Documente Academic
Documente Profesional
Documente Cultură
Drosophila melanogaster
Drosophila melanogaster
Scientific classification Kingdom: Phylum: Class: Order: Family: Genus: Subgenus: Species group: Animalia Arthropoda Insecta Diptera Drosophilidae Drosophila Sophophora melanogaster group
Species subgroup: melanogaster subgroup Species complex: melanogaster complex Species: D. melanogaster Binomial name Drosophila melanogaster Meigen, 1830[1] Drosophila melanogaster (Greek for dark-bellied dew lover : = dew, = lover, = dark-coloured, = belly[2]) is a species of Diptera, or the order of flies, in the family Drosophilidae. The species is known generally as the common fruit fly or vinegar fly. Starting from Charles W. Woodworth, this species is a model organism that is widely used for biological research in studies of genetics, physiology, microbial pathogenesis and life history evolution. It is typically used because it is an animal species that is easy to care for, breeds quickly, and lays many eggs.[3] Flies belonging to the family Tephritidae are also called fruit flies, which can lead to confusion, especially in Australia and South Africa, where the term fruit fly refers to members of the Tephritidae that are economic pests in fruit production, such as Ceratitis capitata, the Mediterranean fruit fly or "Medfly".
Drosophila melanogaster
Physical appearance
Wildtype fruit flies have brick red eyes, are yellow-brown in color, and have transverse black rings across their abdomen. They exhibit sexual dimorphism: females are about 2.5 millimeters (0.098in) long; males are slightly smaller and the back of their bodies is darker. Males are easily distinguished from females based on color differences, with a distinct black patch at the abdomen, less noticeable in recently Male (right) and female D. melanogaster emerged flies (see fig), and the sexcombs (a row of dark bristles on the tarsus of the first leg). Furthermore, males have a cluster of spiky hairs (claspers) surrounding the reproducing parts used to attach to the female during mating. There are extensive images at FlyBase.[4]
Drosophila melanogaster approximately 80% of her offspring. This precedence was found to occur through displacement and incapacitation.[14] The displacement is attributed to sperm handling by the female fly as multiple matings are conducted and is most significant during the first 12 days after copulation. Displacement from the seminal receptacle is more significant than displacement from the spermathecae.[14] Incapacitation of first male sperm by second male sperm becomes significant 27 days after copulation. The seminal fluid of the second male is believed to be responsible for this incapacitation mechanism (without removal of first male sperm) which takes effect before fertilization occurs.[14] The delay in effectiveness of the incapacitation mechanism is believed to be a protective mechanism that prevents a male fly from incapacitating its own sperm should it mate with the same female fly repetitively.[14]
Drosophila melanogaster
D. melanogaster types (clockwise): brown eyes with black body, cinnabar eyes, sepia eyes with ebony body, vermilion eyes, white eyes, and wild-type eyes with yellow body
Genetic markers
Genetic markers are commonly used in Drosophila research, for example within balancer chromosomes or P-element inserts, and most phenotypes are easily identifiable either with the naked eye or under a microscope. In the list of example common markers below, the allele symbol is followed by the name of the gene affected and a description of its phenotype. (Note: Recessive alleles are in lower case, while dominant alleles are capitalised.) Cy1: Curly; The wings curve away from the body, flight may be somewhat impaired. e1: ebony; Black body and wings (heterozygotes are also visibly darker than wild type). Sb1: stubble; Bristles are shorter and thicker than wild type. w1: white; Eyes lack pigmentation and appear white. y1: yellow; Body pigmentation and wings appear yellow. This is the fly analog of albinism.
Drosophila genes are traditionally named after the phenotype they cause when mutated. For example, the absence of a particular gene in Drosophila will result in a mutant embryo that does not develop a heart. Scientists have thus called this gene tinman, named after the Oz character of the same name.[17] This system of nomenclature results in a wider range of gene names than in other organisms.
