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Caenorhabditis Microbiota: Worm Guts Get Populated Laura C
Clark and Hodgkin BMC Biology (2016) 14:37 DOI 10.1186/s12915-016-0260-7 COMMENTARY Open Access Caenorhabditis microbiota: worm guts get populated Laura C. Clark and Jonathan Hodgkin* Please see related Research article: The native microbiome of the nematode Caenorhabditis elegans: Gateway to a new host-microbiome model, http://dx.doi.org/10.1186/s12915-016-0258-1 effects on the life history of the worm are often profound Abstract [2]. It has been increasingly recognized that the worm Until recently, almost nothing has been known about microbiota is an important consideration in achieving a the natural microbiota of the model nematode naturalistic experimental model in which to study, for Caenorhabditis elegans. Reporting their research in instance, host–pathogen interactions or worm behavior. BMC Biology, Dirksen and colleagues describe the first Dirksen et al [3] present the first step towards under- sequencing effort to characterize the gut microbiota standing understanding the complex interactions of the of environmentally isolated C. elegans and the related natural worm microbiota by reporting a 16S rDNA-based taxa Caenorhabditis briggsae and Caenorhabditis “head count” of the bacterial population present in wild remanei In contrast to the monoxenic, microbiota-free nematode isolates (Fig. 1). Interestingly, it appears that cultures that are studied in hundreds of laboratories, it nematodes isolated from diverse natural environment- appears that natural populations of Caenorhabditis s—and even those that have been maintained for a short harbor distinct microbiotas. time on E. coli following isolation—share a “core” host- defined microbiota. This finding is in agreement with work by Berg et al. -
Recent Advances in Drosophila Models of Charcot-Marie-Tooth Disease
International Journal of Molecular Sciences Review Recent Advances in Drosophila Models of Charcot-Marie-Tooth Disease Fukiko Kitani-Morii 1,2,* and Yu-ichi Noto 2 1 Department of Molecular Pathobiology of Brain Disease, Kyoto Prefectural University of Medicine, Kyoto 6028566, Japan 2 Department of Neurology, Kyoto Prefectural University of Medicine, Kyoto 6028566, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-75-251-5793 Received: 31 August 2020; Accepted: 6 October 2020; Published: 8 October 2020 Abstract: Charcot-Marie-Tooth disease (CMT) is one of the most common inherited peripheral neuropathies. CMT patients typically show slowly progressive muscle weakness and sensory loss in a distal dominant pattern in childhood. The diagnosis of CMT is based on clinical symptoms, electrophysiological examinations, and genetic testing. Advances in genetic testing technology have revealed the genetic heterogeneity of CMT; more than 100 genes containing the disease causative mutations have been identified. Because a single genetic alteration in CMT leads to progressive neurodegeneration, studies of CMT patients and their respective models revealed the genotype-phenotype relationships of targeted genes. Conventionally, rodents and cell lines have often been used to study the pathogenesis of CMT. Recently, Drosophila has also attracted attention as a CMT model. In this review, we outline the clinical characteristics of CMT, describe the advantages and disadvantages of using Drosophila in CMT studies, and introduce recent advances in CMT research that successfully applied the use of Drosophila, in areas such as molecules associated with mitochondria, endosomes/lysosomes, transfer RNA, axonal transport, and glucose metabolism. -
Bergmann's Rule in Larval Ant Lions
