scholarly journals Transcriptional Responses of Sclerotinia sclerotiorum to the Infection by SsHADV-1

2021 ◽  
Vol 7 (7) ◽  
pp. 493
Author(s):  
Zheng Qu ◽  
Yanping Fu ◽  
Yang Lin ◽  
Zhenzhen Zhao ◽  
Xuekun Zhang ◽  
...  
Keyword(s):  
Sclerotinia Sclerotiorum ◽  
Rna Silencing ◽  
Morphological Changes ◽  
Transcriptional Responses ◽  
Dna Virus ◽  
Ribosomal Assembly ◽  
Carbohydrate And Lipid Metabolism ◽  
Damage Response ◽  
Genome Transcription ◽  
Virulence Factor Genes

The infection by a single-stranded DNA virus, Sclerotinia sclerotiorum hypovirulence-associated DNA virus 1 (SsHADV-1), causes hypovirulence, a reduced growth rate, and other colony morphological changes in its host Sclerotinia sclerotiorum strain DT-8. However, the mechanisms of the decline are still unclear. Using digital RNA sequencing, a transcriptome analysis was conducted to elucidate the phenotype-related genes with expression changes in response to SsHADV-1 infection. A total of 3110 S. sclerotiorum differentially expressed genes (DEGs) were detected during SsHADV-1 infection, 1741 of which were up-regulated, and 1369 were down-regulated. The identified DEGs were involved in several important pathways. DNA replication, DNA damage response, carbohydrate and lipid metabolism, ribosomal assembly, and translation were the affected categories in S. sclerotiorum upon SsHADV-1 infection. Moreover, the infection of SsHADV-1 also suppressed the expression of antiviral RNA silencing and virulence factor genes. These results provide further detailed insights into the effects of SsHADV-1 infection on the whole genome transcription in S. sclerotiorum.

scholarly journals Suppression of RNA Silencing by a Plant DNA Virus Satellite Requires a Host Calmodulin-Like Protein to Repress RDR6 Expression

2014 ◽  
Vol 10 (2) ◽  
pp. e1003921 ◽  
Author(s):  
Fangfang Li ◽  
Changjun Huang ◽  
Zhenghe Li ◽  
Xueping Zhou
Keyword(s):  
Rna Silencing ◽  
Dna Virus ◽  
Plant Dna

scholarly journals Volatile Compounds of Endophytic Bacillus spp. have Biocontrol Activity Against Sclerotinia sclerotiorum

2018 ◽  
Vol 108 (12) ◽  
pp. 1373-1385 ◽  
Author(s):  
Venance Colman Massawe ◽  
Alvina Hanif ◽  
Ayaz Farzand ◽  
David Kibe Mburu ◽  
Sylvans Ochieng Ochola ◽  
...  
Keyword(s):  
Sclerotinia Sclerotiorum ◽  
Morphological Changes ◽  
Antagonistic Activity ◽  
In Vitro Assays ◽  
Gas Chromatography Mass Spectrometry ◽  
Bromophenol Blue ◽  
Fungal Mycelium ◽  
Negative Effects ◽  
Bacillus Spp

To develop an effective biological agent to control Sclerotinia sclerotiorum, three endophytic Bacillus spp. strains with high antagonistic activity were isolated from maize seed and characterized. In vitro assays revealed that the Bacillus endophytes could produce volatile organic compounds (VOC) that reduced sclerotial production and inhibited mycelial growth of S. sclerotiorum. Gas chromatography–mass spectrometry revealed that the selected strains produced 16 detectable VOC. Eight of the produced VOC exhibited negative effects on S. sclerotiorum, while a further four induced accumulation of reactive oxygen species in mycelial cells. A mixture of VOC produced by Bacillus velezensis VM11 caused morphological changes in the ultrastructure and organelle membranes of S. sclerotiorum mycelial cells. The bromophenol blue assay revealed a yellow color of untreated fungal mycelium, which grew faster and deeper from 24 to 72 h postinoculation, as an indication of reduced pH. The potassium permanganate (KMnO4) titration assay showed that the rate of oxalic acid accumulation was higher in minimal salt liquid medium cultures inoculated with untreated fungal plugs compared with the Bacillus VOC-treated ones. Interestingly, biological control assays using host-plant leaves challenged with treated fungal mycelial plugs produced reduced lesions compared with the control. These findings provide new viable possibilities of controlling diseases caused by S. sclerotiorum using VOC produced by Bacillus endophytes.

scholarly journals Early Transcriptional Response to DNA Virus Infection in Sclerotinia sclerotiorum

Viruses ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 278 ◽  
Author(s):  
Feng Ding ◽  
Jiasen Cheng ◽  
Yanping Fu ◽  
Tao Chen ◽  
Bo Li ◽  
...  
Keyword(s):  
Signal Transduction ◽  
G Protein ◽  
Sclerotinia Sclerotiorum ◽  
Molecular Mechanisms ◽  
Cell Structure ◽  
Differentially Expressed ◽  
Post Inoculation ◽  
Dna Virus ◽  
Fungal Cell ◽  
Small G Protein

