Transcriptional response of oil palm (Elaeis guineensis Jacq.) inoculated simultaneously with both Ganoderma boninense and Trichoderma harzianum

Application of beneficial microbes offers an environmentally friendly alternative for mitigation of basal stem rot (BSR) disease in oil palm. However, the biocontrol mechanisms of Trichoderma against the pathogenic Ganoderma spp. which cause BSR are largely unknown at the molecular level. To identify the transcripts involved during induced systemic resistance (ISR), we analyzed the root transcriptomes of oil palm seedlings inoculated simultaneously with both G. boninense and T. harzianum, and un-inoculated oil palm seedlings, as well as those that were inoculated with either pathogenic or beneficial fungi. Our analyses revealed that the biocontrol mechanisms of T. harzianum against G. boninense involve modulation of genes related to biosynthesis of phytohormones (ethylene, MeJA and MeSA), antioxidant (l-ascorbate and myo-inositol) and unique secondary metabolites such as momilactone, cell wall metabolisms, and detoxification of phytotoxic compounds; in addition to its role as a biofertilizer which improves nutritional status of host plant. The outcomes of this study have fueled our understanding on the biocontrol mechanisms involving T. harizianum against G. boninense infection in oil palm roots

Leaf transcriptome of oil palm (Elaeis guineensis Jacq.) infected by Ganoderma boninense

Oil palm is susceptible to Ganoderma infection which causes basal stem rot (BSR). Induced defense gene profiles in oil palm leaves will assist the identification of markers for detection of infected oil palms. In this study, we have sequenced the mRNA samples from the leaves of G. boninense infected oil palm seedlings (LG) and in control treatment (LC). Differential gene expression analysis showed 711 and 482 genes that were up-and down-regulated more than fourfold in LG, respectively, compared to the LC. Differential gene expression analyses revealed the modulation of oil palm genes involved in defense response such as chitinases, glucanases, and thaumatin-like proteins that showed up-regulation in LG. In addition, genes for enzymes related to the biosynthesis of flavonoids, alkaloids, and terpenes were up-regulated, while many genes involved in photosynthesis were found to be suppressed in LG. Our findings provided information on how infected oil palm leaves diverting their resources into defense at the cost of other biological processes, contributing towards identification of candidate markers for the detection of infected oil palms

De novo transcriptome analyses of hostfungal interactions in oil palm (Elaeis guineensis Jacq.)

Background: Basal stem rot (BSR) is a fungal disease in oil palm (Elaeis guineensis Jacq.) which is caused by hemibiotrophic white rot fungi belonging to the Ganoderma genus. Molecular responses of oil palm to these pathogens are not well known although this information is crucial to strategize effective measures to eradicate BSR. In order to elucidate the molecular interactions between oil palm and G. boninense and its biocontrol fungus Trichoderma harzianum, we compared the root transcriptomes of untreated oil palm seedlings with those inoculated with G. boninense and T. harzianum, respectively. Results: Differential gene expression analyses revealed that jasmonate (JA) and salicylate (SA) may act in an antagonistic manner in affecting the hormone biosynthesis, signaling, and downstream defense responses in G. boninense-treated oil palm roots. In addition, G. boninense may compete with the host to control disease symptom through the transcriptional regulation of ethylene (ET) biosynthesis, reactive oxygen species (ROS) production and scavenging. The strengthening of host cell walls and production of pathogenesis-related proteins as well as antifungal secondary metabolites in host plants, are among the important defense mechanisms deployed by oil palm against G. boninense. Meanwhile, endophytic T. harzianum was shown to improve the of nutrition status and nutrient transportation in host plants. Conclusion: The findings of this analysis have enhanced our understanding on the molecular interactions of G. boninense and oil palm, and also the biocontrol mechanisms involving T. harzianum, thus contributing to future formulations of better strategies for prevention and treatment of BSR

Identification and Characterization of a Rare Fungus, Quambalaria cyanescens, Isolated from the Peritoneal Fluid of a Patient after Nocturnal Intermittent Peritoneal Dialysis.

Peritonitis is the leading complication of peritoneal dialysis, which is primarily caused by bacteria rather than fungi. Peritonitis is responsible for approximately 18% of the infection-related mortality in peritoneal dialysis patients. In this paper, we report the isolation of a rare fungus, Quambalaria cyanescens, from the peritoneal fluid of a man after he switched from continuous ambulatory peritoneal dialysis to nocturnal intermittent peritoneal dialysis. Based on the morphological examination and multigene phylogeny, the clinical isolate was confirmed as Q. cyanescens. This pathogen exhibited low sensitivity to all tested echinocandins and 5-flucytosine. Interestingly, morphological characterization revealed that Q. cyanescens UM 1095 produced different pigments at low temperatures (25°C and 30°C) on various culture media. It is important to monitor the emergence of this rare fungus as a potential human pathogen in the tropics. This study provides insight into Q. cyanescens UM 1095 phenotype profiles using a Biolog phenotypic microarray (PM). Of the 760 nutrient sources tested, Q. cyanescens UM 1095 utilized 42 compounds, and the fungus can adapt to a broad range of osmotic and acidic environments. To our knowledge, this is the first report of the isolation of Q. cyanescens from peritoneal fluid, revealing this rare fungus as a potential human pathogen that may be misidentified using conventional methods. The detailed morphological, molecular and phenotypic characterization of Q. cyanescens UM 1095 provides the basis for future studies on its biology, lifestyle, and potential pathogenicity

Additional file 2: Figure S1. of The genome of newly classified Ochroconis mirabilis: Insights into fungal adaptation to different living conditions