Ecological Entomology (2003) 28, 645–650 Bergmann’s rule in larval ant lions: testing the starvation resistance hypothesis AMY E. ARNETT andNICHOLAS J. GOTELLI Department of Biology, University of Vermont, U.S.A. Abstract. 1. Body size of the ant lion Myrmeleon immaculatus follows Bergmann’s rule – an increase in body size towards higher latitudes. The hypothesis that ant lion body size is larger in the north as an adaptation for starvation resistance was tested. 2. In a laboratory experiment testing starvation resistance, survivorship curves differed among 10 ant lion populations for both a starved and a fed treatment. 3. The average number of months survived by each population was correlated positively with latitude for both treatments. Across both treatments and all populations, large individuals survived longer than small individuals; however individuals from high latitudes had higher survivorship, even after factoring out variation due to initial body size. 4. These results suggest that starvation resistance may be an adaptation for coping with reduced prey availability in high latitudes. Starvation resistance may contribute to latitudinal gradients in body size of ant lions and other ectotherms. Key words. Ant lion, Bergmann’s rule, body size, latitudinal gradients, Myrmeleon immaculatus, starvation resistance. Introduction body size (Cushman et al., 1993). If food availability decreases at high latitudes, starvation resistance may be Bergmann’s rule – an increase in body size with latitude – is genetically based and promote large body size at high lati- a common geographic pattern that has been described for tudes. Size-dependent resistance to starvation is supported many taxa including birds (James, 1970; Graves, 1991), by many studies of both endotherms and ectotherms mammals (Boyce, 1978; Sand et al., 1995; Sharples et al., (Brodie, 1975; Kondoh, 1977; Boyce, 1978; Lindstedt & 1996), fish (L’Abe´e-Lund et al., 1989; Taylor & Gotelli, Boyce, 1985; Murphy, 1985; Cushman et al., 1993). -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Modulation in the Feeding Prey Capture of the Antlion, Myrmeleon Crudelis
RESEARCH ARTICLE Modulation in the Feeding Prey CaptureoftheAnt-lion, Myrmeleon crudelis à ERIC PATTEN LAMBERT , PHILIP JAY MOTTA, AND DAYV LOWRY Department of Integrative Biology, University of South Florida, Tampa, Florida ABSTRACT Ant-lions are pit-building larvae (Neuroptera: Myrmeleontidae), which possess relatively large mandibles used for catching and consuming prey. Few studies involving terrestrial arthropod larva have investigated prey capture behavior and kinematics and no study has shown modulation of strike kinematics. We examined feeding kinematics of the ant-lion, Myrmeleon crudelis,using high-speed video to investigate whether larvae modulate strike behavior based on prey location relative to the mandible. Based on seven capture events from five M. crudelis,thestriketook 17.6072.92 msec and was characterized by near-simultaneous contact of both mandibles with the prey. Modulation of the angular velocity of the mandibles based on prey location was clearly demonstrated. M. crudelis larvae attempted to simultaneously contact prey with both mandibles by increasing mean angular velocity of the far mandible (65721 rad secÀ1) compared with the near mandible (35714 rad secÀ1). Furthermore, kinematic results showed a significant difference for mean angular velocity between the two mandibles (Po0.005). Given the lengthy strike duration compared with other fast-striking arthropods, these data suggest that there is a tradeoff between the ability to modulate strike behavior for accurate simultaneous mandible contact and the overall velocity of the strike. The ability to modulate prey capture behavior may increase dietary breadth and capture success rate in these predatory larvae by allowing responsive adjustment to small-scale variations in prey size, presentation, and escape response. -
Preference of Antlion and Wormlion Larvae (Neuroptera: Myrmeleontidae; Diptera: Vermileonidae) for Substrates According to Substrate Particle Sizes
