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Project description:The low efficiency of fungal growth and substrate utilization is a barrier to high yield and productivity of target products during fungal fermentation. However, elaborated and intricate regulatory mechanisms of fungal growth remains inconclusive. In this study, we found deletion of putative methyltransferase LaeA enhanced sugar consumption and fungal growth rate of M. thermophila. The exploration of the mechanism of LaeA regulation revealed that transcription factor (Cre-1, Grf-1, Grf-2 and Grf-3) acted as negative repressor of intracellular metabolism, of which expression was indirectly regulated by LaeA. Moreover, higher gluconeogenesis activity is crucial for elevated fugal growth rate and PCK might be the core notes of metabolism network relative to fungal vegetative growth. Further in vivo global histone methylation assay and in vitro biochemical analysis declared LaeA was a methyltransferase with histone H3 lysine 9 (H3K9) as the substrate and regulated growth properties by directly modulating H3K9 methylation levels. ChIP-seq analysis displayed significantly reduced H3K9me3 in region of pck locus in strain ΔlaeA, implying methylation modification of pck might be the way of LaeA regulating growth phenotypes. Additionally, whole-genome bisulfite sequencing (WGBS) analysis demonstrated methylation of cytosines (5mC) in genomic DNA was carried out and correlated to the methylation of H3K9 modified by LaeA. Taken together, our research declared LaeA possessed methyltransferase activity, targeting H3K9 and participated in regulation of fugal properties, including on sugar consumption, mycelium growth, cellulase production, secondary metabolism, and oxidative stress tolerance, providing new insights into the epigenetics of filamentous fungi.
2023-04-12 | GSE213573 | GEO
Project description:The low efficiency of fungal growth and substrate utilization is a barrier to high yield and productivity of target products during fungal fermentation. However, elaborated and intricate regulatory mechanisms of fungal growth remains inconclusive. In this study, we found deletion of putative methyltransferase LaeA enhanced sugar consumption and fungal growth rate of M. thermophila. The exploration of the mechanism of LaeA regulation revealed that transcription factor (Cre-1, Grf-1, Grf-2 and Grf-3) acted as negative repressor of intracellular metabolism, of which expression was indirectly regulated by LaeA. Moreover, higher gluconeogenesis activity is crucial for elevated fugal growth rate and PCK might be the core notes of metabolism network relative to fungal vegetative growth. Further in vivo global histone methylation assay and in vitro biochemical analysis declared LaeA was a methyltransferase with histone H3 lysine 9 (H3K9) as the substrate and regulated growth properties by directly modulating H3K9 methylation levels. ChIP-seq analysis displayed significantly reduced H3K9me3 in region of pck locus in strain ΔlaeA, implying methylation modification of pck might be the way of LaeA regulating growth phenotypes. Additionally, whole-genome bisulfite sequencing (WGBS) analysis demonstrated methylation of cytosines (5mC) in genomic DNA was carried out and correlated to the methylation of H3K9 modified by LaeA. Taken together, our research declared LaeA possessed methyltransferase activity, targeting H3K9 and participated in regulation of fugal properties, including on sugar consumption, mycelium growth, cellulase production, secondary metabolism, and oxidative stress tolerance, providing new insights into the epigenetics of filamentous fungi.
2023-04-12 | GSE213575 | GEO
Project description:The low efficiency of fungal growth and substrate utilization is a barrier to high yield and productivity of target products during fungal fermentation. However, elaborated and intricate regulatory mechanisms of fungal growth remains inconclusive. In this study, we found deletion of putative methyltransferase LaeA enhanced sugar consumption and fungal growth rate of M. thermophila. The exploration of the mechanism of LaeA regulation revealed that transcription factor (Cre-1, Grf-1, Grf-2 and Grf-3) acted as negative repressor of intracellular metabolism, of which expression was indirectly regulated by LaeA. Moreover, higher gluconeogenesis activity is crucial for elevated fugal growth rate and PCK might be the core notes of metabolism network relative to fungal vegetative growth. Further in vivo global histone methylation assay and in vitro biochemical analysis declared LaeA was a methyltransferase with histone H3 lysine 9 (H3K9) as the substrate and regulated growth properties by directly modulating H3K9 methylation levels. ChIP-seq analysis displayed significantly reduced H3K9me3 in region of pck locus in strain ΔlaeA, implying methylation modification of pck might be the way of LaeA regulating growth phenotypes. Additionally, whole-genome bisulfite sequencing (WGBS) analysis demonstrated methylation of cytosines (5mC) in genomic DNA was carried out and correlated to the methylation of H3K9 modified by LaeA. Taken together, our research declared LaeA possessed methyltransferase activity, targeting H3K9 and participated in regulation of fugal properties, including on sugar consumption, mycelium growth, cellulase production, secondary metabolism, and oxidative stress tolerance, providing new insights into the epigenetics of filamentous fungi.
