are consistent with the Ca2+ responses occurring in parallel with the NAP1 and PIR1 induced cytoskeletal changes, although the possibility of a low level or localised change in Ca2+ cannot be excluded.
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