Eur. J. Entomol. 112(3): 000–000, 2015 doi: 10.14411/eje.2015.052 ISSN 1210-5759 (print), 1802-8829 (online) Preference of antlion and wormlion larvae (Neuroptera: Myrmeleontidae; Diptera: Vermileonidae) for substrates according to substrate particle sizes Dušan DEVETAK 1 and AMY E. ARNETT 2 1 Department of Biology, Faculty of Natural Sciences and Mathematics, University of Maribor, Koroška cesta 160, SI-2000 Maribor, Slovenia; e-mail: [email protected] 2 Center for Biodiversity, Unity College, 90 Quaker Hill Road, Unity, ME 04915, U.S.A.; e-mail: [email protected] Key words. Neuroptera, Myrmeleontidae, Diptera, Vermileonidae, antlions, wormlions, substrate particle size, substrate selection, pit-builder, non-pit-builder, habitat selection Abstract. Sand-dwelling wormlion and antlion larvae are predators with a highly specialized hunting strategy, which either construct efficient pitfall traps or bury themselves in the sand ambushing prey on the surface. We studied the role substrate particle size plays in these specialized predators. Working with thirteen species of antlions and one species of wormlion, we quantified the substrate particle size in which the species were naturally found. Based on these particle sizes, four substrate types were established: fine substrates, fine to medium substrates, medium substrates, and coarse substrates. Larvae preferring the fine substrates were the wormlion Lampromyia and the antlion Myrmeleon hyalinus originating from desert habitats. Larvae preferring fine to medium and medium substrates belonged to antlion genera Cueta, Euroleon, Myrmeleon, Nophis and Synclisis and antlion larvae preferring coarse substrates were in the genera Distoleon and Neuroleon. In addition to analyzing naturally-occurring substrate, we hypothesized that these insect larvae will prefer the substrate type that they are found in. -
Kif1b Rab7a Lmna
Title: Charcot-Marie-Tooth Neuropathy Type 2 GeneReview Molecular Genetics: Less Commonly Involved Genes Author: Bird TD Updated: March 2016 KIF1B Gene structure. KIF1B comprises 47 exons and 167.13 kb of DNA. Pathogenic allelic variants. See Table A, Locus Specific and HGMD Normal gene product. Kinesin-like protein KIF1B is involved in axonal transport of synaptic vesicle precursors [Zhao et al 2001]. The kinesin superfamily of proteins is essential for intracellular transport along microtubules. Abnormal gene product. There may be a defect in the transport of synaptic vesicles. RAB7A Gene structure. RAB7A has six exons and 87.9 kb of DNA. Pathogenic allelic variants. See Table A. Normal gene product. Ras-related protein Rab-7a belongs to the RAB family of Ras- related GTPases essential for the regulation of intracellular membrane trafficking. Rab- 7a is involved in transport between late endosomes and lysosomes. RAB-interacting lysosomal protein (RILP) induces the recruitment of dynein-dynactin motors and regulates transport toward the minus-end of microtubules [Verhoeven et al 2003]. Abnormal gene product. Abnormal Rab-7a may cause malfunction of lysosomes and inhibit neurite outgrowth [Spinosa et al 2008, Bucci & Deluca 2012]. LMNA Gene structure. LMNA has 12 exons spread over 24 kb of genomic DNA. Pathogenic allelic variants. The most common pathogenic variant found in individuals with CMT2B1 is p.Arg298Cys, a founder mutation in North Africa [Bouhouche et al 2007, De Sandre-Giovannoli et al 2002]. See also Table A. Table 5. Selected LMNA Variants DNA Nucleotide Protein Amino Acid Class of Variant Allele Reference Sequences Change Change Benign c.1908C>T p.= 1 c.398G>T p.Arg133Leu NM_170707.2 c.892C>T p.Arg298Cys Pathogenic NP_733821.1 c.1411C>T p.Arg471Cys c.1579C>T p.Arg527Cys Note on variant classification: Variants listed in the table have been provided by the author. -
The Ubiquitin Proteasome System in Neuromuscular Disorders: Moving Beyond Movement
International Journal of Molecular Sciences Review The Ubiquitin Proteasome System in Neuromuscular Disorders: Moving Beyond Movement 1, , 2, 3,4 Sara Bachiller * y , Isabel M. Alonso-Bellido y , Luis Miguel Real , Eva María Pérez-Villegas 5 , José Luis Venero 2 , Tomas Deierborg 1 , José Ángel Armengol 5 and Rocío Ruiz 2 1 Experimental Neuroinflammation Laboratory, Department of Experimental Medical Science, Lund University, Sölvegatan 19, 221 84 Lund, Sweden; [email protected] 2 Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla/Instituto de Biomedicina de Sevilla-Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, 41012 Sevilla, Spain; [email protected] (I.M.A.