scholarly journals The nuclear effector ArPEC25 from the necrotrophic fungus Ascochyta rabiei targets the chickpea transcription factor CaβLIM1a and negatively modulates lignin biosynthesis for host susceptibility

2021 ◽  
Author(s):  
Shreenivas Kumar Singh ◽  
Sandhya Verma ◽  
Kunal Singh ◽  
Ankita Shree ◽  
Ritu Singh ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fungal Pathogens ◽  
Ascochyta Blight ◽  
Lignin Biosynthesis ◽  
Phenylpropanoid Pathway ◽  
Host Cells ◽  
Host Susceptibility ◽  
Ascochyta Rabiei ◽  
Underlying Mechanisms ◽  
Blight Disease

Fungal pathogens deploy a barrage of secreted effectors to subvert host immunity, often by evading, disrupting, or altering key components of transcription, defense signaling, and metabolic pathways. However, the underlying mechanisms of effectors and their host targets are largely unexplored in necrotrophic fungal pathogens. Here, we describe the effector protein ArPEC25, which is secreted by the necrotroph Ascochyta rabiei, the causal agent of Ascochyta blight disease in chickpea (Cicer arietinum), and is indispensable for virulence. After entering host cells, ArPEC25 localizes to the nucleus and targets the host LIM transcription factor CaβLIM1a. CaβLIM1a is a transcriptional regulator of CaPAL1, which encodes phenylalanine ammonia lyase, the regulatory, gatekeeping enzyme of the phenylpropanoid pathway. ArPEC25 inhibits the transactivation of Ca?LIM1a by interfering with its DNA binding ability. This results in negative regulation of the phenylpropanoid pathway and decreased levels of intermediates of lignin biosynthesis, thereby suppressing lignin production. Our findings illustrate the role of fungal effectors in enhancing virulence by targeting a key defense pathway that leads to the biosynthesis of various secondary metabolites and antifungal compounds. This study provides a template for the study of less explored necrotrophic effectors and their host target functions.

scholarly journals Efficacy of fungicides, plant extracts and biocontrol agents against Ascochyta blight (Ascochyta rabiei) of chickpea (Cicer arietinum L.) under field conditions

2021 ◽  
Vol 8 (2) ◽  
pp. 255-262
Author(s):  
Salman Ahmad ◽  
Muhammad Aslam Khan ◽  
Irfan Ahmad ◽  
Zafar Iqbal ◽  
Ejaz Ashraf ◽  
...  
Keyword(s):  
Disease Severity ◽  
Plant Extracts ◽  
Biocontrol Agent ◽  
Ascochyta Blight ◽  
Field Conditions ◽  
Ascochyta Rabiei ◽  
Melia Azedarach ◽  
Sulphur Compounds ◽  
Cicer Arietinum L ◽  
Blight Disease

Two fungicides, Aliette and ThiovitJet @ 0.15%, containing Aluminum tris (O-ethyl phosphonate) and sulphur compounds, respectively; two plant extracts, Melia azedarach and Azadirachta indica @ 8% and one biocontrol agent, Trichoderma harzianum @ 107 conidia ml-1 were investigated against ascochyta blight of chickpea under field conditions. Treatments were evaluated on three varieties susceptible to chickpea blight. Field trial revealed that Aliette and ThiovitJet significantly decreased disease severity to 17 and 23% respectively, followed by M. azedarach and A. indica which decreased severity to 50 and 56% respectively, compared to control with 75% disease severity. T. harzianum, with a severity of 63%, was significantly less effective than fungicides and both plant extracts in controlling blight disease. The current research revealed that systemic and sulphur containing fungicides, both plant extracts and the biocontrol agent have the potential to control ascochyta blight of chickpea.

scholarly journals Current population structure and pathogenicity patterns of Ascochyta rabiei in Australia

2021 ◽  
Vol 7 (7) ◽  
Author(s):  
Ido Bar ◽  
Prabhakaran Thanjavur Sambasivam ◽  
Jenny Davidson ◽  
Lina M. Farfan-Caceres ◽  
Robert C. Lee ◽  
...  
Keyword(s):  
Continuous Monitoring ◽  
Molecular Diversity ◽  
Clonal Selection ◽  
Gene Diversity ◽  
Ascochyta Blight ◽  
Genotyping By Sequencing ◽  
Ascochyta Rabiei ◽  
Detailed Knowledge ◽  
Comprehensive Collection ◽  
Blight Disease

