A Rough Guide to Drosophila Mating Schemes 1
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The Joy of Balancers
REVIEW The joy of balancers 1,2 3 4,5 Danny E. MillerID *, Kevin R. Cook , R. Scott HawleyID * 1 Department of Medicine, Division of Medical Genetics, University of Washington, Seattle, Washington, United States of America, 2 Department of Pediatrics, Division of Genetic Medicine, University of Washington, Seattle, Washington and Seattle Children's Hospital, Seattle, Washington, United States of America, 3 Department of Biology, Indiana University, Bloomington, Indiana, United States of America, 4 Stowers Institute for Medical Research, Kansas City, Missouri, United States of America, 5 Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, United States of America * [email protected] (DEM); [email protected] (RSH) Abstract Balancer chromosomes are multiply inverted and rearranged chromosomes that are widely used in Drosophila genetics. First described nearly 100 years ago, balancers are used extensively in stock maintenance and complex crosses. Recently, the complete molecular a1111111111 structures of several commonly used balancers were determined by whole-genome a1111111111 sequencing. This revealed a surprising amount of variation among balancers derived from a a1111111111 a1111111111 common progenitor, identified genes directly affected by inversion breakpoints, and cata- a1111111111 loged mutations shared by balancers. These studies emphasized that it is important to choose the optimal balancer, because different inversions suppress meiotic recombination in different chromosomal regions. In this review, we provide a brief history of balancers in Drosophila, discuss how they are used today, and provide examples of unexpected recom- bination events involving balancers that can lead to stock breakdown. OPEN ACCESS Citation: Miller DE, Cook KR, Hawley RS (2019) The joy of balancers. -
Additional Miscellaneous Information About Drosophila
Supplemental handout Background on flies Spring, 2013 --------------------------------------------- Miscellaneous useful information about Drosophila A diploid Drosopihila melanogaster fruit fly has two sex chromosomes (XX in the female and XY in the male) and three pairs of autosomes, designated chromosomes 2, 3 and 4; the X is designated chromosome 1. Chromosome 4 is very small. The X is telocentric, meaning that the centromere is at one end. Centromeric heterochromatin is not amplified in polytene nuclei, and all polytene chromosomes are attached to the chromocenter (unamplified heterochromatin), so that a good squash of a polytene nucleus shows five arms extending from a central point. These arms are the euchromatic portions of X, 2L, 2R, 3L and 3R. The pattern of bands is reproducible, and Calvin Bridges devised a nomenclature for them in the 1930's. Each major chromosome arm is divided into 20 numbered sections (X = 1-20, 2L = 21-40, 2R = 41-60, 3L = 61-80, 3R = 81-100 and 4 = 101-102). Each numbered unit is divided into six lettered regions, A-F, and each letter into some number of bands, depending on what Bridges saw. The correlation of these polytene maps and cloned DNA can be accomplished by in situ hybridization, and polytene maps can be correlated with genetic maps based on recombination by testing for complementation between mutant alleles and cytologically visible deletions. A summary of such correlated information is available on Flybase and links available through Flybase. Genes are given a full name, like speck, and a symbol, like sp. In general, gene symbols are capitalized if the original allele was dominant. -
Determination of the Chromosomal Position of Three Mutations Using Recombination Mapping in Drosophila Melanogaster Zane Bryant Coleman University of Mississippi
University of Mississippi eGrove Honors College (Sally McDonnell Barksdale Honors Theses Honors College) 2018 Determination of the Chromosomal Position of Three Mutations Using Recombination Mapping in Drosophila Melanogaster Zane Bryant Coleman University of Mississippi. Sally McDonnell Barksdale Honors College Follow this and additional works at: https://egrove.olemiss.edu/hon_thesis Part of the Biology Commons Recommended Citation Coleman, Zane Bryant, "Determination of the Chromosomal Position of Three Mutations Using Recombination Mapping in Drosophila Melanogaster" (2018). Honors Theses. 