DOCSLIB.ORG

UNIVERSITY of CALIFORNIA, SAN DIEGO Microsporidia Growth And

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
UNIVERSITY of CALIFORNIA, SAN DIEGO Microsporidia Growth And UNIVERSITY OF CALIFORNIA, SAN DIEGO Microsporidia growth and host resistance in Nematocida-Caenorhabditis elegans interactions A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Biology by Keir Morgan Balla Committee in charge: Professor Emily Troemel, Chair Professor Sreekanth Chalasani Professor Lars Eckmann Professor Kit Pogliano Professor Scott Rifkin 2016 Copyright Keir Morgan Balla, 2016 All rights reserved. The Dissertation of Keir Morgan Balla is approved, and it is acceptable in quality and form for publication on microfilm and electronically: Chair University of California, San Diego 2016 iii DEDICATION With love to my wife, grandparents, parents and their partners, brothers, in-laws, friends, and cat iv TABLE OF CONTENTS SIGNATURE PAGE….……………………………………………………………………... iii DEDICATION ............................................................................................................... iv TABLE OF CONTENTS ................................................................................................ v LIST OF FIGURES ...................................................................................................... vi LIST OF TABLES ....................................................................................................... viii PREFACE .................................................................................................................... ix ACKNOWLEDGEMENTS ............................................................................................. x VITA ............................................................................................................................ xii ABSTRACT OF THE DISSERTATION ....................................................................... xiii 1 Introduction: Microsporidia growth in the host environment ................................... 1 2 Introduction: Caenorhabiditis elegans as a model for intracellular pathogen infection ................................................................................................................ 16 3 Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia ......................................................................................................... 27 4 A wild C. elegans strain has enhanced epithelial immunity to a natural microsporidian parasite ......................................................................................... 41 5 Associations of host ubiquitin and autophagy proteins with microsporidia cells during elimination of infection in intestinal epithelial cells ..................................... 73 Appendix ..................................................................................................................... 91 v LIST OF FIGURES Figure 2-1. Features of the C. elegans intestine ................................................... 18 Figure 2-2. Intracellular pathogens studied in C. elegans and the cell biology of natural intracellular infections in C. elegans intestinal cells ................ 21 Figure 3-1. A single N. parisii cell can grow to fill most of the C. elegans intestine ... ............................................................................................................ 29 Figure 3-2. N.parisii can spread across and fuse host intestinal cells into a syncytial organ .................................................................................... 30 Figure 3-3. Spreading across host cells is a conserved microsporidia growth strategy with distinct host cell fusion patterns caused by distantly related Nematocida species ................................................................ 30 Figure 3-4. Nematocida vary in growth and virulence, and the density of infection alters developmental speed ................................................................ 31 Figure 3-S1. Quantification of N. parisii spreading across host intestinal cells over time ..................................................................................................... 35 Figure 3-S2. Quantification of red Dendra signal diffusion in 10 uninfected cells of infected animals, or 10 infected cells .................................................. 36 Figure 3-S3. The C. elegans fusogens AFF-1 and EFF-1 are not required for N. parisii-induced fusion of intestinal cells .......................................... 37 Figure 3-S4. Quantification of the number of host cells occupied by parasite by the time of sporulation ............................................................................... 38 Figure 3-S5. N. displodere causes syncytia formation in the anterior hypodermal cells of C. elegans. .............................................................................. 39 Figure 3-S6. Quantification of N. parisii growth rate in size mutants and increased initial infections. ................................................................................... 40 Figure 4-1. Natural variation in C. elegans response to N. parisii infection ........... 45 Figure 4-2. Age-dependent variation in resistance to N. parisii infection .............. 46 Figure 4-3. Age- and strain-dependent variation in clearance of N. parisii infection... ............................................................................................ 48 Figure 4-4. Survival, fecundity, and competition between N2 and HW strains in the presence and absence of infection ..................................................... 50 Figure 4-5. Linkage mapping results for N2 and HW resistance to N. parisii infection ............................................................................................... 