RUNX2 Transcriptional Regulation in Development and Disease

Brusgard, Jessica L.; Passaniti, Antonino

doi:10.1007/978-1-4614-8039-6_3

Cited by 5 publications

(4 citation statements)

References 136 publications

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“…Nearly all the genes found to be up-regulated in infected 24h clustered in module blue-host ( n = 2352; 98.5%). Not surprisingly, the main driver genes (‘hub-genes’) include several transcriptional activators, such as, for module turquoise-host , several Zinc finger proteins, Transcription factor GATA-3 ( gata-3 ), Forkhead box protein O3 ( foxpo3 ), activators of the autophagy pathways and the main drivers of naïve specific T-cell differentiation and activation [ 54 ], Runt-related transcription factor 2- ( runt2 ) coding genes, involved in osteoblast differentiation, mineral- depositing cells and sialoproteins [ 55 , 56 ]. In module blue-host , ‘hub-genes’ mainly reported actors of the innate immune system, inflammatory response, wound healing, oxidative and adhesion activity (Fig.…”

Section: Resultsmentioning

confidence: 99%

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

et al. 2021

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Background Tenacibaculum maritimum is a fish pathogen known for causing serious damage to a broad range of wild and farmed marine fish populations worldwide. The recently sequenced genome of T. maritimum strain NCIMB 2154T provided unprecedented information on the possible molecular mechanisms involved in the virulence of this species. However, little is known about the dynamic of infection in vivo, and information is lacking on both the intrinsic host response (gene expression) and its associated microbiota. Here, we applied complementary omic approaches, including dual RNAseq and 16S rRNA gene metabarcoding sequencing using Nanopore and short-read Illumina technologies to unravel the host–pathogen interplay in an experimental infection system using the tropical fish Platax orbicularis as model. Results We showed that the infection of the host is characterised by an enhancement of functions associated with antibiotic and glucans catabolism functions but a reduction of sulfate assimilation process in T. maritimum. The fish host concurrently displays a large panel of immune effectors, notably involving innate response and triggering acute inflammatory response. In addition, our results suggest that fish activate an adaptive immune response visible through the stimulation of T-helper cells, Th17, with congruent reduction of Th2 and T-regulatory cells. Fish were, however, largely sensitive to infection, and less than 25% survived after 96 hpi. These surviving fish showed no evidence of stress (cortisol levels) or significant difference in microbiome diversity compared with controls at the same sampling time. The presence of T. maritimum in resistant fish skin and the total absence of any skin lesions suggest that these fish did not escape contact with the pathogen, but rather that some mechanisms prevented pathogens entry. In resistant individuals, we detected up-regulation of specific immune-related genes differentiating resistant individuals from controls at 96 hpi, which suggests a possible genomic basis of resistance, although no genetic variation in coding regions was found. Conclusion Here we focus in detail on the interplay between common fish pathogens and host immune response during experimental infection. We further highlight key actors of defence response, pathogenicity and possible genomic bases of fish resistance to T. maritimum.

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Section: Resultsmentioning

confidence: 99%

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

et al. 2021

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“…Nearly all the genes found to be upregulated in infected 24h clustered in module blue−host (n = 2,352; 98.5%). Not surprisingly, the main driver genes ('hub-genes') include several transcriptional activators, such as, for module turquoise−host , several Zinc nger proteins, Transcription factor GATA-3 (gata-3), Forkhead box protein O3 (foxpo3), activators of the autophagy pathways and the main drivers of naïve speci c T-cell differentiation and activation [56], Runt-related transcription factor 2-(runt2) coding genes, involved in osteoblast differentiation, mineraldepositing cells and sialoproteins [57,58]. In module blue−host , 'hub-genes' mainly reported actors of the innate immune system, in ammatory response, wound healing, oxidative and adhesion activity (Fig.…”

Section: B) Dynamics Of Host Transcriptomic Response To Infection Andmentioning

confidence: 99%

Dual RNAseq Highlights the Kinetics of Skin Microbiome and Fish Host Responsiveness to Bacterial Infection

