Prakash Pragya, Roychowdhury-Sinha Arghyashree, Goto Akira
Verloren negatively regulates the expression of IMD pathway dependent antimicrobial peptides in Drosophila Journal Article
In: Scientific Reports, vol. 11, no. 15549, 2021.
Abstract | Links | BibTeX | Tags: bacteria, Biochemistry, DNA, Fungi, Gene Expression, gene regulation, Genetics, hoffmann, Immunochemistry, Immunology, infection, inflammation, Innate immune cells, innate immunity, M3i, microbiology, Molecular Biology, pathogens, RNA, RNAi, Signal Transduction, Transcription
@article{Goto2021,
title = {Verloren negatively regulates the expression of IMD pathway dependent antimicrobial peptides in Drosophila},
author = {Pragya Prakash and Arghyashree Roychowdhury-Sinha and Akira Goto},
url = {https://www.nature.com/articles/s41598-021-94973-0},
doi = {10.1038/s41598-021-94973-0},
year = {2021},
date = {2021-07-30},
journal = {Scientific Reports},
volume = {11},
number = {15549},
abstract = {Drosophila immune deficiency (IMD) pathway is similar to the human tumor necrosis factor receptor (TNFR) signaling pathway and is preferentially activated by Gram-negative bacterial infection. Recent studies highlighted the importance of IMD pathway regulation as it is tightly controlled by numbers of negative regulators at multiple levels. Here, we report a new negative regulator of the IMD pathway, Verloren (Velo). Silencing of Velo led to constitutive expression of the IMD pathway dependent antimicrobial peptides (AMPs), and Escherichia coli stimulation further enhanced the AMP expression. Epistatic analysis indicated that Velo knock-down mediated AMP upregulation is dependent on the canonical members of the IMD pathway. The immune fluorescent study using overexpression constructs revealed that Velo resides both in the nucleus and cytoplasm, but the majority (~ 75%) is localized in the nucleus. We also observed from in vivo analysis that Velo knock-down flies exhibit significant upregulation of the AMP expression and reduced bacterial load. Survival experiments showed that Velo knock-down flies have a short lifespan and are susceptible to the infection of pathogenic Gram-negative bacteria, P. aeruginosa. Taken together, these data suggest that Velo is an additional new negative regulator of the IMD pathway, possibly acting in both the nucleus and cytoplasm.},
keywords = {bacteria, Biochemistry, DNA, Fungi, Gene Expression, gene regulation, Genetics, hoffmann, Immunochemistry, Immunology, infection, inflammation, Innate immune cells, innate immunity, M3i, microbiology, Molecular Biology, pathogens, RNA, RNAi, Signal Transduction, Transcription},
pubstate = {published},
tppubtype = {article}
}
Majzoub Karim, Imler Jean-Luc
Encyclopedia of Molecular Cell Biology and Molecular Medicine Book Chapter
In: Verlag, Wiley-VCH (Ed.): vol. 1, Chapter « RNAi to treat virus infections », pp. 192-228, GmbH & Co. KGaA, 2015.
Abstract | Links | BibTeX | Tags: antiviral, Argonaute, Delivery, imler, Immunity, lipofection, M3i, microRNA (miRNA), RNA Virus Infections, RNAi, small hairpin RNA (shRNA), small interfering RNA (siRNA)
@inbook{Majzoub2015,
title = {Encyclopedia of Molecular Cell Biology and Molecular Medicine},
author = {Karim Majzoub and Jean-Luc Imler},
editor = {Wiley-VCH Verlag},
doi = {10.1002/3527600906.mcb.201500003},
year = {2015},
date = {2015-04-28},
volume = {1},
pages = {192-228},
publisher = {GmbH & Co. KGaA},
chapter = {« RNAi to treat virus infections »},
abstract = {In spite of its young age, the field of RNA interference has already yielded major advances in the laboratory. This sequence-specific mechanism of gene regulation also holds strong promise for the development of a new generation of drugs, in particular to control the everlasting threat of viral infections. Here, the mechanisms and pathways of RNA interference are reviewed, with emphasis placed on how RNA silencing forms a potent antiviral immune mechanism in plants and invertebrates. The approaches developed to use RNA interference to control viral infections in mammals are then described. Finally, the problems encountered while translating this revolutionary technology into the clinic are presented, and the advances currently developed to overcome these limitations are discussed.},
keywords = {antiviral, Argonaute, Delivery, imler, Immunity, lipofection, M3i, microRNA (miRNA), RNA Virus Infections, RNAi, small hairpin RNA (shRNA), small interfering RNA (siRNA)},
pubstate = {published},
tppubtype = {inbook}
}
Lamacchia Marina, Clayton John Randy, Wang-Sattler R, Steinmetz Lars M, Levashina Elena A, Blandin Stéphanie A
Silencing of Genes and Alleles by RNAi in Anopheles gambiae Journal Article
In: Methods Mol Biol., vol. 923, pp. 161-76, 2013.
