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Articles 1 - 12 of 12
Full-Text Articles in Life Sciences
Iiv-6 Inhibits Nf-Kappab Responses In Drosophila, Cara C. West, Florentina Rus, Ying Chen, Anni Kleino, Monique Gangloff, Don B. Gammon, Neal S. Silverman
Iiv-6 Inhibits Nf-Kappab Responses In Drosophila, Cara C. West, Florentina Rus, Ying Chen, Anni Kleino, Monique Gangloff, Don B. Gammon, Neal S. Silverman
Neal Silverman
The host immune response and virus-encoded immune evasion proteins pose constant, mutual selective pressure on each other. Virally encoded immune evasion proteins also indicate which host pathways must be inhibited to allow for viral replication. Here, we show that IIV-6 is capable of inhibiting the two Drosophila NF-kappaB signaling pathways, Imd and Toll. Antimicrobial peptide (AMP) gene induction downstream of either pathway is suppressed when cells infected with IIV-6 are also stimulated with Toll or Imd ligands. We find that cleavage of both Imd and Relish, as well as Relish nuclear translocation, three key points in Imd signal transduction, occur …
Regulation Of The Drosophila Imd Pathway By Signaling Amyloids, Anni Kleino, Neal S. Silverman
Regulation Of The Drosophila Imd Pathway By Signaling Amyloids, Anni Kleino, Neal S. Silverman
Neal Silverman
Fruit flies elicit effective defense responses against numerous microbes. The responses against Gram-negative bacteria are mediated by the Imd pathway, an evolutionarily conserved NF-kappaB pathway recognizing meso-diaminopimelic acid (DAP)-type peptidoglycan from bacterial cell walls. Several reviews already provide a detailed view of ligand recognition and signal transduction during Imd signaling, but the formation and regulation of the signaling complex immediately downstream of the peptidoglycan-sensing receptors is still elusive. In this review, we focus on the formation of the Imd amyloidal signaling center and post-translational modifications in the assembly and disassembly of the Imd signaling complex.
Leishmania Amazonensis Engages Cd36 To Drive Parasitophorous Vacuole Maturation, Kendi Okuda, Mei Tong, Brian Dempsey, Kathryn J. Moore, Ricardo T. Gazzinelli, Neal S. Silverman
Leishmania Amazonensis Engages Cd36 To Drive Parasitophorous Vacuole Maturation, Kendi Okuda, Mei Tong, Brian Dempsey, Kathryn J. Moore, Ricardo T. Gazzinelli, Neal S. Silverman
Neal Silverman
Leishmania amastigotes manipulate the activity of macrophages to favor their own success. However, very little is known about the role of innate recognition and signaling triggered by amastigotes in this host-parasite interaction. In this work we developed a new infection model in adult Drosophila to take advantage of its superior genetic resources to identify novel host factors limiting Leishmania amazonensis infection. The model is based on the capacity of macrophage-like cells, plasmatocytes, to phagocytose and control the proliferation of parasites injected into adult flies. Using this model, we screened a collection of RNAi-expressing flies for anti-Leishmania defense factors. Notably, we …
Genomic Insights Into The Ixodes Scapularis Tick Vector Of Lyme Disease, Monika Gulia-Nuss,, Daniel R. Caffrey, Neal S. Silverman, Adam R. Wespiser, Catherine A. Hill
Genomic Insights Into The Ixodes Scapularis Tick Vector Of Lyme Disease, Monika Gulia-Nuss,, Daniel R. Caffrey, Neal S. Silverman, Adam R. Wespiser, Catherine A. Hill
Neal Silverman