52 Figure 4-S1. Lifecycle of N. parisii in C. elegans.. ................................................... 63 Figure 4-S2. Longevity of wild strains in the absence of infection ........................... 64 Figure 4-S3. Correlation between pathogen load and survival upon N. parisii infection.. ............................................................................................. 65 Figure 4-S4. Variation in the response of N2 and HW C. elegans strains to infection by N. parisii strain ERTm1 from France. ............................................. 66 Figure 4-S5. Measurement of feeding rate in N2 and HW L1 animals .................... 67 Figure 4-S6. Analysis of resistance against N. parisii in C. elegans strains that vary in the npr-1 gene ................................................................................. 68 Figure 4-S7. HW resistance to N. parisii is dominant to N2 ..................................... 69 Figure 4-S8. Pathogen load distribution in parents and RIAILs. .............................. 70 Figure 4-S9. Pathogen load in NILs measured by FISH. ......................................... 71 vi Figure 5-1. Host ubiquitin and autophagy proteins localize around microsporidia cells with distinct patterns in the resistant HW strain and susceptible N2 strain .............................................................................................. 78 Figure 5-2. GFP-fusion ubiquitin and autophagy protein expression varies among transgenic N2 and HW strains. ........................................................... 79 Figure 5-3. Clearance of N. ironsii (ERTm5) infections occurs gradually over time in HW animals at both 25°C and 20°C ................................................ 81 Figure 5-4. Nematocida species vary in their ability to evade elimination by L1 stage HW hosts ................................................................................... 83 Figure 5-5. The localization of host ubiquitin around Nematocida cells is most frequent in contexts where infection is eliminated ............................... 84 Figure A.1-1. Linkage mapping results for N2 and HW size and resistance to N. parisii (ERTm1) infection ..................................................................... 94 Figure A.1-2. Natural variation among 54 wild C. elegans strains in resistance to N. ironsii (ERTm5) infection maps to two unique genomic loci ................ 95 Figure A.1-3. Inhibiting gene function by RNAi or mutation to investigate functions for candidate genes identified by GWAS in controlling N. ironsii (ERTm5) levels ................................................................................................... 98 Figure A.2-1. Example of the percentage of infected L1 animals and number of infectious events per L1 animal in samples used for RNAseq .......... 104 Figure A.2-2. Pathogen load and infection-induced host gene expression in samples used for RNAseq ............................................................................... 105 vii LIST OF TABLES Table 2-S1. Pathogens tested for intracellular infection in C. elegans and features of the immune response. ..................................................................... 26 Table 3-S1. Quantification of infection distributions ................................................ 34 Table A.1-1. Ranked genes based on variation between C. elegans strains and correlation with pathogen load. ........................................................... 97 Table A.2-1. RNA sample concentrations and absorbance used for RNAseq ...... 103 Table A.2-2. Uniquely expressed genes in N. parisii-infected HW L1 animals (only genes annotated with gene names are shown) ................................ 107 Table A.2-3. Enrichment for functional classes among genes uniquely expressed in N. parisii-infected HW L1
Load more

Recommended publications
  • Downloaded (Additional File 1, Table S4)
    Phylogenomics supports microsporidia as the earliest diverging clade of sequenced fungi Capella-Gutiérrez et al. Capella-Gutiérrez et al. BMC Biology 2012, 10:47 http://www.biomedcentral.com/1741-7007/10/47 (31 May 2012) Capella-Gutiérrez et al. BMC Biology 2012, 10:47 http://www.biomedcentral.com/1741-7007/10/47 RESEARCHARTICLE Open Access Phylogenomics supports microsporidia as the earliest diverging clade of sequenced fungi Salvador Capella-Gutiérrez, Marina Marcet-Houben and Toni Gabaldón* Abstract Background: Microsporidia is one of the taxa that have experienced the most dramatic taxonomic reclassifications. Once thought to be among the earliest diverging eukaryotes, the fungal nature of this group of intracellular pathogens is now widely accepted. However, the specific position of microsporidia within the fungal tree of life is still debated. Due to the presence of accelerated evolutionary rates, phylogenetic analyses involving microsporidia are prone to methodological artifacts, such as long-branch attraction, especially when taxon sampling is limited. Results: Here we exploit the recent availability of six complete microsporidian genomes to re-assess the long- standing question of their phylogenetic position. We show that microsporidians have a similar low level of conservation of gene neighborhood with other groups of fungi when controlling for the confounding effects of recent segmental duplications. A combined analysis of thousands of gene trees supports a topology in which microsporidia is a sister group to all other sequenced fungi. Moreover, this topology received increased support when less informative trees were discarded. This position of microsporidia was also strongly supported based on the combined analysis of 53 concatenated genes, and was robust to filters controlling for rate heterogeneity, compositional bias, long branch attraction and heterotachy.
