The soybean gene GmHsp22.4 is involved in the resistance response to Meloidogyne javanica in Arabidopsis thaliana.

BACKGROUND: Small heat shock proteins (sHSPs) belong to the class of molecular chaperones that respond to biotic and abiotic stresses in plants. A previous study has showed strong induction of the gene GmHsp22.4 in response to the nematode Meloidogyne javanica in a resistant soybean genotype, while repression in a susceptible one. This study aimed to investigate the functional involvement of this small chaperone in response to M. javanica in Arabidopsis thaliana. First, it was evaluated the activation of the promoter region after the nematode inoculation, and the occurrence of polymorphisms between resistant and susceptible re-sequenced soybean accessions. Then functional analysis using A. thaliana lines overexpressing the soybean GmHsp22.4 gene, and knocked-out mutants were challenged with M. javanica infestation. RESULTS: High expression levels of the GFP gene marker in transformed A. thaliana plants revealed that the promoter region of GmHsp22.4 was strongly activated after nematode inoculation. Moreover, the multiplication of the nematode was significantly reduced in plants overexpressing GmHsp22.4 gene in A. thaliana compared to the wild type. Additionally, the multiplication of M. javanica in the A. thaliana mutants was significantly increased mainly in the event athsp22.0-2. This increase was not that evident in the event athsp22.0-1, the one that preserved a portion of the promoter region, including the HSEs in the region around - 83 bp. However, structural analysis at sequence level among soybean resistant and susceptible genotypes did not detect any polymorphisms in the whole gene model. CONCLUSIONS: The soybean chaperone GmHsp22.4 is involved in the defense response to root-knot nematode M. javanica in A. thaliana. Specifically, the promoter region covering until - 191 from the transcriptional start site (TSS) is necessary to promoter activation after nematode infection in Arabidopsis. No polymorphisms that could explain these differences in the defense response were detected in the GmHsp22.4 gene between resistant and susceptible soybean genotypes. Therefore, further investigation is needed to elucidate the triggering factor of the plant's defense mechanism, both at the sequence level of the soybean genotypes presenting contrasting reaction to root-knot nematode and by detecting cis-elements that are essential for the activation of the GmHsp22.4 gene promoter.

Phakopsora pachyrhizi triggers the jasmonate signaling pathway during compatible interaction in soybean and GmbZIP89 plays a role of major component in the pathway.

The biotrophic fungus Phakopsora pachyrhizi is currently the major pathogen affecting soybean production worldwide. It has already been suggested for the non-host interaction between P. pachyrhizi and Arabidopsis thaliana that the fungus in early infection induces jasmonic acid (JA) pathway to the detriment of the salicylic acid (SA) pathway as a mechanism to the establishment of infection. In this study, we verified that this mechanism might also be occurring during the compatible interaction in soybean (Glycine max L. Merril). It was demonstrated that P. pachyrhizi triggers a JA pathway during the early and late stages of infection in a susceptible soybean cultivar. The expression of the GmbZIP89 was induced in a biphasic profile, similarly to other JA responsive genes, which indicates a new marker gene for this signaling pathway. Additionally, plants silenced for GmbZIP89 (iGmZIP89) by the virus-induced gene silencing (VIGS) approach present lower severity of infection and higher expression of pathogenesis related protein 1 (PR1). The lower disease severity showed that the iGmbZIP89 plants became more resistant to infection. These data corroborate the hypothesis that the GmbZIP89 may be a resistance negative regulator. In conclusion, we demonstrated that P. pachyrhizi mimics a necrotrophic fungus and activates the JA/ET pathway in soybean. It is possible to suppose that its direct penetration on epidermal cells or fungal effectors may modulate the expression of target genes aiming the activation of the JA pathway and inhibition of SA defense.