Abstract | BibTeX | Tags: blandin, dsRNA, M3i, RNAi
@article{M2013,
title = {Silencing of Genes and Alleles by RNAi in Anopheles gambiae},
author = {Marina Lamacchia and John Randy Clayton and R Wang-Sattler and Lars M Steinmetz and Elena A Levashina and Stéphanie A Blandin},
year = {2013},
date = {2013-06-13},
journal = {Methods Mol Biol.},
volume = {923},
pages = {161-76},
abstract = {Anopheles gambiae mosquitoes are the major vectors of human malaria parasites. However, mosquitoes are not passive hosts for parasites, actively limiting their development in vivo. Our current understanding of the mosquito antiparasitic response is mostly based on the phenotypic analysis of gene knockdowns obtained by RNA interference (RNAi), through the injection or transfection of long dsRNAs in adult mosquitoes or cultured cells, respectively. Recently, RNAi has been extended to silence specifically one allele of a given gene in a heterozygous context, thus allowing to compare the contribution of different alleles to a phenotype in the same genetic background.},
keywords = {blandin, dsRNA, M3i, RNAi},
pubstate = {published},
tppubtype = {article}
}
Catteruccia Flaminia, Levashina Elena A
RNAi in the malaria vector, Anopheles gambiae Journal Article
In: Methods Mol Biol., vol. 555, pp. 63-75, 2009.
Abstract | Links | BibTeX | Tags: RNAi
@article{F2009,
title = {RNAi in the malaria vector, Anopheles gambiae},
author = {Flaminia Catteruccia and Elena A Levashina},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19495688},
year = {2009},
date = {2009-01-01},
journal = {Methods Mol Biol.},
volume = {555},
pages = {63-75},
abstract = {Malaria is a disease that kills more than a million people each year in tropical and subtropical countries. The disease is caused by Plasmodium parasites and is transmitted to humans exclusively by mosquitoes of the genus Anopheles. The lack of functional approaches has hampered study of the biological networks that determine parasite transmission by the insect vector. The recent discovery of RNA interference and its adaptation to mosquitoes is now providing crucial tools for the dissection of vector-parasite interactions and for the analysis of aspects of mosquito biology influencing the vectorial capacity. Two RNAi approaches have been established in mosquitoes: transient gene silencing by direct injection of double-stranded RNA, and stable expression of hairpin RNAs from transgenes integrated in the genome. Here we describe these methods in detail, providing information about their use and limitations.},
keywords = {RNAi},
pubstate = {published},
tppubtype = {article}
}
Blandin Stéphanie A, Levashina Elena A
Reverse Genetics Analysis of Antiparasitic Responses in the Malaria Vector, Anopheles gambiae Journal Article
In: Methods Mol Biol., vol. 415, pp. 365-77, 2008.