Luyer

Schull

Auffret

et al. 2020

Preprint

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a) BackgroundTenacibaculum maritimum is a fish pathogen known for causing serious damage to a broad range of wild and farmed marine fish populations worldwide. The recently sequenced genome of T. maritimum strain NCIMB 2154T provided unprecedented information on the possible molecular mechanisms involved in the virulence of this species. However, little is known about the dynamic of infection in vivo, and information is lacking on both the intrinsic host response (gene expression) and its associated microbiome community. Here, we applied complementary omic approaches, including dual RNAseq and 16S rRNA gene metabarcoding sequencing using Nanopore and short-read Illumina technologies to unravel the host–pathogen interplay in an experimental infection system using the tropical fish Platax orbicularis as model.b) ResultsWe showed that the T. maritimum transcriptomic landscape during infection is characterised by an enhancement of antibiotic catalytic and glucan catalytic functions but a decrease in the sulfate assimilation process, compared with in vitro cultures. The fish host concurrently displays a large panel of immune effectors, notably involving innate response and triggering acute inflammatory response. In addition, our results suggest that fish activate an adaptive immune response visible through the stimulation of T-helper cells, Th17, with congruent reduction of Th2 and T-regulatory cells. Fish were, however, largely sensitive to infection, and less than 25% survived after 96 hpi. These surviving fish showed no evidence of stress (cortisol levels) or significant difference in microbiome diversity compared with controls at the same sampling time. The presence of Tenacibaculum in resistant fish skin and the total absence of any skin lesions suggest that these fish did not escape contact with the pathogen, but rather that they prevented pathogen entry. In these individuals, we detected up-regulation of specific immune-related genes differentiating resistant individuals from controls at 96 hpi, which suggests a possible genomic basis of resistance, although no genetic variation in coding regions were found.c) ConclusionHere we focus in detail on the interplay between common fish pathogens and host immune response during experimental infection. We further highlight key actors of defence response, pathogenicity and possible genomic bases of fish resistance to T. maritimum.

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“…Nearly all the genes found to be up-regulated in infected 24h clustered in module blue-host (n = 2,352; 98.5%). Not surprisingly, the main driver genes ('hub-genes') include several transcriptional activators, such as, for module turquoise-host , several Zinc nger proteins, Transcription factor GATA-3 (gata-3), Forkhead box protein O3 (foxpo3), activators of the autophagy pathways and the main drivers of naïve speci c T-cell differentiation and activation [56], Runtrelated transcription factor 2-(runt2) coding genes, involved in osteoblast differentiation, mineraldepositing cells and sialoproteins [57,58]. In module blue-host , 'hub-genes' mainly reported actors of the innate immune system, in ammatory response, wound healing, oxidative and adhesion activity ( Figure 3B).…”

Section: B) Dynamics Of Host Transcriptomic Response To Infection Andmentioning

confidence: 99%

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

Luyer

Schull

Auffret

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Tenacibaculum maritimum is a fish pathogen known for causing serious damage to a broad range of wild and farmed marine fish populations worldwide. The recently sequenced genome of T. maritimum strain NCIMB 2154 T provided unprecedented information on the possible molecular mechanisms involved in the virulence of this species. However, little is known about the dynamic of infection in vivo, and information is lacking on both the intrinsic host response (gene expression) and its associated microbiome community. Here, we applied complementary omic approaches, including dual RNAseq and 16S rRNA gene metabarcoding sequencing using Nanopore and short-read Illumina technologies to unravel the host–pathogen interplay in an experimental infection system using the tropical fish Platax orbicularis as model. Results: We showed that the T. maritimum transcriptomic landscape during infection is characterised by an enhancement of antibiotic catalytic and glucan catalytic functions but a decrease in the sulfate assimilation process, compared with in vitro cultures. The fish host concurrently displays a large panel of immune effectors, notably involving innate response and triggering acute inflammatory response. In addition, our results suggest that fish activate an adaptive immune response visible through the stimulation of T-helper cells, Th17, with congruent reduction of Th2 and T-regulatory cells. Fish were, however, largely sensitive to infection, and less than 25% survived after 96 hpi. These surviving fish showed no evidence of stress (cortisol levels) or significant difference in microbiome diversity compared with controls at the same sampling time. The presence of Tenacibaculum in resistant fish skin and the total absence of any skin lesions suggest that these fish did not escape contact with the pathogen, but rather that they prevented pathogen entry. In these individuals, we detected up-regulation of specific immune-related genes differentiating resistant individuals from controls at 96 hpi, which suggests a possible genomic basis of resistance, although no genetic variation in coding regions were found. Conclusions: Here we focus in detail on the interplay between common fish pathogens and host immune response during experimental infection. We further highlight key actors of defence response, pathogenicity and possible genomic bases of fish resistance to T. maritimum .

show abstract

RUNX2 Transcriptional Regulation in Development and Disease

Cited by 5 publications

References 136 publications

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

Dual RNAseq Highlights the Kinetics of Skin Microbiome and Fish Host Responsiveness to Bacterial Infection

Dual RNAseq highlights the kinetics of skin microbiome and fish host responsiveness to bacterial infection

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