Drosophila melanogaster
Genome
The genome of D. melanogaster (sequenced in 2000, and curated at the FlyBase database[16]) contains four pairs of chromosomes: an X/Y pair, and three autosomes labeled 2, 3, and 4. The fourth chromosome is so tiny that it is often ignored, aside from its important eyeless gene. The D. melanogaster sequenced genome of 139.5 million base pairs has been annotated[19] and contains approximately 15,016 genes. More than 60% of the genome appears to be functional non-protein-coding DNA[20] involved in gene expression control. D. melanogaster chromosomes to scale with megabase-pair references oriented as in the [18] National Center for Biotechnology Information database . Centimorgan distances are Determination of sex in Drosophila approximate and estimated from the locations of selected mapped loci. occurs by the ratio of X chromosomes to autosomes, not because of the presence of a Y chromosome as in human sex determination. Although the Y chromosome is entirely heterochromatic, it contains at least 16 genes, many of which are thought to have male-related functions.[21]
Similarity to humans
About 75% of known human disease genes have a recognizable match in the genome of fruit flies,[22] and 50% of fly protein sequences have mammalian homologs. An online database called Homophila is available to search for human disease gene homologues in flies and vice versa.[23] Drosophila is being used as a genetic model for several human diseases including the neurodegenerative disorders Parkinson's, Huntington's, spinocerebellar ataxia and Alzheimer's disease. The fly is also being used to study mechanisms underlying aging and oxidative stress, immunity, diabetes, and cancer, as well as drug abuse.
Drosophila melanogaster
Development
Embryogenesis in Drosophila has been extensively studied, as its small size, short generation time, and large brood size makes it ideal for genetic studies. It is also unique among model organisms in that cleavage occurs in a syncytium. During oogenesis, cytoplasmic bridges called "ring canals" connect the forming oocyte to nurse cells. Nutrients and developmental control molecules move from the nurse cells into the oocyte. In the figure to the left, the forming oocyte can be seen to be covered by follicular support cells. After fertilization of the oocyte the early embryo (or syncytial embryo) undergoes rapid DNA replication and 13 nuclear divisions until approximately 5000 to 6000 nuclei accumulate in the unseparated cytoplasm of the embryo. By the end of the 8th division most nuclei have migrated to the surface, surrounding the yolk sac (leaving behind only a few nuclei, which will become the yolk nuclei). After the 10th Drosophila melanogaster oogenesis division the pole cells form at the posterior end of the embryo, segregating the germ line from the syncytium. Finally, after the 13th division cell membranes slowly invaginate, dividing the syncytium into individual somatic cells. Once this process is completed gastrulation starts.[24] Nuclear division in the early Drosophila embryo happens so quickly there are no proper checkpoints so mistakes may be made in division of the DNA. To get around this problem, the nuclei that have made a mistake detach from their centrosomes and fall into the centre of the embryo (yolk sac), which will not form part of the fly. The gene network (transcriptional and protein interactions) governing the early development of the fruit fly embryo is one of the best understood gene networks to date, especially the patterning along the antero-posterior (AP) and dorso-ventral (DV) axes (See under morphogenesis).[24] The embryo undergoes well-characterized morphogenetic movements during gastrulation and early development, including germ-band extension, formation of several furrows, ventral invagination of the mesoderm, posterior and anterior invagination of endoderm (gut), as well as extensive body segmentation until finally hatching from the surrounding cuticle into a 1st-instar larva. During larval development, tissues known as imaginal discs grow inside the larva. Imaginal discs develop to form most structures of the adult body, such as the head, legs, wings, thorax and genitalia. Cells of the imaginal disks are set aside during embryogenesis and continue to grow and divide during the larval stagesunlike most other cells of the larva, which have differentiated to perform specialized functions and grow without further cell division. At metamorphosis, the larva forms a pupa, inside which the larval tissues are reabsorbed and the imaginal tissues undergo extensive morphogenetic movements to form adult structures.
Drosophila melanogaster
Sex Determination
Drosophila have both X and Y chromosomes as well as autosomes. Unlike humans, the Y chromosome does not confer maleness, rather it encodes genes necessary for making sperm. Sex is instead determined by the ratio of autosomes to X chromosomes. Further, each cell "decides" whether to be male or female independently of the rest of the organism resulting in the occasional occurrence of gynandromorphs.
