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      Lucilia cuprina genome unlocks parasitic fly biology to underpin future interventions

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          Abstract

          Lucilia cuprina is a parasitic fly of major economic importance worldwide. Larvae of this fly invade their animal host, feed on tissues and excretions and progressively cause severe skin disease (myiasis). Here we report the sequence and annotation of the 458-megabase draft genome of Lucilia cuprina. Analyses of this genome and the 14,544 predicted protein-encoding genes provide unique insights into the fly's molecular biology, interactions with the host animal and insecticide resistance. These insights have broad implications for designing new methods for the prevention and control of myiasis.

          Abstract

          Lucilia cuprina is a parasitic blowfly of major economic importance worldwide that feeds on the tissues of animals such as sheep. Here, the authors sequence the genome of L. cuprina and provide insights into the fly's molecular biology, interactions with the host animal and insecticide resistance.

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          Most cited references49

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          An optimized transgenesis system for Drosophila using germ-line-specific phiC31 integrases.

          Germ-line transformation via transposable elements is a powerful tool to study gene function in Drosophila melanogaster. However, some inherent characteristics of transposon-mediated transgenesis limit its use for transgene analysis. Here, we circumvent these limitations by optimizing a phiC31-based integration system. We generated a collection of lines with precisely mapped attP sites that allow the insertion of transgenes into many different predetermined intergenic locations throughout the fly genome. By using regulatory elements of the nanos and vasa genes, we established endogenous sources of the phiC31 integrase, eliminating the difficulties of coinjecting integrase mRNA and raising the transformation efficiency. Moreover, to discriminate between specific and rare nonspecific integration events, a white gene-based reconstitution system was generated that enables visual selection for precise attP targeting. Finally, we demonstrate that our chromosomal attP sites can be modified in situ, extending their scope while retaining their properties as landing sites. The efficiency, ease-of-use, and versatility obtained here with the phiC31-based integration system represents an important advance in transgenesis and opens up the possibility of systematic, high-throughput screening of large cDNA sets and regulatory elements.
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            Two chemosensory receptors together mediate carbon dioxide detection in Drosophila.

            Blood-feeding insects, including the malaria mosquito Anopheles gambiae, use highly specialized and sensitive olfactory systems to locate their hosts. This is accomplished by detecting and following plumes of volatile host emissions, which include carbon dioxide (CO2). CO2 is sensed by a population of olfactory sensory neurons in the maxillary palps of mosquitoes and in the antennae of the more genetically tractable fruitfly, Drosophila melanogaster. The molecular identity of the chemosensory CO2 receptor, however, remains unknown. Here we report that CO2-responsive neurons in Drosophila co-express a pair of chemosensory receptors, Gr21a and Gr63a, at both larval and adult life stages. We identify mosquito homologues of Gr21a and Gr63a, GPRGR22 and GPRGR24, and show that these are co-expressed in A. gambiae maxillary palps. We show that Gr21a and Gr63a together are sufficient for olfactory CO2-chemosensation in Drosophila. Ectopic expression of Gr21a and Gr63a together confers CO2 sensitivity on CO2-insensitive olfactory neurons, but neither gustatory receptor alone has this function. Mutant flies lacking Gr63a lose both electrophysiological and behavioural responses to CO2. Knowledge of the molecular identity of the insect olfactory CO2 receptors may spur the development of novel mosquito control strategies designed to take advantage of this unique and critical olfactory pathway. This in turn could bolster the worldwide fight against malaria and other insect-borne diseases.
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              Climate change and vector-borne diseases: a regional analysis.

              Current evidence suggests that inter-annual and inter-decadal climate variability have a direct influence on the epidemiology of vector-borne diseases. This evidence has been assessed at the continental level in order to determine the possible consequences of the expected future climate change. By 2100 it is estimated that average global temperatures will have risen by 1.0-3.5 degrees C, increasing the likelihood of many vector-borne diseases in new areas. The greatest effect of climate change on transmission is likely to be observed at the extremes of the range of temperatures at which transmission occurs. For many diseases these lie in the range 14-18 degrees C at the lower end and about 35-40 degrees C at the upper end. Malaria and dengue fever are among the most important vector-borne diseases in the tropics and subtropics; Lyme disease is the most common vector-borne disease in the USA and Europe. Encephalitis is also becoming a public health concern. Health risks due to climatic changes will differ between countries that have developed health infrastructures and those that do not. Human settlement patterns in the different regions will influence disease trends. While 70% of the population in South America is urbanized, the proportion in sub-Saharan Africa is less than 45%. Climatic anomalies associated with the El Niño-Southern Oscillation phenomenon and resulting in drought and floods are expected to increase in frequency and intensity. They have been linked to outbreaks of malaria in Africa, Asia and South America. Climate change has far-reaching consequences and touches on all life-support systems. It is therefore a factor that should be placed high among those that affect human health and survival.
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                Author and article information

                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Pub. Group
                2041-1723
                25 June 2015
                2015
                : 6
                : 7344
                Affiliations
                [1 ]Faculty of Veterinary and Agricultural Sciences, The University of Melbourne , Parkville, Victoria 3010, Australia
                [2 ]Department of Human and Molecular Genetics, Baylor College of Medicine , Houston, Texas 77030, USA
                [3 ]School of Biosciences, The University of Melbourne , Parkville, Victoria 3010, Australia
                [4 ]Structural Chemistry Program, Eskitis Institute for Drug Discovery, Griffith University , Brisbane, Queensland 4111, Australia
                [5 ]Department of Genetic Medicine and Development, University of Geneva & Swiss Institute of Bioinformatics , CH-1211 Geneva, Switzerland
                [6 ]Ecosciences Precinct, Queensland Alliance for Agriculture and Food Innovation (QAAFI), Queensland Bioscience Precinct, The University of Queensland , St Lucia, Brisbane, Queensland 4072, Australia
                [7 ]CSIRO Agriculture Flagship, Queensland Bioscience Precinct , St Lucia, Brisbane, Queensland 4067, Australia
                Author notes
                Author information
                http://orcid.org/0000-0003-0939-6745
                Article
                ncomms8344
                10.1038/ncomms8344
                4491171
                26108605
                fc44f38e-f5bc-478f-8952-1b8995eb76c2
                Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 09 February 2015
                : 29 April 2015
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