978. https://egrove.olemiss.edu/hon_thesis/978 This Undergraduate Thesis is brought to you for free and open access by the Honors College (Sally McDonnell Barksdale Honors College) at eGrove. It has been accepted for inclusion in Honors Theses by an authorized administrator of eGrove. For more information, please contact [email protected]. DETERMINATION OF THE CHROMOSOMAL POSITION OF THREE MUTATIONS USING RECOMBINATION MAPPING IN DROSOPHILA MELANOGASTER by Zane Bryant Coleman A thesis submitted to the faculty of The University of Mississippi in partial fulfillment of the requirements of the Sally McDonnell Barksdale Honors College. Oxford May 2018 Approved by ____________________________________ Advisor: Dr. Bradley Jones ____________________________________ Reader: Dr. Joshua Bloomekatz ____________________________________ Reader: Dr. Colin Jackson Ó 2018 Zane Bryant Coleman ALL RIGHTS RESERVED ii ACKNOWLEDGEMENTS I would like to thank Dr. Jones for allowing me to work in his lab, mentoring me throughout my college career, and helping me during the research process. Through patience and understanding, Dr. Jones has molded me into a scientist capable of overcoming obstacles. I would also like to thank Drs. Bloomekatz and Jackson for participating as readers. -
Engineering New Balancer Chromosomes in C. Elegans Via
www.nature.com/scientificreports OPEN Engineering new balancer chromosomes in C. elegans via CRISPR/Cas9 Received: 19 May 2016 Satoru Iwata1, Sawako Yoshina1, Yuji Suehiro1, Sayaka Hori1 & Shohei Mitani1,2 Accepted: 02 September 2016 Balancer chromosomes are convenient tools used to maintain lethal mutations in heterozygotes. We Published: 21 September 2016 established a method for engineering new balancers in C. elegans by using the CRISPR/Cas9 system in a non-homologous end-joining mutant. Our studies will make it easier for researchers to maintain lethal mutations and should provide a path for the development of a system that generates rearrangements at specific sites of interest to model and analyse the mechanisms of action of genes. Genetic balancers (including inversions, translocations and crossover-suppressors) are essential tools to maintain lethal or sterile mutations in heterozygotes. Recombination is suppressed within these chromosomal rearrange- ments. However, despite efforts to isolate genetic balancers since 19781–5, approximately 15% (map units) of the C. elegans genome has not been covered6 (Supplementary Fig. 1). Because the chromosomal rearrangements gen- erated by gamma-ray and X-ray mutagenesis are random, it is difficult to modify specific chromosomal regions. Here, we used the CRISPR/Cas9 genome editing system to solve this problem. The CRISPR/Cas9 system has enabled genomic engineering of specific DNA sequences and has been successfully applied to the generation of gene knock-outs and knock-ins in humans, rats, mice, zebrafish, flies and nematodes7. Recently, the CRISPR/ Cas9 system has been shown to induce inversions and translocations in human cell lines and mouse somatic cells8–10. -
Identification and Characterization of Breakpoints and Mutations on Drosophila Melanogaster Balancer Chromosomes
G3: Genes|Genomes|Genetics Early Online, published on September 24, 2020 as doi:10.1534/g3.120.401559 1 Identification and characterization of breakpoints and mutations on Drosophila 2 melanogaster balancer chromosomes 3 Danny E. Miller*, Lily Kahsai†, Kasun Buddika†, Michael J. Dixon†, Bernard Y. Kim‡, Brian R. 4 Calvi†, Nicholas S. Sokol†, R. Scott Hawley§** and Kevin R. Cook† 5 *Department of Pediatrics, Division of Genetic Medicine, University of Washington, and Seattle 6 Children's Hospital, Seattle, WA, 98105 7 †Department of Biology, Indiana University, Bloomington, IN 47405 8 ‡Department of Biology, Stanford University, Stanford, CA 94305 9 §Department of Molecular and Integrative Physiology, University of Kansas Medical Center, 10 Kansas City, KS 66160 11 **Stowers Institute for Medical Research, Kansas City, MO 64110 12 ORCIDs: 0000-0001-6096-8601 (D.E.M.), 0000-0003-3429-445X (L.K.), 0000-0002-9872-4765 13 (K.B.), 0000-0003-0208-0641 (M.J.D.), 0000-0002-5025-1292 (B.Y.K.), 0000-0001-5304-0047 14 (B.R.C.), 0000-0002-2768-4102 (N.S.S.), 0000-0002-6478-0494 (R.S.H.), 0000-0001-9260- 15 364X (K.R.C.) 1 © The Author(s) 2020. Published by the Genetics Society of America. 16 Running title: Balancer breakpoints and phenotypes 17 18 Keywords: balancer chromosomes, chromosomal inversions, p53, Ankyrin 2, 19 Fucosyltransferase A 20 21 Corresponding author: Kevin R. Cook, Department of Biology, Indiana University, 1001 E. 22 Third St., Bloomington, IN 47405, 812-856-1213, [email protected] 23 2 24 ABSTRACT 25 Balancers are rearranged chromosomes used in Drosophila melanogaster to maintain 26 deleterious mutations in stable populations, preserve sets of linked genetic elements and 27 construct complex experimental stocks. -