X Chromosomes Autosomes Ratio of X:A XXXX XXX XX X XXX XXXX XX X AAAA AAA AA AA AA AAA AAA AAA 1 1 1 0.50 1.50 1.33 0.66 0.33 Sex Normal Female Normal Female Normal Female Normal Male Metafemale Metafemale Intersex Metamale
3 major genes are involved in determination of Drosophila sex. These are Sex-lethal, Sisterless and Deadpan. Deadpan is an autosomal gene which inhibits sex-lethal while sisterless is carried on the X chromosome and inhibits the action of deadpan. An AAX cell has twice as much deadpan as sisterless and so sex-lethal will be inhibited creating a male. On the other hand an AAXX cell will produce enough sisterless to inhibit the action of deadpan allowing the sex-lethal gene to be transcribed creating a female. Later control by deadpan and sisterless disappears and what becomes important is the form of the sex-lethal gene. A secondary promoter causes transcription in both males and females. Analysis of the cDNA has shown that different forms are expressed in males and females. Sex-lethal has been shown to affect the splicing of its own mRNA. In males the 3rd exon is included which encodes a stop codon causing a truncated form to be produced. In the female version, the presence of sex-lethal causes this exon to be missed out the other 7 amino acids are produced as a full peptide chain, again giving us a difference between males and females. [25] Presence or absence of functional Sex-lethal proteins now go on to affect the transcription of another protein known as Doublesex. In the absence of sex-lethal, Doublesex will have the 4th exon removed and be translated up to and including exon 6 (DSX-M[ale]), while in its presence the 4 exon which encodes a stop codon will produce a truncated version of the protein (DSX-F[emale]). DSX-F causes transcription of Yolk proteins 1 and 2 in somatic cells which will be pumped into the oocyte on its production.
Immunity
Unlike mammals, Drosophila only have innate immunity and lack an adaptive immune response. The D. melanogaster immune system can be divided into two responses: humoral and cell-mediated. The former is a systemic response mediated through the Toll and imd pathways, which are parallel systems for detecting microbes. The Toll pathway in Drosophila is known as the homologue of Toll-Like pathways in mammals. Spatzle, a known ligand for the Toll pathway in flies, is produced in response to Gram-positive bacteria, parasites, and fungal infection. Upon infection, pro-Spatzle will be cleaved by protease SPE (Spatzle processing enzyme) to become active Spatzle, which then binds to the Toll receptor located on the cell surface (Fat body, hemocytes) and dimerise for activation of downstream NF-B signaling pathways. On the other hand, the imd pathway is triggered by Gram-negative bacteria through soluble and surface receptors (PGRP-LE and LC, respectively). D. melanogaster have a "fat body", which is thought to be homologous to the human liver. It is the primary secretory organ and produces antimicrobial peptides. These peptides are secreted into the hemolymph and bind infectious bacteria,
Drosophila melanogaster killing them by forming pores in their cell walls. Years ago[when?] many drug companies wanted to purify these peptides and use them as antibiotics. Other than the fat body, hemocytes, the blood cells in drosophila, are known as the homologue of mammalian monocyte/macrophages, possessing a significant role in immune responses. It is known from the literature that in response to immune challenge, hemocytes are able to secrete cytokines, for example Spatzle, to activate downstream signaling pathways in the fat body. However, the mechanism still remains unclear.
Vision