    [Show full text]
  • A Model for Evolutionary Ecology of Disease: the Case for Caenorhabditis Nematodes and Their Natural Parasites
    Journal of Nematology 49(4):357–372. 2017. Ó The Society of Nematologists 2017. A Model for Evolutionary Ecology of Disease: The Case for Caenorhabditis Nematodes and Their Natural Parasites AMANDA K. GIBSON AND LEVI T. M ORRAN Abstract: Many of the outstanding questions in disease ecology and evolution call for combining observation of natural host– parasite populations with experimental dissection of interactions in the field and the laboratory. The ‘‘rewilding’’ of model systems holds great promise for this endeavor. Here, we highlight the potential for development of the nematode Caenorhabditis elegans and its close relatives as a model for the study of disease ecology and evolution. This powerful laboratory model was disassociated from its natural habitat in the 1960s. Today, studies are uncovering that lost natural history, with several natural parasites described since 2008. Studies of these natural Caenorhabditis–parasite interactions can reap the benefits of the vast array of experimental and genetic tools developed for this laboratory model. In this review, we introduce the natural parasites of C. elegans characterized thus far and discuss resources available to study them, including experimental (co)evolution, cryopreservation, behavioral assays, and genomic tools. Throughout, we present avenues of research that are interesting and feasible to address with caenorhabditid nematodes and their natural parasites, ranging from the maintenance of outcrossing to the community dynamics of host-associated microbes. In combining natural relevance with the experimental power of a laboratory supermodel, these fledgling host–parasite systems can take on fundamental questions in evolutionary ecology of disease. Key words: bacteria, Caenorhabditis, coevolution, evolution and ecology of infectious disease, experimental evolution, fungi, host–parasite interactions, immunology, microbiome, microsporidia, virus.
    [Show full text]
  • Functional Genomic Screening of Nematocida Parisii Host-Exposed Proteins
    Functional Genomic Screening of Nematocida parisii host-exposed proteins By Eashwar Mohan A thesis submitted in conformity with the requirements for the degree of Master of Science Department of Molecular Genetics University of Toronto © Copyright by Eashwar Mohan 2021 Functional Genomic Screening of Nematocida parisii host-exposed proteins Eashwar Mohan Master of Science Department of Molecular Genetics University of Toronto 2021 Abstract Microsporidia are a divergent group of obligate, intracellular pathogens that are relatively poorly understood. The Caenorhabditis elegans intestinal infecting Nematocida parisii, has been shown to secrete a diverse arsenal of proteins to their cells upon infection, labelled “host-exposed” proteins. These secreted proteins may be serving roles as effector proteins, and the model organism Saccharomyces cerevisiae has proven to be a reliable system for the study of bacterial effectors. This uses yeast to study microsporidian host-exposed proteins. I have generated a pipeline to clone N. parisii genes into yeast expression vectors and demonstrated reliability by generating a gene set of 97 N. parisii host-exposed genes along with additional controls. Screening this gene collection identified 23 toxic genes, demonstrating that this strategy may help further understanding of microsporidian infection biology by identifying novel microsporidian effector proteins and learning more about the rules of these proteins and their expression in yeast. ii Table of Contents ABSTRACT……………………………………………………………………………………...ii TABLE OF CONTENTS……………………………………………………………………….iii LIST OF TABLES……………………………………………………………………………….v LIST OF FIGURES……………………………………………………………………………..vi LIST OF ABBREVATIONS………………………………………………………………...…vii 1. INTRODUCTION 1.1. Microsporidia……………………………………………………………………………1 1.1.1. Microsporidia History, Evolution and Host Range………………………………..1 1.1.2. Microsporidia Genetic and Cellular Biology……………………………………...2 1.1.3.