Abstract | Links | BibTeX | Tags: blandin, M3i, RNAi
@article{SA2008b,
title = {Reverse Genetics Analysis of Antiparasitic Responses in the Malaria Vector, Anopheles gambiae},
author = {Stéphanie A Blandin and Elena A Levashina},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18370165},
year = {2008},
date = {2008-01-01},
journal = {Methods Mol Biol.},
volume = {415},
pages = {365-77},
abstract = {Anopheles mosquitoes are the major vectors of human malaria parasites. Mosquito-parasite interactions are critical for disease transmission and therefore represent a potential target for malaria control strategies. Mosquitoes mount potent antiparasitic responses, and identification of mosquito factors that limit parasite development is one of the major objectives in the field. To address this question, we have developed a convenient reverse genetics approach by injection of double-stranded RNA (dsRNA) in adult mosquitoes, to evaluate the function of candidate genes in mosquito antiparasitic responses.},
keywords = {blandin, M3i, RNAi},
pubstate = {published},
tppubtype = {article}
}
Blandin Stéphanie A, Levashina Elena A
Phagocytosis in mosquito immune responses Journal Article
In: Immunol Rev., vol. 219, pp. 8-16, 2007.
Abstract | Links | BibTeX | Tags: blandin, M3i, Phagocytosis, RNAi
@article{SA2007,
title = {Phagocytosis in mosquito immune responses},
author = {Stéphanie A Blandin and Elena A Levashina},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17850478},
year = {2007},
date = {2007-10-01},
journal = {Immunol Rev.},
volume = {219},
pages = {8-16},
abstract = {Anopheles mosquitoes are the only vectors of human malaria parasites. Mosquito-parasite interactions are critical for disease transmission and therefore are a potential target for malaria control strategies. Mosquitoes mount potent immune responses that efficiently limit proliferation of a variety of infectious agents, including microbial pathogens and malaria parasites. The recent completion of the Anopheles gambiae genome sequencing project combined with the development of the powerful RNA interference-based gene silencing helped to identify major players of the immune defenses and uncovered evolutionarily conserved mechanisms in the anti-bacterial and anti-Plasmodium responses. The anti-bacterial responses are based on phagocytosis at early steps of infections, followed, several hours later, by the synthesis of anti-microbial peptides. The principal regulators of anti-parasitic responses are predominantly synthesized by the mosquito blood cells; however, the exact molecular mechanisms of parasite killing remain unclear. Several regulators of phagocytosis are also required for efficient parasite killing. Here, we summarize our current knowledge of the anti-bacterial and anti-parasitic responses, with the particular emphasis on the role of phagocytosis in mosquito immunity.},
keywords = {blandin, M3i, Phagocytosis, RNAi},
pubstate = {published},
tppubtype = {article}
}
Moita L F, Wang R, Michel K, Blandin Stéphanie A, Zimmermann T, Levashina Elena A, Kafatos Fotis C
In Vivo Identification of Novel Regulators and Conserved Pathways of Phagocytosis in A. gambiae Journal Article
In: Immunity., vol. 23, no. 1, pp. 65-73, 2005.
Abstract | Links | BibTeX | Tags: blandin, M3i, RNAi
@article{LF2005,
title = {In Vivo Identification of Novel Regulators and Conserved Pathways of Phagocytosis in A. gambiae},
author = {L F Moita and R Wang and K Michel and Stéphanie A Blandin and T Zimmermann and Elena A Levashina and Fotis C Kafatos},
url = {http://www.ncbi.nlm.nih.gov/pubmed/16039580},
year = {2005},
date = {2005-07-01},
journal = {Immunity.},
volume = {23},
number = {1},
pages = {65-73},
abstract = {Anopheles gambiae uses effective immune responses, including phagocytosis, to fight microbial infection. We have developed a semiquantitative phagocytosis test and used it in conjunction with dsRNA gene silencing to test the in vivo roles of 71 candidate genes in phagocytosis of Escherichia coli and Staphylococcus aureus. Here, we show that inactivation of 26 genes changes the phagocytic activity by more than 45% and that two pathways similar to those that mediate apoptotic cell removal in Caenorhabditis elegans are used in A. gambiae for phagocytosis of microorganisms. Simultaneous inactivation of the identified regulators of phagocytosis and conserved components defining each signaling pathway permitted provisional assignment of the novel regulators to one or the other pathway. Pathway inactivation enhances at least three times the ability of E. coli and S. aureus to proliferate in the mosquito. Interestingly, mosquito survival is not compromised even if both pathways are perturbed simultaneously.},
keywords = {blandin, M3i, RNAi},
pubstate = {published},
tppubtype = {article}
}