Ascochyta blight disease, caused by the necrotrophic fungus Ascochyta rabiei, is a major biotic constraint to chickpea production in Australia and worldwide. Detailed knowledge of the structure of the pathogen population and its potential to adapt to our farming practices is key to informing optimal management of the disease. This includes understanding the molecular diversity among isolates and the frequency and distribution of the isolates that have adapted to overcome host resistance across agroecologically distinct regions. Thanks to continuous monitoring efforts over the past 6 years, a comprehensive collection of A. rabiei isolates was collated from the major Australian chickpea production regions. To determine the molecular structure of the entire population, representative isolates from each collection year and growing region have been genetically characterized using a DArTseq genotyping-by-sequencing approach. The genotyped isolates were further phenotyped to determine their pathogenicity levels against a differential set of chickpea cultivars and genotype-phenotype associations were inferred. Overall, the Australian A. rabiei population displayed a far lower genetic diversity (average Nei’s gene diversity of 0.047) than detected in other populations worldwide. This may be explained by the presence of a single mating-type in Australia, MAT1-2, limiting its reproduction to a clonal mode. Despite the low detected molecular diversity, clonal selection appears to have given rise to a subset of adapted isolates that are highly pathogenic on commonly employed resistance sources, and that are occurring at an increasing frequency. Among these, a cluster of genetically similar isolates was identified, with a higher proportion of highly aggressive isolates than in the general population. The discovery of distinct genetic clusters associated with high and low isolate pathogenicity forms the foundation for the development of a molecular pathotyping tool for the Australian A. rabiei population. Application of such a tool, along with continuous monitoring of the genetic structure of the population will provide crucial information for the screening of breeding material and integrated disease management packages.

scholarly journals In Vitro and In Vivo Antifungal Activity of Sorbicillinoids Produced by Trichoderma longibrachiatum

2021 ◽  
Vol 7 (6) ◽  
pp. 428
Author(s):  
Men Thi Ngo ◽  
Minh Van Nguyen ◽  
Jae Woo Han ◽  
Myung Soo Park ◽  
Hun Kim ◽  
...  
Keyword(s):  
Late Blight ◽  
Culture Filtrate ◽  
Fungal Pathogens ◽  
Gray Mold ◽  
Trichoderma Longibrachiatum ◽  
Chemical Structures ◽  
Natural Agents ◽  
Blight Disease

In the search for antifungal agents from marine resources, we recently found that the culture filtrate of Trichoderma longibrachiatum SFC100166 effectively suppressed the development of tomato gray mold, rice blast, and tomato late blight. The culture filtrate was then successively extracted with ethyl acetate and n-butanol to identify the fungicidal metabolites. Consequently, a new compound, spirosorbicillinol D (1), and a new natural compound, 2′,3′-dihydro-epoxysorbicillinol (2), together with 11 known compounds (3–13), were obtained from the solvent extracts. The chemical structures were determined by spectroscopic analyses and comparison with literature values. The results of the in vitro antifungal assay showed that of the tested fungal pathogens, Phytophthora infestans was the fungus most sensitive to the isolated compounds, with MIC values ranging from 6.3 to 400 µg/mL, except for trichotetronine (9) and trichodimerol (10). When tomato plants were treated with the representative compounds (4, 6, 7, and 11), bisvertinolone (6) strongly reduced the development of tomato late blight disease compared to the untreated control. Taken together, our results revealed that the culture filtrate of T. longibrachiatum SFC100166 and its metabolites could be useful sources for the development of new natural agents to control late blight caused by P. infestans.

scholarly journals Brassinosteroids repress the seed maturation program during the seed-to-seedling transition

2021 ◽  
Author(s):  
Jiuxiao Ruan ◽  
Huhui Chen ◽  
Tao Zhu ◽  
Yaoguang Yu ◽  
Yawen Lei ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Abscisic Acid ◽  
Plant Hormone ◽  
Flowering Plants ◽  
Seed Maturation ◽  
Domain Protein ◽  
Abscisic Acid Insensitive3 ◽  
Underlying Mechanisms ◽  
Embryonic Structure