    [Show full text]
  • Transcription Factor Evolution in Eukaryotes and the Assembly of the Regulatory Toolkit in Multicellular Lineages
    Transcription factor evolution in eukaryotes and the assembly of the regulatory toolkit in multicellular lineages Alex de Mendozaa,b,1, Arnau Sebé-Pedrósa,b,1, Martin Sebastijan Sestakˇ c, Marija Matejciˇ cc, Guifré Torruellaa,b, Tomislav Domazet-Losoˇ c,d, and Iñaki Ruiz-Trilloa,b,e,2 aInstitut de Biologia Evolutiva (Consejo Superior de Investigaciones Científicas–Universitat Pompeu Fabra), 08003 Barcelona, Spain; bDepartament de Genètica, Universitat de Barcelona, 08028 Barcelona, Spain; cLaboratory of Evolutionary Genetics, Ruder Boskovic Institute, HR-10000 Zagreb, Croatia; dCatholic University of Croatia, HR-10000 Zagreb, Croatia; and eInstitució Catalana de Recerca i Estudis Avançats, 08010 Barcelona, Spain Edited by Walter J. Gehring, University of Basel, Basel, Switzerland, and approved October 31, 2013 (received for review June 25, 2013) Transcription factors (TFs) are the main players in transcriptional of life (6, 15–22). However, it is not yet clear whether the evo- regulation in eukaryotes. However, it remains unclear what role lutionary scenarios previously proposed are robust to the in- TFs played in the origin of all of the different eukaryotic multicellular corporation of genome data from key phylogenetic taxa that lineages. In this paper, we explore how the origin of TF repertoires were previously unavailable. shaped eukaryotic evolution and, in particular, their role into the In this paper, we present an updated analysis of TF diversity emergence of multicellular lineages. We traced the origin and ex- and evolution in different eukaryote supergroups, focusing on pansion of all known TFs through the eukaryotic tree of life, using the various unicellular-to-multicellular transitions. We report genome broadest possible taxon sampling and an updated phylogenetic background.
    [Show full text]
  • C. Elegans Identified Upregulation of Lipid Metabolites in Three Lipid Biosynthesis Pathways: Phosphatidylcholines, Acylcarnitines and Ceramides
    Characterizing the role of host lipid metabolism on microsporidia infection in Caenorhabditis elegans by JiHae Jeon A thesis submitted in conformity with the requirements for the degree of Master's of Science Graduate Department of Molecular Genetics University of Toronto © Copyright by JiHae Jeon 2021 Characterizing the role of host lipid metabolism on microsporidia infection using the nematode Caenorhabditis elegans JiHae Jeon Master’s of Science Department of Molecular Genetics University of Toronto 2021 Abstract Microsporidia are fungal obligate intracellular pathogens that primarily manifest in immunocompromised individuals. Microsporidia have reduced metabolic capabilities and so they have strong host-dependence for many metabolic processes. However, despite their growing medical importance, microsporidia are poorly understood. I investigated the impact of host lipid metabolism on microsporidia infection using the nematode Caenorhabditis elegans and its natural microsporidian pathogen Nematocida parisii. A previous metabolomics screen performed on N. parisii infected C. elegans identified upregulation of lipid metabolites in three lipid biosynthesis pathways: phosphatidylcholines, acylcarnitines and ceramides. I also identified an increase in the level of lipid droplet associated lipase, ATGL-1, upon infection. In addition, by screening 25 lipid mutant strains, animals defective in producing sphingosine showed resistance to infection whereas supplementing sphingosine increased susceptibility, suggesting sphingosine may be involved in promoting microsporidian growth. Together, my research of lipid regulation by microsporidia can help to determine new therapeutic targets for microsporidian infection. ii Acknowledgment First and foremost, I’d like to thank my supervisor, Dr. Aaron Reinke, for giving me the opportunity to do this project in his lab and his continual support and guidance throughout my master’s degree.