-B.); [email protected] (J.L.V.); [email protected] (R.R.) 3 Unidad Clínica de Enfermedades Infecciosas, Hospital Universitario de Valme, 41014 Sevilla, Spain; [email protected] 4 Departamento de Especialidades Quirúrgicas, Bioquímica e Inmunología, Facultad de Medicina, 29071 Universidad de Málaga, Spain 5 Departamento de Fisiología, Anatomía y Biología Celular, Universidad Pablo de Olavide, 41013 Sevilla, Spain; [email protected] (E.M.P.-V.); [email protected] (J.Á.A.) * Correspondence: [email protected] These authors contributed equally to the work. y Received: 14 July 2020; Accepted: 31 August 2020; Published: 3 September 2020 Abstract: Neuromuscular disorders (NMDs) affect 1 in 3000 people worldwide. There are more than 150 different types of NMDs, where the common feature is the loss of muscle strength. These disorders are classified according to their neuroanatomical location, as motor neuron diseases, peripheral nerve diseases, neuromuscular junction diseases, and muscle diseases. Over the years, numerous studies have pointed to protein homeostasis as a crucial factor in the development of these fatal diseases. -
Caenorhabditis Elegans and Caenorhabditis Briggsae
Mol Gen Genomics (2005) 273: 299–310 DOI 10.1007/s00438-004-1105-6 ORIGINAL PAPER Richard Jovelin Æ Patrick C. Phillips Functional constraint and divergence in the G protein family in Caenorhabditis elegans and Caenorhabditis briggsae Received: 2 July 2004 / Accepted: 9 December 2004 / Published online: 27 April 2005 Ó Springer-Verlag 2005 Abstract Part of the challenge of the post-genomic Keywords Caenorhabditis elegans Æ Caenorhabditis world is to identify functional elements within the wide briggsae Æ G protein Æ Divergence Æ Gene regulation array of information generated by genome sequencing. Although cross-species comparisons and investigation of rates of sequence divergence are an efficient approach, the relationship between sequence divergence and func- Introduction tional conservation is not clear. Here, we use a com- parative approach to examine questions of evolutionary Recent whole genome sequencing projects have revealed rates and conserved function within the guanine nucle- that a substantial portion of genome evolution consists otide-binding protein (G protein) gene family in nema- of divergence and diversification of gene families (e.g., todes of the genus Caenorhabditis. In particular, we Chervitz et al. 1998; Lander et al. 2001; Venter et al. show that, in cases where the Caenorhabditis elegans 2001; Zdobnov et al. 2002). One of the primary chal- ortholog shows a loss-of-function phenotype, G protein lenges in this emerging field is to use information on genes of C. elegans and Caenorhabditis briggsae diverge sequence similarity and divergence among genomes to on average three times more slowly than G protein genes infer gene function. Very low rates of change might that do not exhibit any phenotype when mutated in C. -
Zootaxa,Comparison of the Cryptic Nematode Species Caenorhabditis
Zootaxa 1456: 45–62 (2007) ISSN 1175-5326 (print edition) www.mapress.com/zootaxa/ ZOOTAXA Copyright © 2007 · Magnolia Press ISSN 1175-5334 (online edition) Comparison of the cryptic nematode species Caenorhabditis brenneri sp. n. and C. remanei (Nematoda: Rhabditidae) with the stem species pattern of the Caenorhabditis Elegans group WALTER SUDHAUS1 & KARIN KIONTKE2 1Institut für Biologie/Zoologie, AG Evolutionsbiologie, Freie Universität Berlin, Königin-Luise Straße 1-3, 14195 Berlin, Germany. [email protected] 2Department of Biology, New York University, 100 Washington Square E., New York, NY10003, USA. [email protected] Abstract The new gonochoristic member of the Caenorhabditis Elegans group, C. brenneri sp. n., is described. This species is reproductively isolated at the postmating level from its sibling species, C. remanei. Between these species, only minute morphological differences are found, but there are substantial genetic differences. The stem species pattern of the Ele- gans group is reconstructed. C. brenneri sp. n. deviates from this character pattern only in small diagnostic