Abstract In flowering plants, repression of the seed maturation program is essential for the transition from the seed to the vegetative phase, but the underlying mechanisms remain poorly understood. The B3-domain protein VIVIPAROUS1/ABSCISIC ACID-INSENSITIVE3-LIKE 1 (VAL1) is involved in repressing the seed maturation program. Here we uncovered a molecular network triggered by the plant hormone brassinosteroid (BR) that inhibits the seed maturation program during the seed-to-seedling transition in Arabidopsis (Arabidopsis thaliana). val1-2 mutant seedlings treated with a BR biosynthesis inhibitor form embryonic structures, whereas BR signaling gain-of-function mutations rescue the embryonic structure trait. Furthermore, the BR-activated transcription factors BRI1-EMS-SUPPRESSOR 1 and BRASSINAZOLE-RESISTANT 1 bind directly to the promoter of AGAMOUS-LIKE15 (AGL15), which encodes a transcription factor involved in activating the seed maturation program, and suppress its expression. Genetic analysis indicated that BR signaling is epistatic to AGL15 and represses the seed maturation program by downregulating AGL15. Finally, we showed that the BR-mediated pathway functions synergistically with the VAL1/2-mediated pathway to ensure the full repression of the seed maturation program. Together, our work uncovered a mechanism underlying the suppression of the seed maturation program, shedding light on how BR promotes seedling growth.

scholarly journals Metabolome and proteome analyses reveal transcriptional misregulation in glycolysis of engineered E. coli

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chun-Ying Wang ◽  
Martin Lempp ◽  
Niklas Farke ◽  
Stefano Donati ◽  
Timo Glatter ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Binding Site ◽  
Metabolic Pathways ◽  
Glycerol Production ◽  
Inducible Promoters ◽  
E Coli ◽  
Inhibition Of Glycolysis ◽  
Underlying Mechanisms ◽  
Rate Limiting ◽  
Engineered Bacteria

AbstractSynthetic metabolic pathways are a burden for engineered bacteria, but the underlying mechanisms often remain elusive. Here we show that the misregulated activity of the transcription factor Cra is responsible for the growth burden of glycerol overproducing E. coli. Glycerol production decreases the concentration of fructose-1,6-bisphoshate (FBP), which then activates Cra resulting in the downregulation of glycolytic enzymes and upregulation of gluconeogenesis enzymes. Because cells grow on glucose, the improper activation of gluconeogenesis and the concomitant inhibition of glycolysis likely impairs growth at higher induction of the glycerol pathway. We solve this misregulation by engineering a Cra-binding site in the promoter controlling the expression of the rate limiting enzyme of the glycerol pathway to maintain FBP levels sufficiently high. We show the broad applicability of this approach by engineering Cra-dependent regulation into a set of constitutive and inducible promoters, and use one of them to overproduce carotenoids in E. coli.

scholarly journals Post-Translational Modifications Drive Success and Failure of Fungal–Host Interactions

2021 ◽  
Vol 7 (2) ◽  
pp. 124
Author(s):  
Charmaine Retanal ◽  
Brianna Ball ◽  
Jennifer Geddes-McAlister
Keyword(s):  
Fungal Pathogens ◽  
Fungal Infections ◽  
Treatment Options ◽  
Global Scale ◽  
Host Cells ◽  
Candida Spp ◽  
Post Translational Modifications ◽  
Fungal Host ◽  
Resistant Species

Post-translational modifications (PTMs) change the structure and function of proteins and regulate a diverse array of biological processes. Fungal pathogens rely on PTMs to modulate protein production and activity during infection, manipulate the host response, and ultimately, promote fungal survival. Given the high mortality rates of fungal infections on a global scale, along with the emergence of antifungal-resistant species, identifying new treatment options is critical. In this review, we focus on the role of PTMs (e.g., phosphorylation, acetylation, ubiquitination, glycosylation, and methylation) among the highly prevalent and medically relevant fungal pathogens, Candida spp., Aspergillus spp., and Cryptococcus spp. We explore the role of PTMs in fungal stress response and host adaptation, the use of PTMs to manipulate host cells and the immune system upon fungal invasion, and the importance of PTMs in conferring antifungal resistance. We also provide a critical view on the current knowledgebase, pose questions key to our understanding of the intricate roles of PTMs within fungal pathogens, and provide research opportunities to uncover new therapeutic strategies.