    [Show full text]
  • Ncomms8121.Pdf
    ARTICLE Received 9 Dec 2014 | Accepted 7 Apr 2015 | Published 13 May 2015 DOI: 10.1038/ncomms8121 OPEN Contrasting host–pathogen interactions and genome evolution in two generalist and specialist microsporidian pathogens of mosquitoes Christopher A. Desjardins1, Neil D. Sanscrainte2, Jonathan M. Goldberg1, David Heiman1, Sarah Young1, Qiandong Zeng1, Hiten D. Madhani3, James J. Becnel2 & Christina A. Cuomo1 Obligate intracellular pathogens depend on their host for growth yet must also evade detection by host defenses. Here we investigate host adaptation in two Microsporidia, the specialist Edhazardia aedis and the generalist Vavraia culicis, pathogens of disease vector mosquitoes. Genomic analysis and deep RNA-Seq across infection time courses reveal fundamental differences between these pathogens. E. aedis retains enhanced cell surface modification and signalling capacity, upregulating protein trafficking and secretion dynamically during infection. V. culicis is less dependent on its host for basic metabolites and retains a subset of spliceosomal components, with a transcriptome broadly focused on growth and replication. Transcriptional profiling of mosquito immune responses reveals that response to infection by E. aedis differs dramatically depending on the mode of infection, and that antimicrobial defensins may play a general role in mosquito defense against Microsporidia. This analysis illuminates fundamentally different evolutionary paths and host interplay of specialist and generalist pathogens. 1 Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. 2 USDA, ARS, Center for Medical, Agricultural and Veterinary Entomology, 1600 SW 23rd Drive, Gainesville, Florida 32608, USA. 3 Department of Biochemistry and Biophysics, University of California-San Francisco, San Francisco, California 94158, USA. Correspondence and requests for materials should be addressed to J.J.B.
    [Show full text]
  • Discovery of a Natural Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis Elegans
    RESEARCH ARTICLE Discovery of a Natural Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis elegans Robert J. Luallen1, Aaron W. Reinke1, Linda Tong1, Michael R. Botts1, Marie-Anne Félix2, Emily R. Troemel1* 1 Division of Biological Sciences, Section of Cell and Developmental Biology, University of California San Diego (UCSD), La Jolla, California, United States of America, 2 École Normale Supérieure, Institut de Biologie de l’ENS (IBENS), CNRS-INSERM, Paris, France a11111 * [email protected] Abstract Microbial pathogens often establish infection within particular niches of their host for replica- OPEN ACCESS tion. Determining how infection occurs preferentially in specific host tissues is a key aspect Citation: Luallen RJ, Reinke AW, Tong L, Botts MR, of understanding host-microbe interactions. Here, we describe the discovery of a natural Félix M-A, Troemel ER (2016) Discovery of a Natural microsporidian parasite of the nematode Caenorhabditis elegans that displays a unique tis- Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis elegans. PLoS Pathog 12 sue tropism compared to previously described parasites of this host. We characterize the (6): e1005724. doi:10.1371/journal.ppat.1005724 life cycle of this new species, Nematocida displodere, including pathogen entry, intracellular Editor: James B. Lok, University of Pennsylvania, replication, and exit. N. displodere can invade multiple host tissues, including the epidermis, UNITED STATES muscle, neurons, and intestine of C. elegans. Despite robust invasion of the intestine very Received: April 7, 2016 little replication occurs there, with the majority of replication occurring in the muscle and epi- dermis. This feature distinguishes N. displodere from two closely related microsporidian Accepted: June 3, 2016 pathogens, N.