The compound eye of the fruit fly contains 760 unit eyes or ommatidia, and are one of the most advanced among insects. Each ommatidium contains 8 photoreceptor cells (R1-8), support cells, pigment cells, and a cornea. Wild-type flies have reddish pigment cells, which serve to absorb excess blue light so the fly isn't blinded by ambient light. Each photoreceptor cell consists of two main sections, the cell body Stereo images of the fly eye and the rhabdomere. The cell body contains the nucleus while the 100-m-long rhabdomere is made up of toothbrush-like stacks of membrane called microvilli. Each microvillus is 12 m in length and ~60 nm in diameter.[26] The membrane of the rhabdomere is packed with about 100 million rhodopsin molecules, the visual protein that absorbs light. The rest of the visual proteins are also tightly packed into the microvillar space, leaving little room for cytoplasm. The photoreceptors in Drosophila express a variety of rhodopsin isoforms. The R1-R6 photoreceptor cells express Rhodopsin1 (Rh1), which absorbs blue light (480nm). The R7 and R8 cells express a combination of either Rh3 or Rh4, which absorb UV light (345nm and 375nm), and Rh5 or Rh6, which absorb blue (437nm) and green (508nm) light respectively. Each rhodopsin molecule consists of an opsin protein covalently linked to a carotenoid chromophore, 11-cis-3-hydroxyretinal.[27]
Drosophila melanogaster As in vertebrate vision, visual transduction in invertebrates occurs via a G protein-coupled pathway. However, in vertebrates the G protein is transducin, while the G protein in invertebrates is Gq (dgq in Drosophila). When rhodopsin (Rh) absorbs a photon of light its chromophore, 11-cis-3-hydroxyretinal, is isomerized to all-trans-3-hydroxyretinal. Rh undergoes a conformational change into its active form, metarhodopsin. Metarhodopsin activates Gq, which in turn activates a phospholipase C (PLC) known as NorpA.[28] PLC hydrolyzes phosphatidylinositol (4,5)-bisphosphate (PIP2), a phospholipid found in the cell membrane, into soluble inositol triphosphate (IP3) and diacylgycerol (DAG), which stays in the cell membrane. DAG or a derivative of DAG causes a calcium selective ion channel known as TRP (transient receptor potential) to open and calcium and sodium flows into the cell. IP3 is thought to bind to IP3 receptors in the subrhabdomeric cisternae, an extension of the endoplasmic reticulum, and cause release of calcium, but this process doesn't seem to be essential for normal vision.[28] Calcium binds to proteins such as calmodulin (CaM) and an eye-specific protein kinase C (PKC) known as InaC. These proteins interact with other proteins and have been shown to be necessary for shut off of the light response. In addition, proteins called arrestins bind metarhodopsin and prevent it from activating more Gq. A sodium-calcium exchanger known as CalX pumps the calcium out of the cell. It uses the inward sodium gradient to export calcium at a stoichiometry of 3 Na+/ 1 Ca++.[29] TRP, InaC, and PLC form a signaling complex by binding a scaffolding protein called InaD. InaD contains five binding domains called PDZ domain proteins, which specifically bind the C termini of target proteins. Disruption of the complex by mutations in either the PDZ domains or the target proteins reduces the efficiency of signaling. For example, disruption of the interaction between InaC, the protein kinase C, and InaD results in a delay in inactivation of the light response. Unlike vertebrate metarhodopsin, invertebrate metarhodopsin can be converted back into rhodopsin by absorbing a photon of orange light (580nm). Approximately two-thirds of the Drosophila brain is dedicated to visual processing.[30] Although the spatial resolution of their vision is significantly worse than that of humans, their temporal resolution is approximately ten times better.
Flight
The wings of a fly are capable of beating at up to 220 times per second. Flies fly via straight sequences of movement interspersed by rapid turns called saccades. During these turns, a fly is able to rotate 90 degrees in fewer than 50 milliseconds. It was long thought that the characteristics of Drosophila flight were dominated by the viscosity of the air, rather than the inertia of the fly body. This view was challenged by research in the lab of Michael Dickinson, which indicated that flies perform banked turns, where the fly accelerates, slows down while turning, and accelerates again at the end of the turn, suggesting that inertia is the dominant force, as is the case with larger flying animals.[31][32] However, subsequent work showed that while the viscous effects on the insect body during flight may be negligible, the aerodynamic forces on the wings themselves actually cause fruit flies' turns to be damped viscously.[33]
