Insights into oleaginous phenotype of the yeast Papiliotrema laurentii.

Oleaginous yeasts have stood out due to their ability to accumulate oil, which can be used for fatty acid-derived biofuel production. Papiliotrema laurentii UFV-1 is capable of starting the lipid accumulation in the late exponential growth phase and achieves maximum lipid content at 48 h of growth; it is, therefore, interesting to study how its oleaginous phenotype is regulated. Herein, we provide for the first time insights into the regulation of this phenotype in P. laurentii UFV-1. We sequenced and assembled its genome, performed comparative genomic analyses and investigated its phylogenetic relationships with other yeasts. Gene expression and metabolomic analyses were carried out on the P. laurentii UFV-1 cultivated under a nitrogen-limiting condition. Our results indicated that the lipogenesis of P. laurentii might have taken place during evolution after the divergence of genera in the phylum Basidiomycota. Metabolomic data indicated the redirection of the carbon flux towards fatty acid synthesis in response to the nitrogen limitation. Furthermore, purine seems to be catabolized to recycle nitrogen and leucine catabolization may provide acetyl-CoA for fatty acid synthesis. Analyses of the expression of genes encoding certain enzymes involved with the oleaginous phenotype indicated that the NADP+-dependent malic enzyme seems to play an important role in the supply of NADPH for fatty acid synthesis. There was a surprising decrease in the expression of the ACC1 gene, which encodes acetyl-CoA carboxylase, during lipid accumulation. Taken together, our results provided a basis for understanding lipid accumulation in P. laurentii under nitrogen limiting conditions.

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.