    [Show full text]
  • Horizontally Acquired Genes in Early-Diverging Pathogenic Fungi Enable the Use of Host Nucleosides and Nucleotides
    Horizontally acquired genes in early-diverging pathogenic fungi enable the use of host nucleosides and nucleotides William G. Alexandera, Jennifer H. Wisecaverb, Antonis Rokasb, and Chris Todd Hittingera,1 aLaboratory of Genetics, DOE (Department of Energy) Great Lakes Bioenergy Research Center, Wisconsin Energy Institute, Genome Center of Wisconsin, J. F. Crow Institute for the Study of Evolution, University of Wisconsin-Madison, Madison, WI 53706; and bDepartment of Biological Sciences, Vanderbilt University, Nashville, TN 37235 Edited by Wen-Hsiung Li, Academia Sinica, Taipei, Taiwan, and approved March 2, 2016 (received for review August 28, 2015) Horizontal gene transfer (HGT) among bacteria, archaea, and include the following: (i) the ADP/ATP translocase gene family, viruses is widespread, but the extent of transfers from these lineages originating from an HGT event that transferred the founding gene into eukaryotic organisms is contentious. Here we systematically from a member of the bacterial phylum Chlamydia (10), which are identify hundreds of genes that were likely acquired horizontally known to steal energy-bearing molecules from their host; (ii)asix- from a variety of sources by the early-diverging fungal phyla gene folate synthesis pathway transferred into Encephalitozoon Microsporidia and Cryptomycota. Interestingly, the Microsporidia hellem from multiple donors, a transfer hypothesized to reduce have acquired via HGT several genes involved in nucleic acid host metabolic stress (11); and (iii) the acquisition of a glutamate- synthesis and salvage, such as those encoding thymidine kinase (TK), ammonia ligase from an unknown prokaryotic source by Spraguea cytidylate kinase, and purine nucleotide phosphorylase. We show lophii, which is thought to provide spores a mechanism for defense that these HGT-derived nucleic acid synthesis genes tend to function against the ammonia generated by the decomposing flesh in which at the interface between the metabolic networks of the host and they are embedded (12).
    [Show full text]
  • A Large Collection of Novel Nematode-Infecting Microsporidia and Their Diverse Interactions with C
    bioRxiv preprint doi: https://doi.org/10.1101/074757; this version posted September 12, 2016. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. A large collection of novel nematode-infecting microsporidia and their diverse interactions with C. elegans and other related nematodes Gaotian Zhanga, b, Martin Sachsec, Marie-Christine Prevostc, Robert Luallend, Emily Troemeld and Marie-Anne Félixa a Institut de Biologie de l’Ecole Normale Supérieure, CNRS, Inserm, ENS, PSL Research University, 75005 Paris, France b School of Life Sciences, East China Normal University, 200062 Shanghai, China c Ultrapole, Institute Pasteur, 75015 Paris, France. d Division of Biological Sciences, Section of Cell and Developmental Biology, University of California San Diego, La Jolla, California, 92093 United States of America. Correspondence: M.-A. Félix, Institut de Biologie de l’Ecole Normale Supérieure, 46 rue d’Ulm, 75005 Paris, France Telephone number: +33 144323944; FAX number: +33 144323935 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/074757; this version posted September 12, 2016. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. ABSTRACT Microsporidia are fungi-related intracellular pathogens that may infect virtually all animals, but are poorly understood.
    [Show full text]
  • Microsporidia Are Natural Intracellular Parasites of the Nematode Caenorhabditis Elegans
    Microsporidia are Natural Intracellular Parasites of the Nematode Caenorhabditis Elegans The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Troemel, Emily R., Marie-Anne Félix, Noah K. Whiteman, Antoine Barrière, and Frederick M. Ausubel. 2008. Microsporidia are natural intracellular parasites of the nematode Caenorhabditis elegans. PLoS Biology 6(12): e309. Published Version doi:10.1371/journal.pbio.0060309 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:4455972 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA PLoS BIOLOGY Microsporidia Are Natural Intracellular Parasites of the Nematode Caenorhabditis elegans Emily R. Troemel1¤*, Marie-Anne Fe´lix2, Noah K. Whiteman3, Antoine Barrie`re2, Frederick M. Ausubel1 1 Department of Genetics, Harvard Medical School, Department of Molecular Biology and Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America, 2 Institut Jacques Monod, Centre National de la Recherche Scientifique, Universities Paris 6 and 7, Paris, France, 3 Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts, United States of America For decades the soil nematode Caenorhabditis elegans has been an important model system for biology, but little is known about its natural ecology. Recently, C. elegans has become the focus of studies of innate immunity and several pathogens have been shown to cause lethal intestinal infections in C.