Forward Genetics and Reverse Phenotyping in Pulmonary Arterial Hypertension
G C A T T A C G G C A T genes Review ‘There and Back Again’—Forward Genetics and Reverse Phenotyping in Pulmonary Arterial Hypertension Emilia M. Swietlik 1,2,3, Matina Prapa 1,3, Jennifer M. Martin 1 , Divya Pandya 1, Kathryn Auckland 1 , Nicholas W. Morrell 1,2,3,4 and Stefan Gräf 1,4,5,* 1 Department of Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK; [email protected] (E.M.S.); [email protected] (M.P.); [email protected] (J.M.M.); [email protected] (D.P.); [email protected] (K.A.); [email protected] (N.W.M.) 2 Royal Papworth Hospital NHS Foundation Trust, Cambridge CB2 0AY, UK 3 Addenbrooke’s Hospital NHS Foundation Trust, Cambridge CB2 0QQ, UK 4 NIHR BioResource for Translational Research, University of Cambridge, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK 5 Department of Haematology, University of Cambridge, Cambridge Biomedical Campus, Cambridge CB2 0PT, UK * Correspondence: [email protected] Received: 26 October 2020; Accepted: 23 November 2020; Published: 26 November 2020 Abstract: Although the invention of right heart catheterisation in the 1950s enabled accurate clinical diagnosis of pulmonary arterial hypertension (PAH), it was not until 2000 when the landmark discovery of the causative role of bone morphogenetic protein receptor type II (BMPR2) mutations shed new light on the pathogenesis of PAH. Since then several genes have been discovered, which now account for around 25% of cases with the clinical diagnosis of idiopathic PAH. Despite the ongoing efforts, in the majority of patients the cause of the disease remains elusive, a phenomenon often referred to as “missing heritability”. -
Dikar-Induced Synthetic Lethality in a Drosophila Model of CAG Repeat
University of Connecticut OpenCommons@UConn Honors Scholar Theses Honors Scholar Program Spring 5-12-2013 Dikar-Induced Synthetic Lethality in a Drosophila Model of CAG Repeat Diseases Does Not Result from an Expression Feedback Loop Daniel Camacho University of Connecticut - Storrs, [email protected] Follow this and additional works at: https://opencommons.uconn.edu/srhonors_theses Part of the Cell Biology Commons, and the Molecular Biology Commons Recommended Citation Camacho, Daniel, "Dikar-Induced Synthetic Lethality in a Drosophila Model of CAG Repeat Diseases Does Not Result from an Expression Feedback Loop" (2013). Honors Scholar Theses. 295. https://opencommons.uconn.edu/srhonors_theses/295 1 HONORS THESIS DIKAR-INDUCED SYNTHETIC LETHALITY IN A DROSOPHILA MODEL OF CAG REPEAT DISEASES DOES NOT RESULT FROM AN EXPRESSION FEEDBACK LOOP Presented by Daniel R. Camacho Department of Molecular and Cell Biology The University of Connecticut 2013 2 Abstract Human CAG repeat diseases manifest themselves through the common pathology of neurodeneration. This pathological link is attributed to the property shared by all nine of these diseases: an expanded polyglutamine (polyQ) tract. The most evident result of polyQ expansion is protein aggregation, and it is believed that this phenomenon is partly responsible for conferring cytotoxic properties on the mutated protein. Apart from sequestering the mutated protein, cellular aggregates are able to incorporate native proteins via polyQ-mediated aggregation, thus disrupting important cellular pathways. Using Drosophila melanogaster as a disease model, researchers have been able to compile collections of these so-called disease modifiers for most of the CAG repeat diseases. Moreover, a recently characterized Drosophila gene, Dikar, appears to synergistically react with polyQ-expanded proteins in an especially strong fashion, causing a synthetic lethal phenotype. -
Genetics on the Fly: a Primer on the Drosophila Model System