We previously determined that virions of Sclerotinia sclerotiorum hypovirulence associated DNA virus 1 (SsHADV-1) could directly infect hyphae of Sclerotinia sclerotiorum, resulting in hypovirulence of the fungal host. However, the molecular mechanisms of SsHADV-1 virions disruption of the fungal cell wall barrier and entrance into the host cell are still unclear. To investigate the early response of S. sclerotiorum to SsHADV-1 infection, S. sclerotiorum hyphae were inoculated with purified SsHADV-1 virions. The pre- and post-infection hyphae were collected at one–three hours post-inoculation for transcriptome analysis. Further, bioinformatic analysis showed that differentially expressed genes (DEGs) regulated by SsHADV-1 infection were identified in S. sclerotiorum. In total, 187 genes were differentially expressed, consisting of more up-regulated (114) than down-regulated (73) genes. The identified DEGs were involved in several important pathways. Metabolic processes, biosynthesis of antibiotics, and secondary metabolites were the most affected categories in S. sclerotiorum upon SsHADV-1 infection. Cell structure analysis suggested that 26% of the total DEGs were related to membrane tissues. Furthermore, 10 and 27 DEGs were predicted to be located in the cell membrane and mitochondria, respectively. Gene ontology enrichment analyses of the DEGs were performed, followed by functional annotation of the genes. Interestingly, one third of the annotated functional DEGs could be involved in the Ras-small G protein signal transduction pathway. These results revealed that SsHADV-1 virions may be able to bind host membrane proteins and influence signal transduction through Ras-small G protein-coupled receptors during early infection, providing new insight towards the molecular mechanisms of virions infection in S. sclerotiorum.

scholarly journals Roles of Argonautes and Dicers on Sclerotinia sclerotiorum Antiviral RNA Silencing

2019 ◽  
Vol 10 ◽  
Author(s):  
Achal Neupane ◽  
Chenchen Feng ◽  
Pauline K. Mochama ◽  
Huma Saleem ◽  
Shin-Yi Lee Marzano
Keyword(s):  
Sclerotinia Sclerotiorum ◽  
Rna Silencing

scholarly journals Quantitative conversion of biomass in giant DNA virus infection

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mikael Kördel ◽  
Martin Svenda ◽  
Hemanth K. N. Reddy ◽  
Emelie Fogelqvist ◽  
Komang G. Y. Arsana ◽  
...  
Keyword(s):  
Cellular Response ◽  
Chemical Engineering ◽  
Viral Infections ◽  
Morphological Changes ◽  
Burst Size ◽  
Gravimetric Analysis ◽  
Dna Virus ◽  
X Ray ◽  
Large Size ◽  
Viral Factory

AbstractBioconversion of organic materials is the foundation of many applications in chemical engineering, microbiology and biochemistry. Herein, we introduce a new methodology to quantitatively determine conversion of biomass in viral infections while simultaneously imaging morphological changes of the host cell. As proof of concept, the viral replication of an unidentified giant DNA virus and the cellular response of an amoebal host are studied using soft X-ray microscopy, titration dilution measurements and thermal gravimetric analysis. We find that virions produced inside the cell are visible from 18 h post infection and their numbers increase gradually to a burst size of 280–660 virions. Due to the large size of the virion and its strong X-ray absorption contrast, we estimate that the burst size corresponds to a conversion of 6–12% of carbonaceous biomass from amoebal host to virus. The occurrence of virion production correlates with the appearance of a possible viral factory and morphological changes in the phagosomes and contractile vacuole complex of the amoeba, whereas the nucleus and nucleolus appear unaffected throughout most of the replication cycle.

scholarly journals Herpes Simplex Virus 1 Manipulates Host Cell Antiviral and Proviral DNA Damage Responses

mBio ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Max E. Mertens ◽  
David M. Knipe
Keyword(s):  
Dna Damage ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Damage Response ◽  
Dna Virus ◽  
Herpes Simplex Virus 1 ◽  
Damage Response ◽  
Simplex Virus ◽  
The Relationship ◽  
Hsv 1

ABSTRACT Cells activate their DNA damage response (DDR) in response to DNA virus infection, including adenoviruses, papillomaviruses, polyomaviruses, and herpesviruses. In this study, we found that the DDR kinase pathways activated in normal human fibroblasts by herpes simplex virus 1 (HSV-1) input genomic DNA, HSV-1 replicating DNA, and progeny DNA and in uninfected cells treated with etoposide are different. We also found using clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 technology that different host gene products are required for the DDR in uninfected versus infected cells. Individual DDR components can be proviral or antiviral in that ataxia-telangiectasia mutated (ATM) and p53 promote and Mre11 restricts replication of ICP0-null HSV-1, but ICP0 expression eliminates these DDR effects. Thus, in total, these results argue that HSV-1 manipulates the host cell DDR to utilize specific components for its optimal replication while inactivating the antiviral aspects of the DDR. IMPORTANCE We investigated the relationship between the DNA damage response, a collection of vital cellular pathways that repair potentially lethal damage to the genome, and the DNA virus herpes simplex virus 1. We found that infection by the virus triggers the DNA damage response, and key proteins that mediate this response have opposing effects on the replication and production of progeny viruses. Our work provides novel insights into the relationship between DNA virus infection and the cellular response to the viral genome. We speculate that viral gene products modulate this response, providing potentially novel targets for therapeutic intervention against the virus.