    [Show full text]
  • Shared Signatures of Parasitism and Phylogenomics Unite Cryptomycota and Microsporidia
    Current Biology 23, 1548–1553, August 19, 2013 ª2013 Elsevier Ltd All rights reserved http://dx.doi.org/10.1016/j.cub.2013.06.057 Report Shared Signatures of Parasitism and Phylogenomics Unite Cryptomycota and Microsporidia Timothy Y. James,1,* Adrian Pelin,2 Linda Bonen,2 investigations into the cell biology and genome content that Steven Ahrendt,3 Divya Sain,3 Nicolas Corradi,2 were previously unfeasible. and Jason E. Stajich3 Rozella allomycis can be cultivated as an obligate endopar- 1Department of Ecology and Evolutionary Biology, University asite of the water mold Allomyces. The parasite grows in the of Michigan, Ann Arbor, MI 48109, USA host as a naked, mitochondriate protoplast suspected of using 2Canadian Institute for Advanced Research, Department of phagocytosis to devour the cytoplasm of its host [6, 7]. For Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada reproduction, it either stimulates the host to form a cell wall 3Department of Plant Pathology and Microbiology and around developing zoosporangia containing motile zoospores Institute for Integrative Genome Biology, University of or produces a thick-walled resting spore that stains positive California, Riverside, CA 92521, USA for chitin or cellulose [8]. Using a combination of Illumina and Pacific Biosciences (PacBio) sequencing technologies, we assembled the genome of Rozella into 1,060 contigs totaling Summary 11.86 Mbp. The genome is apparently diploid, with 3,972 high-quality heterozygous SNPs and 6,350 predicted genes. Fungi grow within their food, externally digesting it and We identified four chitin synthase genes, all of which are in absorbing nutrients across a semirigid chitinous cell wall.
    [Show full text]
  • Evolution of a Morphological Novelty Occurred Before Genome Compaction in a Lineage of Extreme Parasites,” by Karen L
    Correction EVOLUTION Correction for “Evolution of a morphological novelty occurred before genome compaction in a lineage of extreme parasites,” by Karen L. Haag, Timothy Y. James, Jean-François Pombert, Ronny Larsson, Tobias M. M. Schaer, Dominik Refardt, and Dieter Ebert, which appeared in issue 43, October 28, 2014, of Proc Natl Acad Sci USA (111:15480–15485; first published October 13, 2014; 10.1073/pnas.1410442111). The authors note, “We described a new basal microsporidian, Mitosporidium daphniae gen. et sp. nov. As was noted in our paper, microsporidians are now classified by some workers in Fungi, but they are nonetheless explicitly excluded from the In- ternational Code of Botanical Nomenclature (1). Having pre- viously been considered animal protists, classified among the so- called ‘sporozoans’, microsporidians continue to fall within the remit of the International Code of Zoological Nomenclature (2). Our paper did not meet all of the conditions mandated by the Zoological Code for making their new generic and specific names nomenclaturally available. In particular, no name-bearing type (holotype, syntypes, or hapantotype) was fixed for the new species, and because the specific name was thus unavailable, so was the new generic name, for which fixation of an available type species was also necessary. Here we propose to remedy this sit- uation by again proposing the new taxon Mitosporidium daphniae gen. et sp. nov., with the generic and specific diagnoses as given by Haag et al. and with M. daphniae designated as the type species of Mitosporidium. The type series of M. daphniae consists of two type slides (120309-A-1 and 120309-A-2) bearing hapantotypes, which have been deposited in the International Protozoan Type Slide Collection at the Department of Invertebrate Zoology, National Museum of Natural History, Smithsonian Institution, Suitland, MD, USA, under the registration numbers 1251929 and 1251930, respectively.
    [Show full text]