2023-04-12 | GSE213570 | GEO
Project description:Comprehensive Annotation of the transcriptome of the human fugal pathogen Candida albicans using RNA-Seq
| PRJNA79703 | ENA
Project description:A simultaneous engagement of different pathogen recognition receptors provides a tailor made adaptive immunity for an efficient defence against distinct pathogens. For example, cross talk of TLR and c-type lectin signalling effectively shapes distinct gene expression patterns by integrating the signals at the level of NF-κB. Here, we extend this principle to a strong synergism between the Dectin-1 agonist, curdlan, and an inflammatory growth factor, GM-CSF. Both together act in synergy in inducing a strong inflammatory signature which converts immature DCs to potent effector DCs. A variety of cytokines (IL-1β, IL-6, TNF-α, IL-2 and IL-12p70), costimulatory molecules (CD80, CD86, CD40 and CD70), chemokines (CxCl1, CxCl2, CxCl3, CCl12, CCl17) as well as receptors and molecules involved in fugal recognition and immunity such as Mincle, Dectin-1, Dectin-2 and Pentraxin 3 are strongly up-regulated in DC treated simultaneously with curdlan and GM-CSF. The synergistic effect of both stimuli resulted in strong IKBα phosphorylation, in its rapid degradation and in enhanced nuclear translocation of all NF-κB subunits. We further identified MAPK ERK, as one possible integration site of both signals, since its phosphorylation was clearly augmented when curdlan was co-applied with GM-CSF. Our data demonstrate that the immunomodulatory activity of curdlan requires an additional signal provided by GM-CSF to successfully initiate a robust β-glucan specific cytokine and chemokine response. The integration of both signals clearly prime and tailor a more effective innate and adaptive response against invading microbes and fungi. CD11b+ fraction of FLT3L generated BM DCs (3-4 x106) were stimulated for 4 hours with 100 or 1 μg/ml curdlan in presence or absence of 5 ng/ml GM-CSF in triplicates.
2011-10-14 | E-GEOD-32986 | biostudies-arrayexpress
Project description:A simultaneous engagement of different pathogen recognition receptors provides a tailor made adaptive immunity for an efficient defence against distinct pathogens. For example, cross talk of TLR and c-type lectin signalling effectively shapes distinct gene expression patterns by integrating the signals at the level of NF-κB. Here, we extend this principle to a strong synergism between the Dectin-1 agonist, curdlan, and an inflammatory growth factor, GM-CSF. Both together act in synergy in inducing a strong inflammatory signature which converts immature DCs to potent effector DCs. A variety of cytokines (IL-1β, IL-6, TNF-α, IL-2 and IL-12p70), costimulatory molecules (CD80, CD86, CD40 and CD70), chemokines (CxCl1, CxCl2, CxCl3, CCl12, CCl17) as well as receptors and molecules involved in fugal recognition and immunity such as Mincle, Dectin-1, Dectin-2 and Pentraxin 3 are strongly up-regulated in DC treated simultaneously with curdlan and GM-CSF. The synergistic effect of both stimuli resulted in strong IKBα phosphorylation, in its rapid degradation and in enhanced nuclear translocation of all NF-κB subunits. We further identified MAPK ERK, as one possible integration site of both signals, since its phosphorylation was clearly augmented when curdlan was co-applied with GM-CSF. Our data demonstrate that the immunomodulatory activity of curdlan requires an additional signal provided by GM-CSF to successfully initiate a robust β-glucan specific cytokine and chemokine response. The integration of both signals clearly prime and tailor a more effective innate and adaptive response against invading microbes and fungi.
2011-10-15 | GSE32986 | GEO
Project description:Botrytis cinerea (gray mold) is one of the most destructive pathogens of cherry tomatoes, causing fruit decay and economic loss. Fludioxonil is an effective fungicide widely used for crop protec-tion and is essential for controlling tomato gray mold. The emergence of fungicide-resistant strains has made the control of Botrytis cinerea more difficult. While the genome of Botrytis cinerea is available, there are few reports regarding the large-scale functional annotation of the genome using expressed genes derived from transcriptomes, and the mechanism(s) underlying such flu-dioxonil resistance remain unclear. The present study prepared RNA-sequencing (RNA-seq) li-braries for three Botrytis cinerea strains [two highly resistant (LR and FR) versus one highly sen-sitive (S) to fludioxonil], with and without fludioxonil treatment, to identify fludioxonil responsive genes that facilitate fungicide resistance. Functional enrichment analysis identified nine resistant related DEGs in the fludioxonil-induced LR and FR transcriptome that were simultaneously up regulated, and seven resistant related DEGs down regulated. These included adenosine tri-phosphate (ATP)-binding cassette (ABC) transporter-encoding genes, major facilitator super-family (MFS) transporter-encoding genes, and the high-osmolarity glycerol (HOG) pathway homologues or related genes. The expression patterns of twelve out of the sixteen fludioxo-nil-responsive genes, obtained from the RNA-sequence data sets were validated using quantita-tive real-time PCR (qRT-PCR). Based on RNA-sequence analysis it was found that fugal HHKs, like BOS1, BcHHK2, and Bchhk17, were in some way involved in the fludioxonil resistance of B. cinerea, in addition, a number of ABC and MFS transporter genes that were not reported before, such as BcATRO, BMR1, BMR3, BcNMT1, BcAMF1, BcTOP1, BcVBA2, and BcYHK8 were differen-tially expressed in the fludioxonil-resistant strains, indicating that overexpression of these efflux transporters located in the plasma membranes played a crucial role in the fludioxonil resistant mechanism of B. cinerea. These lines of evidence together allowed us to draw a general portrait of the anti-fludioxonil mechanisms for Botrytis cinerea, and the assembled and annotated transcrip-tome data provide valuable genomic resources for further study of the molecular mechanisms of B. cinerea resistance to fludioxonil.
2023-12-12 | GSE221721 | GEO