scholarly journals Small Maf Compound Mutants Display Central Nervous System Neuronal Degeneration, Aberrant Transcription, and Bach Protein Mislocalization Coincident with Myoclonus and Abnormal Startle Response

2003 ◽  
Vol 23 (4) ◽  
pp. 1163-1174 ◽  
Author(s):  
Fumiki Katsuoka ◽  
Hozumi Motohashi ◽  
Yuna Tamagawa ◽  
Shigeo Kure ◽  
Kazuhiko Igarashi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Germ Line ◽  
Neuronal Degeneration ◽  
Gene Dosage ◽  
Morphological Changes ◽  
Glycine Receptor ◽  
Neurological Dysfunction ◽  
Transcriptional Responses ◽  
Nuclear Extracts

ABSTRACT The small Maf proteins form heterodimers with CNC and Bach family proteins to elicit transcriptional responses from Maf recognition elements (MAREs). We previously reported germ line-targeted deficiencies in mafG plus mafK compound mutant mice. The most prominent mutant phenotype was a progressive maf dosage-dependent neuromuscular dysfunction. However, there has been no previous report regarding the effects of altered small-maf gene expression on neurological dysfunction. We show here that MafG and MafK are expressed in discrete central nervous system (CNS) neurons and that mafG::mafK compound mutants display neuronal degeneration coincident with surprisingly selective MARE-dependent transcriptional abnormalities. The CNS morphological changes are concurrent with the onset of a neurological disorder in the mutants, and the behavioral changes are accompanied by reduced glycine receptor subunit accumulation. Bach/small Maf heterodimers, which normally generate transcriptional repressors, were significantly underrepresented in nuclear extracts prepared from maf mutant brains, and Bach proteins fail to accumulate normally in nuclei. Thus compound mafG::mafK mutants develop age- and maf gene dosage-dependent cell-autonomous neuronal deficiencies that lead to profound neurological defects.

scholarly journals Mycoviruses as Triggers and Targets of RNA Silencing in White Mold Fungus Sclerotinia sclerotiorum

Viruses ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 214 ◽  
Author(s):  
Pauline Mochama ◽  
Prajakta Jadhav ◽  
Achal Neupane ◽  
Shin-Yi Lee Marzano
Keyword(s):  
Sclerotinia Sclerotiorum ◽  
Rna Silencing ◽  
White Mold ◽  
Mold Fungus

scholarly journals DnaA and SspA Regulation of the iraD gene of E. coli: an alternative DNA damage response independent of LexA/RecA

2021 ◽  
Author(s):  
Thalia H Sass ◽  
Alexander E Ferrazzoli ◽  
Susan T. Lovett
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Constitutive Expression ◽  
Adaptor Protein ◽  
Sos Response ◽  
Upstream Region ◽  
Mobility Shift ◽  
Transcriptional Responses ◽  
E Coli ◽  
Damage Response

The transcription factor RpoS (σS) of Escherichia coli controls a large number of genes important for tolerance of a variety of stress conditions. IraD promotes the post-translation stability of RpoS by inhibition of RssB, an adaptor protein for ClpXP degradation. We have previously documented DNA damage induction of iraD expression, independent of the SOS response. Both iraD and rpoS are required for tolerance to DNA damaging treatments such as H2O2 and the replication inhibitor azidothymidine in the log phase of growth. Using luciferase gene fusions to the 672 bp iraD upstream region, we show here that both promoters of iraD are induced by AZT. Genetic analysis suggests that both promoters are repressed by DnaA-ATP, partially dependent on a putative DnaA box at -81 bp, and regulated by RIDA (regulatory inactivation of DnaA), dependent on the DnaN processivity clamp. By electrophoretic mobility shift assays we show that purified DnaA protein binds to the iraD upstream region, so DnaA regulation of IraD is likely to be direct. DNA damage induction of iraD during log phase growth is abolished in the dnaA-T174P mutant, suggesting that DNA damage, in some way, relieves DnaA repression, possibly through the accumulation of replication clamps and enhanced RIDA. We demonstrate that the RNA-polymerase associated factor, SspA (stringent starvation protein A), induced by the accumulation of ppGpp, also affects IraD expression, with a positive effect on constitutive expression and a negative effect on AZT-induced expression, in a fashion independent of DnaA. SIGNIFICANCE: DNA damage can lead to cell death or genomic instability. Cells have evolved transcriptional responses that sense DNA damage and up-regulate tolerance and repair factors; the LexA/RecA-regulated SOS response in E. coli was the first example of such a system. This work describes an alternative DNA damage response, controlled by DnaA and the IraD post-translational regulator of RpoS. The cellular signals for this response, we propose, are empty replication processivity (β) clamps that accumulate at replication blocks. IraD expression is also regulated by stringent starvation protein, SspA, induced by nutrient deprivation. This SOS-independent DNA damage response integrates a signal of incomplete replication with starvation to modulate expression of genes that promote the completion of replication.

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