The Experts below are selected from a list of 30249 Experts worldwide ranked by ideXlab platform
Alex S. Flynt - One of the best experts on this subject based on the ideXlab platform.
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Rewired RNAi-mediated genome surveillance in house Dust Mites.
PLoS genetics, 2018Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNA (siRNA)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs highlights the unusual arc of Dust mite evolution.
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Rewired RNAi-Mediated Genome Surveillance in House Dust Mites
2016Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Natalya Ortolano, Kelly E Scott, Caleb Taylor, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNAs (siRNAs)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs provides a mechanism for unusual arc of Dust mite evolution.
Pavel B. Klimov - One of the best experts on this subject based on the ideXlab platform.
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Rewired RNAi-mediated genome surveillance in house Dust Mites.
PLoS genetics, 2018Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNA (siRNA)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs highlights the unusual arc of Dust mite evolution.
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Rewired RNAi-Mediated Genome Surveillance in House Dust Mites
2016Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Natalya Ortolano, Kelly E Scott, Caleb Taylor, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNAs (siRNAs)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs provides a mechanism for unusual arc of Dust mite evolution.
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is permanent parasitism reversible critical evidence from early evolution of house Dust Mites
Systematic Biology, 2013Co-Authors: Pavel B. Klimov, Barry M OconnorAbstract:Long-term specialization may limit the ability of a species to respond to new environmental conditions and lead to a higher likelihood of extinction. For permanent parasites and other symbionts, the most intriguing question is whether these organisms can return to a free-living lifestyle and, thus, escape an evolutionary "dead end." This question is directly related to Dollo's law, which stipulates that a complex trait (such as being free living vs. parasitic) cannot re-evolve again in the same form. Here, we present conclusive evidence that house Dust Mites, a group of medically important free-living organisms, evolved from permanent parasites of warm-blooded vertebrates. A robust, multigene topology (315 taxa, 8942 nt), ancestral character state reconstruction, and a test for irreversible evolution (Dollo's law) demonstrate that house Dust Mites have abandoned a parasitic lifestyle, secondarily becoming free living, and then speciated in several habitats. Hence, as exemplified by this model system, highly specialized permanent parasites may drastically de-specialize to the extent of becoming free living and, thus escape from dead-end evolution. Our phylogenetic and historical ecological framework explains the limited cross-reactivity between allergens from the house Dust Mites and "storage" Mites and the ability of the Dust Mites to inhibit host immune responses. It also provides insights into how ancestral features related to parasitism (frequent ancestral shifts to unrelated hosts, tolerance to lower humidity, and pre-existing enzymes targeting skin and keratinous materials) played a major role in reversal to the free-living state. We propose that parasitic ancestors of pyroglyphids shifted to nests of vertebrates. Later the nest-inhabiting pyroglyphids expanded into human dwellings to become a major source of allergens.
Nicolas Cenac - One of the best experts on this subject based on the ideXlab platform.
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House Dust Mites activate nociceptor–mast cell clusters to drive type 2 skin inflammation
Nature Immunology, 2019Co-Authors: Nadine Serhan, Lilian Basso, Riccardo Sibilano, Camille Petitfils, James Meixiong, Chrystelle Bonnart, Laurent L. Reber, Thomas Marichal, Philipp Starkl, Nicolas CenacAbstract:Allergic skin diseases, such as atopic dermatitis, are clinically characterized by severe itching and type 2 immunity-associated hypersensitivity to widely distributed allergens, including those derived from house Dust Mites (HDMs). Here we found that HDMs with cysteine protease activity directly activated peptidergic nociceptors, which are neuropeptide-producing nociceptive sensory neurons that express the ion channel TRPV1 and Tac1, the gene encoding the precursor for the neuropeptide substance P. Intravital imaging and genetic approaches indicated that HDM-activated nociceptors drive the development of allergic skin inflammation by inducing the degranulation of mast cells contiguous to such nociceptors, through the release of substance P and the activation of the cationic molecule receptor MRGPRB2 on mast cells. These data indicate that, after exposure to HDM allergens, activation of TRPV1+Tac1+ nociceptor–MRGPRB2+ mast cell sensory clusters represents a key early event in the development of allergic skin reactions.
Mosharrof Hossain Mondal - One of the best experts on this subject based on the ideXlab platform.
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Rewired RNAi-mediated genome surveillance in house Dust Mites.
PLoS genetics, 2018Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNA (siRNA)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs highlights the unusual arc of Dust mite evolution.
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Rewired RNAi-Mediated Genome Surveillance in House Dust Mites
2016Co-Authors: Mosharrof Hossain Mondal, Pavel B. Klimov, Natalya Ortolano, Kelly E Scott, Caleb Taylor, Alex S. FlyntAbstract:House Dust Mites are common pests with an unusual evolutionary history, being descendants of a parasitic ancestor. Transition to parasitism is frequently accompanied by genome rearrangements, possibly to accommodate the genetic change needed to access new ecology. Transposable element (TE) activity is a source of genomic instability that can trigger large-scale genomic alterations. Eukaryotes have multiple transposon control mechanisms, one of which is RNA interference (RNAi). Investigation of the Dust mite genome failed to identify a major RNAi pathway: the Piwi-associated RNA (piRNA) pathway, which has been replaced by a novel small-interfering RNAs (siRNAs)-like pathway. Co-opting of piRNA function by Dust mite siRNAs is extensive, including establishment of TE control master loci that produce siRNAs. Interestingly, other members of the Acari have piRNAs indicating loss of this mechanism in Dust Mites is a recent event. Flux of RNAi-mediated control of TEs provides a mechanism for unusual arc of Dust mite evolution.
Nadine Serhan - One of the best experts on this subject based on the ideXlab platform.
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House Dust Mites activate nociceptor–mast cell clusters to drive type 2 skin inflammation
Nature Immunology, 2019Co-Authors: Nadine Serhan, Lilian Basso, Riccardo Sibilano, Camille Petitfils, James Meixiong, Chrystelle Bonnart, Laurent L. Reber, Thomas Marichal, Philipp Starkl, Nicolas CenacAbstract:Allergic skin diseases, such as atopic dermatitis, are clinically characterized by severe itching and type 2 immunity-associated hypersensitivity to widely distributed allergens, including those derived from house Dust Mites (HDMs). Here we found that HDMs with cysteine protease activity directly activated peptidergic nociceptors, which are neuropeptide-producing nociceptive sensory neurons that express the ion channel TRPV1 and Tac1, the gene encoding the precursor for the neuropeptide substance P. Intravital imaging and genetic approaches indicated that HDM-activated nociceptors drive the development of allergic skin inflammation by inducing the degranulation of mast cells contiguous to such nociceptors, through the release of substance P and the activation of the cationic molecule receptor MRGPRB2 on mast cells. These data indicate that, after exposure to HDM allergens, activation of TRPV1+Tac1+ nociceptor–MRGPRB2+ mast cell sensory clusters represents a key early event in the development of allergic skin reactions.