KEGG map of styrene degradation. Genes annotated via KEGG are shaded. Z-phenylacetaldoxime degradation by nitrilase (EC 3.5.5.1), nitrile hydratase (EC 4.2.1.84) and amidase (EC 3.5.1.4). Although the phenylacetaldoxime dehydratase (EC 4.99.1.7) was not mapped, the gene was found in the genome. Figure S2. Alignment of putative phenylacetaldoxime dehydratase of O. mirabilis UM 578 (UM578_4049) with Bacillus sp. OxB-1 (P82604). Identical and similar residues are black and gray shaded respectively. The haem-containing dehydratase region is indicated by asterisk. Figure S3. Putative aldoxime-nitrile pathway gene cluster of UM 578. The phyenylacetaldoxime dehydratase (UM578_4049) and nitrilase (UM578_5050). The direction of transcription is indicated by the arrow for each gene. Figure S4. KEGG map of atrazine degradation. Genes annotated via KEGG are shaded. Cyanamide was degraded by cyanamide hydratase (EC 4.2.1.69) and urease (EC 35.1.5). Figure S5. Alignment of predicted metallopeptidase M14A of O. mirabilis UM 578 (UM578_1644). Alignment was carried out with metallopeptidase MeCPA from Metarhizium anisopliae (AAB68600) and TruMcpA from Trichophyton rubrum (ABW79919). Identical and similar residues are black and gray shaded, respectively. The zinc-binding residues are indicated by an asterisk. The active-site residues are indicated by circles. Conserved residues involved in substrate binding are indicated by solid triangles. The conserved Cys residues forming disulfide bridges are indicated by solid rhombus. Figure S6. Alignment of predicted serine carboxypeptidase of O.mirabilis UM 578 (UM578_13449). Alignment was carried out with TruSCPA from Trichophyton rubrum (AAS76667) and AfuCp1 from Aspergillus fumigatus (AAR91697). Identical and similar residues are black and gray shaded respectively. The consensus active residues are indicated by asterisk (Ser228, Asp439 and His497). Figure S7. Alignment of predicted leucine aminopeptidase (LAP) of O. mirabilis UM 578 (UM578_7056). Alignment was carried out with TruLAP1 from Trichophyton rubrum (AAS76670) and AfuLAP1 from Aspergillus fumigatus (AAR996058). Identical and similar residues are black and gray shaded respectively. The consensus binding sites for the first and the second Zn2+ ion binding sites are indicated in triangle (His180 and Asp265) and in rhombus (Glu238 and His347) respectively. The Asp199 is the residue bridging the two Zn2+ ions is indicated in circle. The active sites (Asp182 and Glu237) are indicated by asterisk. Figure S8. Alignment of predicted leucine aminopeptidase (LAP) of O.mirabilis UM 578 (UM578_5513). Alignment was carried out with TruLAP2 from Trichophyton rubrum (AAS76669) and AfuLAP2 from Aspergillus fumigatus (AAR96059). Identical and similar residues are black and gray shaded respectively. The consensus binding sites for the first and the second Zn2+ ion binding sites are indicated in triangle (His252 and Asp326) and in rhombus (Glu297 and His424) respectively. The Asp264 is the residue bridging the two Zn2+ ions is indicated in circle. The active sites (Asp254 and Glu296) are indicated in asterisk. Figure S9. Alignment of predicted dipeptidyl peptidase IV (DPPIV) of O. mirabilis UM 578 (UM578_9285). Alignment was carried out with TruDPPIV from Trichophyton rubrum (AAS76665) and AfuDPPIV from Aspergillus fumigatus (AAC34310). Identical and similar residues are black and gray shaded respectively. The catalytic triad is indicated in asterisk (Ser619, Asp 696, His731). Figure S10. Alignment of predicted dipeptidyl peptidase V (DPPV) of O. mirabilis UM 578 (UM578_9264). Alignment was carried out with TruDPPIV from Trichophyton rubrum (AAN03632) and AfuDPPIV from Aspergillus fumigatus (AAB67282). Identical and similar residues are black and gray shaded respectively. The catalytic triad is indicated in asterisk (Ser566, Asp647, His679). Figure S11. TMpred output of putative sulphite efflux pump (ssu1) in UM 578. The putative gene, UM578_9214 has ten membrane-spanning helixes and hydrophilic N- and C- termini. Figure S12. Putative melanin biosynthesis cluster in UM 578. The organisation and orientation of genes involved in melanin biosynthesis are similar to that of the reported melanin gene cluster in C. heterostrophus [GenBank: AAR90272] and A. brassicicola [GenBank: BAD22832]. The predicted genes encode polyketide synthase (UM578_2557), transcription factor Cmr1 (UM578_2558) and tetrahydroxynaphthalene reductase (UM578_2559). The direction of transcription is indicated by the arrow for each gene. Figure S13. Putative trichothecene biosynthesis cluster in UM 578. The 6751 bp cluster encompasses the trichodiene synthase (UM578_3030) with two cytochrome P450 encoding genes (UM578_3031 and UM578_3032) and the trichothecene efflux pump (UM578_3033). The direction of transcription is indicated by the arrow for each gene. Figure S14. Putative gene organisation of mating type genes in UM 578. The neighbouring genes of alpha-domain containing gene (UM578_3656) encompass the homeodomain-containing protein (UM578_3655), DNA lyase APN2 (UM578_3657) and cytochrome C oxidase Vla Cox13 (UM578_3658). The direction of transcription is indicated by the arrow for each gene. Figure S15. Phylogenomic tree showing number of each node in expansion/ contraction analysis. The number of genes and P-value for UM 578 (node 24) and the internode (node 23) are shown in Additional file 1: Table S12. (PDF 1000 kb