scholarly journals Accessory Chromosomes in Fusarium oxysporum

2020 ◽  
Vol 110 (9) ◽  
pp. 1488-1496
Author(s):  
He Yang ◽  
Houlin Yu ◽  
Li-Jun Ma
Keyword(s):  
Fusarium Oxysporum ◽  
Fungal Pathogen ◽  
Current Knowledge ◽  
Fungal Species ◽  
Gene Density ◽  
Functional Importance ◽  
The Core ◽  
Gene Functions ◽  
Epigenetic Signatures ◽  
Accessory Chromosomes

Most genomes within the species complex of Fusarium oxysporum are organized into two compartments: the core chromosomes (CCs) and accessory chromosomes (ACs). As opposed to CCs, which are conserved and vertically transmitted to carry out essential housekeeping functions, lineage- or strain-specific ACs are believed to be initially horizontally acquired through unclear mechanisms. These two genomic compartments are different in terms of gene density, the distribution of transposable elements, and epigenetic markers. Although common in eukaryotes, the functional importance of ACs is uniquely emphasized among fungal species, specifically in relationship to fungal pathogenicity and their adaptation to diverse hosts. With a focus on the cross-kingdom fungal pathogen F. oxysporum, this review provides a summary of the differences between CCs and ACs based on current knowledge of gene functions, genome structures, and epigenetic signatures, and explores the transcriptional crosstalk between the core and accessory genomes.

scholarly journals Accessories Make the Outfit: Accessory Chromosomes and Other Dispensable DNA Regions in Plant-Pathogenic Fungi

2018 ◽  
Vol 31 (8) ◽  
pp. 779-788 ◽  
Author(s):  
Stefania Bertazzoni ◽  
Angela H. Williams ◽  
Darcy A. Jones ◽  
Robert A. Syme ◽  
Kar-Chun Tan ◽  
...  
Keyword(s):  
Fungal Pathogen ◽  
Core Genome ◽  
Pathogenic Fungi ◽  
Gene Clusters ◽  
Fungal Species ◽  
Sequencing Technologies ◽  
Fungal Genomes ◽  
Metabolite Synthesis ◽  
Specific Virulence ◽  
Accessory Chromosomes

Fungal pathogen genomes can often be divided into core and accessory regions. Accessory regions ARs) may be comprised of either ARs (within core chromosomes (CCs) or wholly dispensable (accessory) chromosomes (ACs). Fungal ACs and ARs typically accumulate mutations and structural rearrangements more rapidly over time than CCs and many harbor genes relevant to host-pathogen interactions. These regions are of particular interest in plant pathology and include host-specific virulence factors and secondary metabolite synthesis gene clusters. This review outlines known ACs and ARs in fungal genomes, methods used for their detection, their common properties that differentiate them from the core genome, and what is currently known of their various roles in pathogenicity. Reports on the evolutionary processes generating and shaping AC and AR compartments are discussed, including repeat induced point mutation and breakage fusion bridge cycles. Previously ACs have been studied extensively within key genera, including Fusarium, Zymoseptoria, and Alternaria, but are growing in frequency of observation and perceived importance across a wider range of fungal species. Recent advances in sequencing technologies permit affordable genome assembly and resequencing of populations that will facilitate further discovery and routine screening of ACs.

scholarly journals Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Mija Marinković ◽  
Matilda Šprung ◽  
Maja Buljubašić ◽  
Ivana Novak
Keyword(s):  
Therapeutic Strategy ◽  
Current Knowledge ◽  
Therapeutic Agents ◽  
Therapeutic Strategies ◽  
Human Diseases ◽  
The Core ◽  
Future Drug ◽  
Autophagic Activity ◽  
Tumor Types ◽  
Catabolic Process