Drosophila melanogaster
10
References
[1] Meigen JW (1830) (in German) (PDF). Systematische Beschreibung der bekannten europischen zweiflgeligen Insekten. (Volume 6) (https:/ / dlib. stanford. edu:6521/ text1/ dd-ill/ insekten6. pdf). Schulz-Wundermann. . [2] (http:/ / www. greek-language. gr/ greekLang/ index. html) [3] Eric C. R. Reeve, ed. (2001-06-23). "Drosophila melanogaster: The Fruit Fly" (http:/ / books. google. com/ ?id=JjLWYKqehRsC& pg=PA157& lpg=PA157& dq=drosophila+ eggs+ day+ lifetime). Encyclopedia of genetics. USA: Fitzroy Dearborn Publishers, I. pp.157. ISBN978-1-884964-34-3. . Retrieved 2009-07-01. [4] "FlyBase: A database of Drosophila genes and genomes" (http:/ / flybase. bio. indiana. edu/ ). Genetics Society of America. 2009. . Retrieved August 11, 2009. [5] Ashburner M, Thompson JN (1978). "The laboratory culture of Drosophila". In Ashburner M, Wright TRF. The genetics and biology of Drosophila. 2A. Academic Press. 181. [6] Ashburner M, Golic KG, Hawley RS (2005). Drosophila: A Laboratory Handbook. (2nd ed.). Cold Spring Harbor Laboratory Press. pp.1624. ISBN0-87969-706-7. [7] Bloomington Drosophila Stock Center (http:/ / flystocks. bio. indiana. edu/ ) at Indiana University: Basic Methods of Culturing Drosophila (http:/ / flystocks. bio. indiana. edu/ Fly_Work/ culturing. htm#stockkeeping) [8] Chiang HC, Hodson AC (1950). "An analytical study of population growth in Drosophila melanogaster". Ecological Monographs 20 (3): 173206. doi:10.2307/1948580. JSTOR1948580. [9] Bakker K (1961). "An analysis of factors which determine success in competition for food among larvae of Drosophila melanogaster". Archives Neerlandaises de Zoologie 14: 200281. [10] Pitnick S (1996). "Investment in testes and the cost of making long sperm in Drosophila". American Naturalist 148: 5780. doi:10.1086/285911. [11] http:/ / news. nationalgeographic. com/ news/ 2009/ 08/ 090821-fruit-fly-sex. html [12] Houot, B.; Svetec, N.; Godoy-Herrera, R.; Ferveur, J. -F. (2010). "Effect of laboratory acclimation on the variation of reproduction-related characters in Drosophila melanogaster". Journal of Experimental Biology 213 (Pt 13): 23222331. doi:10.1242/jeb.041566. PMID20543131. [13] Gilbert SF (2006). "9: Fertilization in Drosophila" (http:/ / 8e. devbio. com/ article. php?ch=9& id=87). In 8th. Developmental Biology. Sinauer Associates. ISBN978-0-87893-250-4. . [14] Price C et al. (1999). "Sperm competition between Drosophila males involves both displacement and incapacitation". Nature 400 (6743): 449452. Bibcode1999Natur.400..449P. doi:10.1038/22755. PMID10440373. [15] Pierce, Benjamin A (2004). Genetics: A Conceptual Approach (2nd ed.). W. H. Freeman. ISBN978-0-7167-8881-2. [16] Adams MD, Celniker SE, Holt RA, et al. (2000). "The genome sequence of Drosophila melanogaster" (http:/ / www. sciencemag. org/ cgi/ content/ abstract/ 287/ 5461/ 2185). Science 287 (5461): 218595. Bibcode2000Sci...287.2185.. doi:10.1126/science.287.5461.2185. PMID10731132. . Retrieved 2007-05-25. [17] Azpiazu N, Frasch M (1993). "tinman and bagpipe: two homeo box genes that determine cell fates in the dorsal mesoderm of Drosophila". Genes and Development 7 (7b): 13251340. doi:10.1101/gad.7.7b.1325. PMID8101173. [18] http:/ / www. ncbi. nlm. nih. gov/ mapview/ map_search. cgi?taxid=7227 [19] "NCBI (National Center for Biotechnology Information) Genome Database" (http:/ / www. ncbi. nlm. nih. gov/ genome/ ?term=drosophila melanogaster). . Retrieved 2011-11-30. [20] Halligan DL, Keightley PD (2006). "Ubiquitous selective constraints in the Drosophila genome revealed by a genome-wide interspecies comparison". Genome Research 16 (7): 87584. doi:10.1101/gr.5022906. PMC1484454. PMID16751341. [21] Carvalho, AB (2002). "Origin and evolution of the Drosophila Y chromosome". Current Opinion in Genetics & Development 12 (6852): 664668. doi:10.1016/S0959-437X(02)00356-8. [22] Reiter, LT; Potocki, L; Chien, S; Gribskov, M; Bier, E (2001). "A Systematic Analysis of Human Disease-Associated