Ticks transmit more pathogens to humans and animals than any other arthropod. We describe the 2.1 Gbp nuclear genome of the tick, Ixodes scapularis (Say), which vectors pathogens that cause Lyme disease, human granulocytic anaplasmosis, babesiosis and other diseases. The large genome reflects accumulation of repetitive DNA, new lineages of retro-transposons, and gene architecture patterns resembling ancient metazoans rather than pancrustaceans. Annotation of scaffolds representing approximately 57% of the genome, reveals 20,486 protein-coding genes and expansions of gene families associated with tick-host interactions. We report insights from genome analyses into parasitic processes unique to ticks, including host 'questing', prolonged feeding, …
A Single Vertebrate Dna Virus Protein Disarms Invertebrate Immunity To Rna Virus Infection, Don B. Gammon, Sophie Duraffour, Daniel K. Rozelle, Heidi Hehnly, Rita Sharma, Michael E. Sparks, Cara C. West, Ying Chen, James J. Moresco, Graciela Andrei, John H. Connor, Darryl Conte Jr., Dawn E. Gundersen-Rindal, William L. Marshall, John R. Yates, Neal S. Silverman, Craig C. Mello
A Single Vertebrate Dna Virus Protein Disarms Invertebrate Immunity To Rna Virus Infection, Don B. Gammon, Sophie Duraffour, Daniel K. Rozelle, Heidi Hehnly, Rita Sharma, Michael E. Sparks, Cara C. West, Ying Chen, James J. Moresco, Graciela Andrei, John H. Connor, Darryl Conte Jr., Dawn E. Gundersen-Rindal, William L. Marshall, John R. Yates, Neal S. Silverman, Craig C. Mello
Neal Silverman
Virus-host interactions drive a remarkable diversity of immune responses and countermeasures. We found that two RNA viruses with broad host ranges, vesicular stomatitis virus (VSV) and Sindbis virus (SINV), are completely restricted in their replication after entry into Lepidopteran cells. This restriction is overcome when cells are co-infected with vaccinia virus (VACV), a vertebrate DNA virus. Using RNAi screening, we show that Lepidopteran RNAi, Nuclear Factor-kappaB, and ubiquitin-proteasome pathways restrict RNA virus infection. Surprisingly, a highly conserved, uncharacterized VACV protein, A51R, can partially overcome this virus restriction. We show that A51R is also critical for VACV replication in vertebrate cells …
Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien
Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien
Neal Silverman
A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic …
The Genome Of Anopheles Darlingi, The Main Neotropical Malaria Vector, Osvaldo Marinotti, Adam R. Wespiser, Daniel R. Caffrey, Douglas T. Golenbock, Neal S. Silverman
The Genome Of Anopheles Darlingi, The Main Neotropical Malaria Vector, Osvaldo Marinotti, Adam R. Wespiser, Daniel R. Caffrey, Douglas T. Golenbock, Neal S. Silverman
Neal Silverman
Anopheles darlingi is the principal neotropical malaria vector, responsible for more than a million cases of malaria per year on the American continent. Anopheles darlingi diverged from the African and Asian malaria vectors approximately 100 million years ago (mya) and successfully adapted to the New World environment. Here we present an annotated reference A. darlingi genome, sequenced from a wild population of males and females collected in the Brazilian Amazon. A total of 10 481 predicted protein-coding genes were annotated, 72% of which have their closest counterpart in Anopheles gambiae and 21% have highest similarity with other mosquito species. In …
Serine/Threonine Acetylation Of Tgfbeta-Activated Kinase (Tak1) By Yersinia Pestis Yopj Inhibits Innate Immune Signaling, Nicholas Paul Paquette, Joseph E. Conlon, Charles R. Sweet, Florentina Rus, Lindsay Wilson, Andrea J. Pereira, Charles V. Rosadini, Nadege Goutagny, Alexander N. R. Weber, William S. Lane, Scott A. Shaffer, Stephanie Maniatis, Katherine A. Fitzgerald, Lynda M. Stuart, Neal S. Silverman