In the last two decades, accumulating evidence pointed to the importance of autophagy in various human diseases. As an essential evolutionary catabolic process of cytoplasmatic component digestion, it is generally believed that modulating autophagic activity, through targeting specific regulatory actors in the core autophagy machinery, may impact disease processes. Both autophagy upregulation and downregulation have been found in cancers, suggesting its dual oncogenic and tumor suppressor properties during malignant transformation. Identification of the key autophagy targets is essential for the development of new therapeutic agents. Despite this great potential, no therapies are currently available that specifically focus on autophagy modulation. Although drugs like rapamycin, chloroquine, hydroxychloroquine, and others act as autophagy modulators, they were not originally developed for this purpose. Thus, autophagy may represent a new and promising pharmacologic target for future drug development and therapeutic applications in human diseases. Here, we summarize our current knowledge in regard to the interplay between autophagy and malignancy in the most significant tumor types: pancreatic, breast, hepatocellular, colorectal, and lung cancer, which have been studied in respect to autophagy manipulation as a promising therapeutic strategy. Finally, we present an overview of the most recent advances in therapeutic strategies involving autophagy modulators in cancer.

Abstract P457: Systems Analysis To Understand The Impact Of The CDK Module On Cardiomyocyte Proliferation

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Bryana N Harris ◽  
Laura Woo ◽  
Jeffrey J Saucerman
Keyword(s):  
Experimental Data ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Dna Synthesis ◽  
Current Knowledge ◽  
Cycle Phase ◽  
Cyclin D ◽  
Cardiomyocyte Proliferation ◽  
The Core ◽  
The Impact

Rationale: Heart failure is caused by the inability of adult mammalian hearts to overcome the loss of cardiomyocytes (CMs). This is due partly to the limited proliferative capacity of CMs, which exit the cell cycle and do not undergo cell division. Current knowledge in cardiac regeneration lacks an understanding of the molecular regulatory networks that determine whether CMs will progress through the cell cycle to proliferate. Our goal is to use computational modeling to understand the expression and activation levels of the core cell cycle network, specifically cyclins and cyclin-cyclin-dependent kinase (CDK) complexes. Methods: A model of core cell cycle dynamics was curated using previously published studies of CM proliferation regulators. This model incorporates those regulators known to stimulate G1/S and G2/M transitions through the core CDKs. The activity of each of the 22 network nodes (22 reactions) was predicted using a logic-based differential equation approach. The CDK model was then coupled with a minimal ODE model of cell cycle phase distributions and validated based on descriptions and experimental data from the literature. To prioritize key nodes for experimental validation, we performed a sensitivity analysis by stimulating individual knockdown for every node in the network, measuring the fractional activity of all nodes. Results: Our model confirmed that the knockdown of p21 and Rb protein and the overexpression of E2F transcription factor and cyclinD-cdk4 showed an increase in cells going through DNA synthesis and entering mitosis. A combined knockdown of p21 and p27 showed an increase of cells entering mitosis. Cyclin D-cdk4 and p21 overexpression showed a decrease and increase of Rb expression, respectively. Of the 14 model predictions, 12 agreed with experimental data in the literature. A comprehensive knockdown of the model nodes suggests that E2F (a key transcription factor driving DNA synthesis) is positively regulated by cyclin D while negatively regulated by GSK3B, SMAD3, and pRB. Conclusion: This model enables us to predict how cardiomyocytes respond to stimuli in the CDK network and identify potential therapeutic regulators that induce cardiomyocyte proliferation.

scholarly journals Transcription Factors Encoded on Core and Accessory Chromosomes of Fusarium oxysporum Induce Expression of Effector Genes

PLoS Genetics ◽  
2016 ◽  
Vol 12 (11) ◽  
pp. e1006401 ◽  
Author(s):  
H. Charlotte van der Does ◽  
Like Fokkens ◽  
Ally Yang ◽  
Sarah M. Schmidt ◽  
Léon Langereis ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Fusarium Oxysporum ◽  
Effector Genes ◽  
Accessory Chromosomes

scholarly journals Revisiting Bap Multidomain Protein: More Than Sticking Bacteria Together

2020 ◽  
Vol 11 ◽  
Author(s):  
Jaione Valle ◽  
Xianyang Fang ◽  
Iñigo Lasa
Keyword(s):  
Biofilm Formation ◽  
Core Genome ◽  
Current Knowledge ◽  
Surface Proteins ◽  
Structure And Properties ◽  
Diverse Range ◽  
The Core ◽  
Self Assembling ◽  
Abiotic Surfaces ◽  
Range Of Functions