characters. In mating tests of C. brenneri sp. n. females with C. remanei males, fertilization takes place and juveniles occasionally hatch. In the reverse combination, no offspring were observed. Individuals from widely separated populations of each species can be crossed successfully (e.g. C. brenneri sp. n. populations from Guadeloupe and Sumatra, or C. remanei populations from Japan and Germany). Both species have been isolated only from anthropogenic habitats, rich in decom- posing organic material. C. brenneri sp. n. is distributed circumtropically, C. remanei is only found in northern temperate regions. To date, no overlap of the ranges was found. -
Drosophila As a Model for Cmt Peripheral Neuropathy: Mutations in Trna Synthetases As an Example
In: Drosophila Melanogaster Models of Motor Neuron Disease ISBN: 978-1-62618-747-4 Editor: Ruben J. Cauchi © 2013 Nova Science Publishers, Inc. No part of this digital document may be reproduced, stored in a retrieval system or transmitted commercially in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services. Chapter 5 DROSOPHILA AS A MODEL FOR CMT PERIPHERAL NEUROPATHY: MUTATIONS IN TRNA SYNTHETASES AS AN EXAMPLE Georg Steffes1 and Erik Storkebaum1,* 1Molecular Neurogenetics Laboratory, Max Planck Institute for Molecular Biomedicine, Muenster, Germany ABSTRACT Charcot-Marie-Tooth (CMT) disease is characterized by the degeneration of peripheral motor and sensory neurons, leading to progressive muscle weakness and wasting, and sensory loss. Electrophysiological and pathological criteria allow the distinction between demyelinating, axonal and intermediate forms of CMT. The disease is genetically heterogeneous, with currently more than 30 genes causally linked to CMT. The molecular underpinnings of the peripheral motor and sensory neuropathy are poorly understood, and there is no effective drug treatment available. In this chapter, we discuss the use of Drosophila melanogaster as a genetic model organism for CMT. Major advantages include the possibility to study the effect of CMT-associated mutant proteins on motor and sensory neurons in their physiological context, and its suitability to perform genetic screens. -
Cracking the Monoubiquitin Code of Genetic Diseases
International Journal of Molecular Sciences Review Cracking the Monoubiquitin Code of Genetic Diseases 1,2, 1,2, 1,2, Raj Nayan Sewduth y, Maria Francesca Baietti y and Anna A. Sablina * 1 VIB-KU Leuven Center for Cancer Biology, VIB, Herestraat 49, 3000 Leuven, Belgium; [email protected] (R.N.S.); [email protected] (M.F.B.) 2 Department of Oncology, KU Leuven, Herestraat 49, 3000 Leuven, Belgium * Correspondence: [email protected] These authors contributed equally to the work. y Received: 7 April 2020; Accepted: 23 April 2020; Published: 25 April 2020 Abstract: Ubiquitination is a versatile and dynamic post-translational modification in which single ubiquitin molecules or polyubiquitin chains are attached to target proteins, giving rise to mono- or poly-ubiquitination, respectively. The majority of research in the ubiquitin field focused on degradative polyubiquitination, whereas more recent studies uncovered the role of single ubiquitin modification in important physiological processes. Monoubiquitination can modulate the stability, subcellular localization, binding properties, and activity of the target proteins. Understanding the function of monoubiquitination in normal physiology and pathology has important therapeutic implications, as alterations in the monoubiquitin pathway are found in a broad range of genetic diseases. This review highlights a link between monoubiquitin signaling and the pathogenesis of genetic disorders. Keywords: ubiquitin system; genetic diseases; ubiquitin ligase; deubiquitinases; monoubiquitin signaling; vesicular trafficking; protein complex formation 1. Introduction Ubiquitination is a reversible post-translational modification process during which the highly conserved 76-aminoacid protein ubiquitin is conjugated to target proteins. Ubiquitin can be conjugated to a protein substrate via distinct mechanisms.