Leptopilina heterotoma and L. boulardi: Strategies to avoid cellular defense responses of Drosophila melanogaster

1990 ◽  
Vol 70 (4) ◽  
pp. 466-475 ◽  
Author(s):  
T.M. Rizki ◽  
R.M. Rizki ◽  
Y. Carton
Keyword(s):  
Drosophila Melanogaster ◽  
Defense Responses ◽  
Leptopilina Heterotoma ◽  
Cellular Defense

SREBP‐1a Regulates Cellular Defense Responses in Bone Marrow‐Derived Macrophages

2008 ◽  
Vol 22 (S2) ◽  
pp. 273-273
Author(s):  
Seung‐Soon Im ◽  
Linda E Hammond ◽  
Leyla Yousef ◽  
Deborah Fraser ◽  
Andrea J Tenner ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Defense Responses ◽  
Cellular Defense

scholarly journals Rhizobacteria-Induced Priming in Arabidopsis Is Dependent on Ethylene, Jasmonic Acid, and NPR1

2007 ◽  
Vol 20 (7) ◽  
pp. 759-768 ◽  
Author(s):  
Il-Pyung Ahn ◽  
Sang-Woo Lee ◽  
Seok-Cheol Suh
Keyword(s):  
Hydrogen Peroxide ◽  
Disease Resistance ◽  
Jasmonic Acid ◽  
Expression Patterns ◽  
Defense Responses ◽  
Underlying Disease ◽  
Callose Deposition ◽  
Cellular Defense ◽  
Arabidopsis Ecotype ◽  
Hydrogen Peroxide Accumulation

A nonpathogenic rhizobacterium, Pseudomonas putida LSW17S, elicited systemic protection against Fusarium wilt and pith necrosis caused by Fusarium oxysporum f. sp. lycopersici and P. corrugata in tomato (Lycopersicon esculentum L.). LSW17S also confers disease resistance against P. syringae pv. tomato DC3000 (DC3000) on Arabidopsis ecotype Col-0. To investigate mechanisms underlying disease protection, expression patterns of defense-related genes PR1, PR2, PR5, and PDF1.2 and cellular defense responses such as hydrogen peroxide accumulation and callose deposition were investigated. LSW17S treatment exhibited the typical phenomena of priming. Strong and faster transcription of defense-related genes was induced and hydrogen peroxide or callose were accumulated in Arabidopsis treated with LSW17S and infected with DC3000. In contrast, individual actions of LSW17S and DC3000 did not elicit rapid molecular and cellular defense responses. Priming by LSW17S was translocated systemically and retained for more than 10 days. Treatment with LSW17S reduced pathogen proliferation in Arabidopsis ecotype Col-0 expressing bacterial NahG; however, npr1, etr1, and jar1 mutations impaired inhibition of pathogen growth. Cellular and molecular priming responses support these results. In sum, LSW17S primes Arabidopsis for NPR1-, ethylene-, and jasmonic acid-dependent disease resistance, and efficient molecular and cellular defense responses.

scholarly journals Multiple Toll-Spätzle Pathways in Drosophila melanogaster Immunity

2018 ◽  
Author(s):  
Munmun Chowdhury ◽  
Chun-Feng Li ◽  
Zhen He ◽  
Yuzhen Lu ◽  
Xusheng Liu ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Drosophila Melanogaster ◽  
Candida Albicans ◽  
Systemic Infection ◽  
Defense Responses ◽  
Immune Defense ◽  
Adult Males ◽  
Male And Female ◽  
Vesicular Stomatitis ◽  
Males And Females

AbstractThe Drosophila melanogaster Toll-Spätzle pathway plays an important role in development and immunity. Drosophila genome encodes nine Toll receptors and six Spätzle (Spz) proteins, and only the canonical Toll-Spz (Toll-1-Spz-1) pathway has been well investigated. In this study, we compared the nine Drosophila Tolls and showed that similarly to Toll, Toll-7 also strongly activated drosomycin promoter. Importantly, we showed that both Toll and Toll-7 interacted with Spz, Spz-2 and Spz-5, and co-expression of Toll or Toll-7 with Spz, Spz-2 and Spz-5 activated the drosomycin promoter. Furthermore, Toll and Toll-7 both recognized vesicular stomatitis virus (VSV) by binding to the VSV glycoprotein. Septic infection in Toll and Toll-7 mutant flies suggested that Toll and Toll-7 differentially affected defense responses in adult males and females after systemic infection by Enterococcus faecalis, Pseudomonas aeruginosa, Candida albicans or VSV. Our results suggest multiple Toll family members activate the expression of antimicrobial peptides. Our results also provide evidence that Toll and Toll-7 bind multiple Spätzle proteins and differentially affect immune defense against different pathogens in adult male and female flies.

scholarly journals Human Papillomavirus Carcinogenesis: an Identity Crisis in the Retinoblastoma Tumor Suppressor Pathway

2015 ◽  
Vol 89 (9) ◽  
pp. 4708-4711 ◽  
Author(s):  
Karl Munger ◽  
D. Leanne Jones
Keyword(s):  
Tumor Suppressor ◽  
Synthetic Lethality ◽  
Defense Responses ◽  
Human Papillomaviruses ◽  
Host Cells ◽  
Cellular Defense ◽  
Retinoblastoma Tumor Suppressor ◽  
Intracellular Parasites ◽  
Cellular Replication ◽  
Retinoblastoma Tumor

Viruses are obligate intracellular parasites and need to reprogram host cells to establish long-term persistent infection and/or to produce viral progeny. Cellular changes initiated by the virus trigger cellular defense responses to cripple viral replication, and viruses have evolved countermeasures to neutralize them. Established models have suggested that human papillomaviruses target the retinoblastoma (RB1) and TP53 tumor suppressor networks to usurp cellular replication, which drives carcinogenesis. More recent studies, however, suggest that modulating the activity of the Polycomb family of transcriptional repressors and the resulting changes in epigenetic regulation are proximal steps in the rewiring of cellular signaling circuits. Consequently, RB1 inactivation evolved to tolerate the resulting cellular alterations. Therefore, epigenetic reprograming results in cellular “addictions” to pathways for survival. Inhibition of such a pathway could cause “synthetic lethality” in adapted cells while not markedly affecting normal cells and could prove to be an effective therapeutic approach.

scholarly journals An Artificial Intelligence Workflow for Defining Host-Pathogen Interactions

2018 ◽  
Author(s):  
Daniel H Fisch ◽  
Artur Yakimovich ◽  
Barbara Clough ◽  
Joseph Wright ◽  
Monique Bunyan ◽  
...  
Keyword(s):  
Image Analysis ◽  
Defense Responses ◽  
Machine Learning Algorithms ◽  
Host Protein ◽  
Source Image ◽  
Host Pathogen Interactions ◽  
Cellular Defense ◽  
Host Pathogen ◽  
Protein Recruitment ◽  
Analysis Platform

For image-based infection biology, accurate unbiased quantification of host-pathogen interactions is essential, yet often performed manually or using limited enumeration employing simple image analysis algorithms based on image segmentation. Host protein recruitment to pathogens is often refractory to accurate automated assessment due to its heterogeneous nature. An intuitive intelligent image analysis program to assess host protein recruitment within general cellular pathogen defense is lacking. We present HRMAn (Host Response to Microbe Analysis), an open-source image analysis platform based on machine learning algorithms and deep learning. We show that HRMAn has the capability to learn phenotypes from the data, without relying on researcher-based assumptions. Using Toxoplasma gondii and Salmonella typhimurium we demonstrate HRMAn’s capacity to recognize, classify and quantify pathogen killing, replication and cellular defense responses.

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