One of the major components of the staphylococcal biofilm is surface proteins that assemble as scaffold components of the biofilm matrix. Among the different surface proteins able to contribute to biofilm formation, this review is dedicated to the Biofilm Associated Protein (Bap). Bap is part of the accessory genome of Staphylococcus aureus but orthologs of Bap in other staphylococcal species belong to the core genome. When present, Bap promotes adhesion to abiotic surfaces and induces strong intercellular adhesion by self-assembling into amyloid like aggregates in response to the levels of calcium and the pH in the environment. During infection, Bap enhances the adhesion to epithelial cells where it binds directly to the host receptor Gp96 and inhibits the entry of the bacteria into the cells. To perform such diverse range of functions, Bap comprises several domains, and some of them include several motifs associated to distinct functions. Based on the knowledge accumulated with the Bap protein of S. aureus, this review aims to summarize the current knowledge of the structure and properties of each domain of Bap and their contribution to Bap functionality.

scholarly journals Analysis of hepatitis C virus core/NS5A protein co-localization using novel cell culture systems expressing core–NS2 and NS5A of genotypes 1–7

2013 ◽  
Vol 94 (10) ◽  
pp. 2221-2235 ◽  
Author(s):  
Andrea Galli ◽  
Troels K. H. Scheel ◽  
Jannick C. Prentoe ◽  
Lotte S. Mikkelsen ◽  
Judith M. Gottwein ◽  
...  
Keyword(s):  
Cell Culture ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Current Knowledge ◽  
Particle Assembly ◽  
Adaptive Mutations ◽  
Culture Systems ◽  
The Core ◽  
Cell Culture Systems ◽  
Significant Difference

Hepatitis C virus (HCV) is an important human pathogen infecting hepatocytes. With the advent of infectious cell culture systems, the HCV particle assembly and release processes are finally being uncovered. The HCV core and NS5A proteins co-localize on cytoplasmic lipid droplets (cLDs) or on the endoplasmic reticulum (ER) at different stages of particle assembly. Current knowledge on assembly and release is primarily based on studies in genotype 2a cell culture systems; however, given the high genetic heterogeneity of HCV, variations might exist among genotypes. Here, we developed novel HCV strain JFH1-based recombinants expressing core–NS2 and NS5A from genotypes 1–7, and analysed core and NS5A co-localization in infected cells. Huh7.5 cells were transfected with RNA of core–NS2/NS5A recombinants and putative adaptive mutations were analysed by reverse genetics. Adapted core–NS2/NS5A recombinants produced infectivity titres of 102.5–104.5 f.f.u. ml−1. Co-localization analysis demonstrated that the core and NS5A proteins from all genotypes co-localized extensively, and there was no significant difference in protein co-localization among genotypes. In addition, we found that the core and NS5A proteins were highly associated with cLDs at 12 h post-infection but became mostly ER associated at later stages. Finally, we found that different genotypes showed varying levels of core/cLD co-localization, with a possible effect on viral assembly/release. In summary, we developed a panel of HCV genotype 1–7 core–NS2/NS5A recombinants producing infectious virus, and an immunostaining protocol detecting the core and NS5A proteins from seven different genotypes. These systems will allow, for the first time, investigation of core/NS5A interactions during assembly and release of HCV particles of all major genotypes.

scholarly journals Clathrin- and Arp2/3-Independent Endocytosis in the Fungal Pathogen Candida albicans

mBio ◽  
2013 ◽  
Vol 4 (5) ◽  
Author(s):  
Elias Epp ◽  
Elena Nazarova ◽  
Hannah Regan ◽  
Lois M. Douglas ◽  
James B. Konopka ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Membrane Proteins ◽  
Fungal Pathogen ◽  
Mammalian Cells ◽  
Fluid Phase ◽  
Fungal Species ◽  
Endocytic Pathway ◽  
Dependent Manner ◽  
Content Type ◽  
Actin Cables