GENETICS | PRIMER Genetics on the Fly: A Primer on the Drosophila Model System Karen G. Hales,*,1 Christopher A. Korey,† Amanda M. Larracuente,‡ and David M. Roberts§ *Department of Biology, Davidson College, Davidson North Carolina 28035, †Biology Department, College of Charleston, Charleston, South Carolina 29424, ‡Department of Biology, University of Rochester, Rochester, New York 14627, and §Biology Department, Franklin and Marshall College, Lancaster, Pennsylvania 17604 ABSTRACT Fruit flies of the genus Drosophila have been an attractive and effective genetic model organism since Thomas Hunt Morgan and colleagues made seminal discoveries with them a century ago. Work with Drosophila has enabled dramatic advances in cell and developmental biology, neurobiology and behavior, molecular biology, evolutionary and population genetics, and other fields. With more tissue types and observable behaviors than in other short-generation model organisms, and with vast genome data available for many species within the genus, the fly’s tractable complexity will continue to enable exciting opportunities to explore mechanisms of complex developmental programs, behaviors, and broader evolutionary questions. This primer describes the organism’s natural history, the features of sequenced genomes within the genus, the wide range of available genetic tools and online resources, the types of biological questions Drosophila can help address, and historical milestones. KEYWORDS Drosophila; development; comparative genomics; model organism; TABLE OF CONTENTS -
A Toolkit of Engineered Recombinational Balancers in C
View metadata, citation and similar papers at core.ac.uk brought to you by CORE HHS Public Access provided by Caltech Authors Author manuscript Author ManuscriptAuthor Manuscript Author Trends Genet Manuscript Author . Author manuscript; Manuscript Author available in PMC 2019 April 01. Published in final edited form as: Trends Genet. 2018 April ; 34(4): 253–255. doi:10.1016/j.tig.2018.01.009. A toolkit of engineered recombinational balancers in C. elegans Hillel T Schwartz and Paul W Sternberg Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125 Abstract Dejima and colleagues report using CRISPR-Cas9 to generate a new collection of greatly improved balancer chromosomes in the standard laboratory nematode Caenorhabditis elegans, using methods previously reported by the same laboratory [1,2], expanding the set of C. elegans balancers to cover nearly 90% of coding genes. Keywords Caenorhabditis elegans; CRISPR; Cas9; balancer; recombinational suppression Text Balancer chromosomes are a powerful tool in experimental genetics. Balancers are variant chromosomes that when heterozygous with normal chromosomes have a defined region within which there is no or essentially no recombination between the balancer chromosome and the normal chromosome. To achieve this, balancer chromosomes contain rearrangements such as inversions and translocations that disrupt synapsis and so prevent recombination. Any mutations within this recombinationally suppressed region can be reliably followed in trans using the balancer. Balancer chromosomes typically carry markers to make this more efficient: dominantly acting markers such as a gfp transgene to mark the presence of the balancer, and often a mutation with a recessive visible or even lethal phenotype to mark or to prevent the loss of the non-balancer chromosome and the mutations it contains. -
Silencing at Drosophila Telomeres: Nuclear Organization and Chromatin Structure Play Critical Roles
The EMBO Journal Vol.18 No.13 pp.3724–3735, 1999 Silencing at Drosophila telomeres: nuclear organization and chromatin structure play critical roles Diane E.Cryderman, Eric J.Morris, rich tracks, but instead possess tandem repeats of the Harald Biessmann1, Sarah C.R.Elgin2 and retrotransposons HeT-A and TART (Biessmann et al., 1992; Lori L.Wallrath3 Levis et al., 1993; Walter et al., 1995; Danilevskaya et al., 1997). Many parallels have been noted between Department of Biochemistry, 4-772 Bowen Science Building, telomerase-based telomere elongation and this retrotran- 1 University of Iowa, Iowa City, IA 52242, Developmental Biology sposon-based system (Pardue et al., 1997). Center, University of California, Irvine, CA 92697 and 2Department of Biology, Washington University, St Louis, MO 63130, USA Telomeric and pericentric regions of most eukaryotic 3 genomes are packaged into heterochromatin, the relatively Corresponding author gene-poor, late replicating material that remains condensed e-mail: [email protected] throughout the cell cycle (Weiler and Wakimoto, 1995). Transgenes inserted into the telomeric regions of Droso- In contrast, most regions between centromeres and telom- phila melanogaster chromosomes exhibit position effect eres are packaged into euchromatin, the gene-rich, early variegation (PEV), a mosaic silencing characteristic of replicating material that decondenses during interphase. euchromatic genes brought into juxtaposition with When euchromatic genes are brought into juxtaposition heterochromatin. Telomeric transgenes on the second with heterochromatin by chromosomal rearrangement or and third chromosomes are flanked by telomeric associ- transposition, they can exhibit position effect variegation ated sequences (TAS), while fourth chromosome telom- (PEV), a silencing of the gene in a subset of the cells in eric transgenes are most often associated with which it is normally expressed (Weiler and Wakimoto, repetitious transposable elements. -