Serine/Threonine Acetylation Of Tgfbeta-Activated Kinase (Tak1) By Yersinia Pestis Yopj Inhibits Innate Immune Signaling, Nicholas Paul Paquette, Joseph E. Conlon, Charles R. Sweet, Florentina Rus, Lindsay Wilson, Andrea J. Pereira, Charles V. Rosadini, Nadege Goutagny, Alexander N. R. Weber, William S. Lane, Scott A. Shaffer, Stephanie Maniatis, Katherine A. Fitzgerald, Lynda M. Stuart, Neal S. Silverman
Neal Silverman
The Gram-negative bacteria Yersinia pestis, causative agent of plague, is extremely virulent. One mechanism contributing to Y. pestis virulence is the presence of a type-three secretion system, which injects effector proteins, Yops, directly into immune cells of the infected host. One of these Yop proteins, YopJ, is proapoptotic and inhibits mammalian NF-kappaB and MAP-kinase signal transduction pathways. Although the molecular mechanism remained elusive for some time, recent work has shown that YopJ acts as a serine/threonine acetyl-transferase targeting MAP2 kinases. Using Drosophila as a model system, we find that YopJ inhibits one innate immune NF-kappaB signaling pathway (IMD) but not …
Specificity And Signaling In The Drosophila Immune Response, Neal S. Silverman, Nicholas Paul Paquette, Kamna Aggarwal
Specificity And Signaling In The Drosophila Immune Response, Neal S. Silverman, Nicholas Paul Paquette, Kamna Aggarwal
Neal Silverman
The Drosophila immune response is characterized by the rapid and robust production of a battery of antimicrobial peptides immediately following infection. The genes encoding these antimicrobial peptides are controlled by two NF-κB signaling pathways that respond to microbial infection. The IMD pathway is triggered by DAP-type peptidoglycan, from the cell wall of most Gram-negative and certain Gram-positive bacteria, and activates the NF-κB precursor protein Relish. The Toll pathway, on the other hand, is stimulated by lysine-type peptidoglycan from many Gram-positive bacteria, β 1,3 glucans from many fungi, as well as by microbial proteases. Toll signaling leads to the activation and …
Fighting Infection Fly-Style, Louisa Wu, Neal S. Silverman
Fighting Infection Fly-Style, Louisa Wu, Neal S. Silverman
Neal Silverman
No abstract provided.
Nf-Kappab Signaling Pathways In Mammalian And Insect Innate Immunity, Neal S. Silverman, Tom Maniatis
Nf-Kappab Signaling Pathways In Mammalian And Insect Innate Immunity, Neal S. Silverman, Tom Maniatis
Neal Silverman
In this review, we discuss recent advances in understanding the signaling pathways in mammalian and Drosophila innate immunity, with emphasis on the mechanisms by which NF-kappaB/Rel family proteins are activated.
Hormonal Regulation Of The Humoral Innate Immune Response In Drosophila Melanogaster, Thomas Flatt, Andreas Heyland, Florentina Rus, Ermelinda Porpiglia, Chris Sherlock, Rochele Yamamoto, Alina Garbuzov, Subba R. Palli, Marc Tatar, Neal S. Silverman
Hormonal Regulation Of The Humoral Innate Immune Response In Drosophila Melanogaster, Thomas Flatt, Andreas Heyland, Florentina Rus, Ermelinda Porpiglia, Chris Sherlock, Rochele Yamamoto, Alina Garbuzov, Subba R. Palli, Marc Tatar, Neal S. Silverman
Neal Silverman
Juvenile hormone (JH) and 20-hydroxy-ecdysone (20E) are highly versatile hormones, coordinating development, growth, reproduction and aging in insects. Pulses of 20E provide key signals for initiating developmental and physiological transitions, while JH promotes or inhibits these signals in a stage-specific manner. Previous evidence suggests that JH and 20E might modulate innate immunity, but whether and how these hormones interact to regulate the immune response remains unclear. Here we show that JH and 20E have antagonistic effects on the induction of antimicrobial peptide (AMP) genes in Drosophila melanogaster. 20E pretreatment of Schneider S2 cells promoted the robust induction of AMP genes, …