scholarly journals TheEucalyptuslinker histone variant EgH1.3 cooperates with the transcription factor EgMYB1 to control lignin biosynthesis during wood formation

2016 ◽  
Vol 213 (1) ◽  
pp. 287-299 ◽  
Author(s):  
Marçal Soler ◽  
Anna Plasencia ◽  
Romain Larbat ◽  
Cécile Pouzet ◽  
Alain Jauneau ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Lignin Biosynthesis ◽  
Wood Formation ◽  
Histone Variant

CBIO-15. LOSS OF WILLIAMS SYNDROME TRANSCRIPTION FACTOR (WSTF) LEADS TO IMPROVED TEMOZOLOMIDE SENSITIVITY IN HUMAN GLIOBLASTOMA CELLS IRRESPECTIVE OF MGMT EXPRESSION

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi30-vi30
Author(s):  
Katharina Sarnow ◽  
Stephanie Schwab ◽  
Oline Rio ◽  
Joydeep Mukherjee ◽  
Rolf Bjerkvig ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Lines ◽  
Williams Syndrome ◽  
Colony Formation ◽  
Dna Methyltransferase ◽  
Guide Rna ◽  
Methylguanine Dna Methyltransferase ◽  
Development Of Resistance ◽  
Dna Repair Protein ◽  
Underlying Mechanisms

Abstract BACKGROUND The prognosis for glioblastoma multiforme (GBM) patients is poor with a median survival of approximately 15 months. The DNA repair protein O 6-methylguanine-DNA methyltransferase (MGMT) counteracts the effects of temozolomide (TMZ) chemotherapy and is thus associated with poor outcome in GBM patients. Williams Syndrome Transcription Factor (WSTF) has been suggested to regulate the DNA damage response pathway (DDR) in both an indirect (through chromatin remodeling) and direct manner (by phosphorylating H2AX at Tyr142). However, whether WSTF has any role in the development of resistance against chemotherapy through its functions in the DDR in GBMs, is so far unknown. In this study, we investigated whether a loss of WSTF sensitizes different MGMT-proficient and -deficient GBM cell lines to TMZ treatment. METHODS We generated WSTF knockout clones from both MGMT-proficient (LN18, T98G) and -deficient GBM cell lines (U-251) using CRISPR/Cas9 gene-editing technology with lentiviral vectors. The PCR-based screening results combined with the T7 endonuclease mismatch assay for bi-allelic monoclonal knockouts were verified via sequencing and immunoblotting to identify candidate knockout clones. Colony formation assays were performed to determine the survival ability in response to TMZ treatment. Statistical analysis was performed using two-way ANOVA. RESULTS WSTF knockout clones showed a significant decrease in colony formation after TMZ-treatment compared to the corresponding control groups (non-target single guide RNA) (LN18: Clone 59 vs control: p= 0.0456, T98G: All three studied clones vs control: p< 0.0001, U-251: Clone 7/35.1/70.2 vs control: p< 0.0001/p= 0.0107/p= 0.0119). CONCLUSION WSTF is an important factor in both MGMT de- and proficient GBM cell lines for response against TMZ chemotherapy. The loss of WSTF leads to a significantly increased TMZ sensitivity in clinically relevant concentrations for all the studied cell lines. Ongoing studies are investigating the underlying mechanisms and potential alterations in the DDR pathway caused by WSTF loss.

PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle

Circulation ◽  
2021 ◽  
Author(s):  
Tongbin Wu ◽  
Zhengyu Liang ◽  
Zengming Zhang ◽  
Canzhao Liu ◽  
Lunfeng Zhang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Single Cell ◽  
Rna Sequencing ◽  
Mouse Models ◽  
Molecular Mechanisms ◽  
Left Ventricular ◽  
Ventricular Noncompaction ◽  
Chip Sequencing ◽  
Transcriptional Signature ◽  
Underlying Mechanisms

Background: Left ventricular noncompaction cardiomyopathy (LVNC) was discovered half a century ago as a cardiomyopathy with excessive trabeculation and a thin ventricular wall. In the decades since, numerous studies have demonstrated that LVNC primarily impacts left ventricles (LVs), and is often associated with LV dilation and dysfunction. However, owing in part to the lack of suitable mouse models that faithfully mirror the selective LV vulnerability in patients, mechanisms underlying susceptibility of LV to dilation and dysfunction in LVNC remain unknown. Genetic studies have revealed that deletions and mutations in PRDM16 cause LVNC, but previous conditional Prdm16 knockout mouse models do not mirror the LVNC phenotype in patients, and importantly, the underlying molecular mechanisms by which PRDM16 deficiency causes LVNC are still unclear. Methods: Prdm16 cardiomyocyte (CM)-specific knockout ( Prdm16 cKO ) mice were generated and analyzed for cardiac phenotypes. RNA sequencing and ChIP sequencing were performed to identify direct transcriptional targets of PRDM16 in CMs. Single cell RNA sequencing in combination with Spatial Transcriptomics were employed to determine CM identity at single cell level. Results: CM-specific ablation of Prdm16 in mice caused LV-specific dilation and dysfunction, as well as biventricular noncompaction, which fully recapitulated LVNC in patients. Mechanistically, PRDM16 functioned as a compact myocardium-enriched transcription factor, which activated compact myocardial genes while repressing trabecular myocardial genes in LV compact myocardium. Consequently, Prdm16 cKO LV compact myocardial CMs shifted from their normal transcriptomic identity to a transcriptional signature resembling trabecular myocardial CMs and/or neurons. Chamber-specific transcriptional regulation by PRDM16 was in part due to its cooperation with LV-enriched transcription factors Tbx5 and Hand1. Conclusions: These results demonstrate that disruption of proper specification of compact CM may play a key role in the pathogenesis of LVNC. They also shed light on underlying mechanisms of LV-restricted transcriptional program governing LV chamber growth and maturation, providing a tangible explanation for the susceptibility of LV in a subset of LVNC cardiomyopathies.

scholarly journals Rapid evolution of decreased host susceptibility drives a stable relationship between ultrasmall parasite TM7x and its bacterial host

2018 ◽  
Vol 115 (48) ◽  
pp. 12277-12282 ◽  
Author(s):  
Batbileg Bor ◽  
Jeffrey S. McLean ◽  
Kevin R. Foster ◽  
Lujia Cen ◽  
Thao T. To ◽  
...  
Keyword(s):  
Host Cell ◽  
Rapid Evolution ◽  
Host Population ◽  
Host Cells ◽  
Host Susceptibility ◽  
Bacterial Host ◽  
Narrow Host Range ◽  
Stable Relationship ◽  
Candidate Phyla Radiation

Around one-quarter of bacterial diversity comprises a single radiation with reduced genomes, known collectively as the Candidate Phyla Radiation. Recently, we coisolated TM7x, an ultrasmall strain of the Candidate Phyla Radiation phylum Saccharibacteria, with its bacterial host Actinomyces odontolyticus strain XH001 from human oral cavity and stably maintained as a coculture. Our current work demonstrates that within the coculture, TM7x cells establish a long-term parasitic association with host cells by infecting only a subset of the population, which stay viable yet exhibit severely inhibited cell division. In contrast, exposure of a naïve A. odontolyticus isolate, XH001n, to TM7x cells leads to high numbers of TM7x cells binding to each host cell, massive host cell death, and a host population crash. However, further passaging reveals that XH001n becomes less susceptible to TM7x over time and enters a long-term stable relationship similar to that of XH001. We show that this reduced susceptibility is driven by rapid host evolution that, in contrast to many forms of phage resistance, offers only partial protection. The result is a stalemate where infected hosts cannot shed their parasites; nevertheless, parasite load is sufficiently low that the host population persists. Finally, we show that TM7x can infect and form stable long-term relationships with other species in a single clade of Actinomyces, displaying a narrow host range. This system serves as a model to understand how parasitic bacteria with reduced genomes such as those of the Candidate Phyla Radiation have persisted with their hosts and ultimately expanded in their diversity.

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