ABSTRACT Clathrin-mediated endocytosis (CME) is conserved among eukaryotes and has been extensively analyzed at a molecular level. Here, we present an analysis of CME in the human fungal pathogen Candida albicans that shows the same modular structure as those in other fungi and mammalian cells. Intriguingly, C. albicans is perfectly viable in the absence of Arp2/3, an essential component of CME in other systems. In C. albicans, Arp2/3 function remains essential for CME as all 15 proteins tested that participate in CME, including clathrin, lose their characteristic dynamics observed in wild-type (WT) cells. However, since arp2/3 cells are still able to endocytose lipids and fluid-phase markers, but not the Ste2 and Mup1 plasma membrane proteins, there must be an alternate clathrin-independent pathway we term Arp2/3-independent endocytosis (AIE). Characterization of AIE shows that endocytosis in arp2 mutants relies on actin cables and other Arp2/3-independent actin structures, as inhibition of actin functions prevented cargo uptake in arp2/3 mutants. Transmission electron microscopy (TEM) showed that arp2/3 mutants still formed invaginating tubules, cell structures whose proper functions are believed to heavily rely on Arp2/3. Finally, Prk1 and Sjl2, two proteins involved in patch disassembly during CME, were not correctly localized to sites of endocytosis in arp2 mutants, implying a role of Arp2/3 in CME patch disassembly. Overall, C. albicans contains an alternative endocytic pathway (AIE) that relies on actin cable function to permit clathrin-independent endocytosis (CIE) and provides a system to further explore alternate endocytic routes that likely exist in fungal species. IMPORTANCE There is a well-established process of endocytosis that is generally used by eukaryotic cells termed clathrin-mediated endocytosis (CME). Although the details are somewhat different between lower and higher eukaryotes, CME appears to be the dominant endocytic process in all eukaryotes. While fungi such as Saccharomyces cerevisiae have proven excellent models for dissecting the molecular details of endocytosis, loss of CME is so detrimental that it has been difficult to study alternate pathways functioning in its absence. Although the fungal pathogen Candida albicans has a CME pathway that functions similarly to that of S. cerevisiae, inactivation of this pathway does not compromise growth of yeast-form C. albicans. In these cells, lipids and fluid-phase molecules are still endocytosed in an actin-dependent manner, but membrane proteins are not. Thus, C. albicans provides a powerful model for the analysis of CME-independent endocytosis in lower eukaryotes.

Selection for resistance to Fusarium wilt in red clover

1999 ◽  
Vol 79 (3) ◽  
pp. 351-356 ◽  
Author(s):  
B. C. Venuto ◽  
R. R. Smith ◽  
C. R. Grau
Keyword(s):  
Fusarium Oxysporum ◽  
Fungal Pathogen ◽  
Trifolium Pratense ◽  
Red Clover ◽  
Severity Index ◽  
Research Station ◽  
Vascular Wilt ◽  
Trifolium Pratense L ◽  
Selection For ◽  
Overall Resistance

In Wisconsin, Fusarium oxysporum, Schlect., a pathogen causing vascular wilt, is the most prevalent fungal pathogen recovered from diseased red clover (Trifolium pratense L.) plants. This study was conducted to determine the mode of inheritance for red clover resistance to this pathogen and to develop resistant germplasm. Virulent isolates of this pathogen, collected from red clover plants at the Ashland Research Station, Ashland, Wisconsin, were used to screen three populations, the red clover cultivars Arlington and Marathon and the C11 germplasm, for resistant plants. Plants were inoculated with the pathogen and evaluated for reaction, using a disease-severity index (DSI) score from 1 to 5 (1 = no reaction, 5 = plant dead). Selected plants from each cycle were intercrossed to produce subsequent generations. After two and three cycles of selection, the developed populations were simultaneously evaluated for gain from selection. The gain from selection for resistance in these populations (cycle 0 minus cycle 2) ranged from 0.31 to 0.48, 0.12 to 0.75, and 0.13 to 0.83 DSI units, respectively, for Arlington, Marathon, and C11. Estimated narrow-sense heritabilities, based on cycle-1 and cycle-2 progeny, were, respectively, 0.20 and 0.37 for Arlington, 0.15 and 0.13 for Marathon, and 0.06 and 0.17 for C11. These results indicate that resistance is a quantitative trait controlled by many loci, each contributing some portion to overall resistance in the host. Key words: Red clover, Trifolium pratense L., Fusarium oxysporum, vascular wilt, resistance

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