Retention of Induced Mutations in a Drosophila Reverse-Genetic Resource
Genetics: Published Articles Ahead of Print, published on September 9, 2008 as 10.1534/genetics.108.092437 Retention of induced mutations in a Drosophila reverse-genetic resource Jennifer L. Cooper*+, Elizabeth A. Greene*, Bradley J. Till*‡, Christine A. Codomo*, Barbara T. Wakimoto§ and Steven Henikoff*+ *Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA +Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98107, USA §Department of Biology, University of Washington, Box 351800, Seattle, WA 98195, USA ‡Present address: FAO/IAEA Agricultural and Biotechnology Laboratory A-2444 Seibersdorf, Austria Running head: Retention of induced mutations Key words: mutagenesis, TILLING, balancer chromosomes, mutational spectrum, ethyl methanesulfonate Corresponding author: Steven Henikoff, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109-1024; Phone: (206) 667-4515; FAX (206) 667-5889; Email: [email protected] 2 ABSTRACT TILLING (Targeting Induced Local Lesions IN Genomes) is a reverse-genetic method to identify point mutations in chemically mutagenized populations. For functional genomics, it is ideal to have a stable collection of heavily mutagenized lines that can be screened over an extended period of time. However, long-term storage is impractical for Drosophila, so mutant strains must be maintained by continual propagation of live cultures. Here we evaluate a strategy in which ethylmethane sulfonate (EMS) mutagenized chromosomes were maintained as heterozygotes with balancer chromosomes for over 100 generations before screening. The strategy yielded a spectrum of point mutations similar to those found in previous studies of EMS-induced mutations, as well as 2.4% indels (insertions and deletions). Our analysis of 1887 point mutations in 148 targets showed evidence for selection against deleterious lesions and differential retention of lesions among targets based on their position relative to balancer breakpoints, leading to a broad distribution of mutational densities. -
Genetics of Sleep Section Fred W
Genetics of Sleep Section Fred W. Turek 3 11 Introduction 15 Genetic Basis of Sleep in Healthy 12 Circadian Clock Genes Humans 13 Genetics of Sleep in a Simple Model 16 Genetics of Sleep and Sleep Disorders in Organism: Drosophila Humans 14 Genetic Basis of Sleep in Rodents Chapter Introduction Fred W. Turek 11 The inclusion for the first time of a specific Section on all, of 24-hour behavioral, physiologic, and cellular genetics in Principles and Practice of Sleep Medicine is a her- rhythms of the body. The simplicity and ease of moni- alding event as it signifies that the study of the genetic toring a representative “output rhythm” of the central control of the sleep–wake cycle is becoming an important circadian clock from literally thousands of rodents in a approach for understanding not only the regulatory mech- single laboratory, such as the precise rhythm of wheel anisms underlying the regulation of sleep and wake but running in rodents, was a major factor in uncovering the also for elucidating the function of sleep. Indeed, as genetic molecular transcriptional and translational feedback loops approaches are being used for the study of sleep in diverse that give rise to 24-hour output signals.4,5 There is now species from flies to mice to humans (see Chapters 13 to substantial evidence demonstrating that deletion or muta- 16), the evolutionary significance for the many functions tions in many canonical circadian clock genes can lead of sleep that have evolved over time are becoming a trac- to fundamental changes in other sleep–wake traits includ- table subject for research, as many researchers are bringing ing the amount of sleep and the response to sleep depri- the tools of genetics and genomics to the sleep field.