Gene Sequences In Drosophila melanogaster". Genome Research 11 (6): 11141125. doi:10.1101/gr.169101. PMC311089. PMID11381037. [23] Bier lab (2008). "Homophila: Human disease to Drosophila disease database" (http:/ / superfly. ucsd. edu/ homophila). University of California, San Diego. . Retrieved August 11, 2009. [24] Katrin Weigmann, Robert Klapper, Thomas Strasser, Christof Rickert, Gerd Technau, Herbert Jckle, Wilfried Janning & Christian Klmbt (2003). "FlyMove a new way to look at development of Drosophila". Trends in Genetics 19 (6): 310311. doi:10.1016/S0168-9525(03)00050-7. PMID12801722. [25] Gilbert S.F. (2000). Developmental Biology. 6th edition. Sunderland (MA): Sinauer Associates; 2000. [26] Hardie RC, Raghu P (2001). "Visual transduction in Drosophila". Nature 413 (6852): 18693. doi:10.1038/35093002. PMID11557987. [27] Nichols R, Pak WL (1985). "Characterization of Drosophila melanogaster rhodopsin". Journal of Biological Chemistry 260 (23): 126704. PMID3930500. [28] Raghu P, Colley NJ, Webel R, et al. (2000). "Normal phototransduction in Drosophila photoreceptors lacking an InsP(3) receptor gene". Molecular and Cellular Neuroscience 15 (5): 42945. doi:10.1006/mcne.2000.0846. PMID10833300. [29] Wang T, Xu H, Oberwinkler J, Gu Y, Hardie R, Montell C, et al. (2005). "Light activation, adaptation, and cell survival Functions of the Na+/Ca2+ exchanger CalX". Neuron 45 (3): 367378. doi:10.1016/j.neuron.2004.12.046. PMID15694299. [30] Rein, K. and Zockler, M. and Mader, M.T. and Grubel, C. and Heisenberg, M. (2002). "The Drosophila Standard Brain". Current Biology 12 (3): 227231. doi:10.1016/S0960-9822(02)00656-5. PMID11839276.
Drosophila melanogaster
[31] Caltech Press Release 4/17/2003 (http:/ / mr. caltech. edu/ media/ Press_Releases/ PR12371. html) [32] S. Fry and M. Dickinson (2003). "The aerodynamics of free-flight maneuvers in Drosophila". Science 300 (5618): 4958. Bibcode2003Sci...300..495F. doi:10.1126/science.1081944. PMID12702878. [33] T. Hesselberg and F.-O. Lehmann (2007). "Turning behaviour depends on frictional damping in the fruit fly "Drosophila"". The Journal of Experimental Biology 210 (Pt 24): 431934. doi:10.1242/jeb.010389. PMID18055621.
11
Further reading
K. Haug-Collet, et al. (1999). "Cloning and Characterization of a Potassium-Dependent Sodium/Calcium Exchanger in Drosophila". J. Cell Biol. 147 (3): 65970. doi:10.1083/jcb.147.3.659. PMC2151195. PMID10545508. R. Ranganathan, et al. (1995). "Signal transduction in Drosophila photoreceptors". Annu. Rev. Neurosci. 18: 283317. doi:10.1146/annurev.ne.18.030195.001435. PMID7605064. Adams MD, et al. (2000). "The genome sequence of Drosophila melanogaster". Science 287 (5461): 218595. Bibcode2000Sci...287.2185.. doi:10.1126/science.287.5461.2185. PMID10731132. Kohler, Robert E. (1994). Lords of the Fly: Drosophila genetics and the experimental life. Chicago: University of Chicago Press. ISBN0-226-45063-5. Gilbert S.F. (2000). Developmental Biology. 6th edition. Sunderland (MA): Sinauer Associates; 2000.
Popular media
"Inside the Fly Lab" (http://www.thirteen.org/curious/episodes/inside-the-fly-lab/) broadcast by WGBH and PBS, in the program series "Curious", January 2008. "How a Fly Detects Poison" (http://whyfiles.org/shorties/285fly_taste/) WhyFiles.org article describes how the fruit fly tastes a larva-killing chemical in food.
External links
External identifiers for Drosophila melanogaster Encyclopedia of Life ITIS 733739 (http://www.eol.org/pages/733739) 146290 (http://www.itis.gov/servlet/SingleRpt/SingleRpt?search_topic=TSN&
search_value=146290)
NCBI
7227 (http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.
cgi?mode=Info& id=7227)
Drosophila Melanogaster (http://www.thebugsquad.com/fruit-flies/drosophila-melanogaster) - Great information for school projects (http://www.thebugsquad.com/fruit-flies/drosophila-melanogaster) A quick and simple introduction to Drosophila melanogaster (http://ceolas.org/VL/fly/intro.html) FlyBase A Database of Drosophila Genes & Genomes (http://flybase.net/) NCBI page on Drosophila melanogaster (http://www.ncbi.nlm.nih.gov/mapview/map_search. cgi?taxid=7227) The WWW Virtual Library: Drosophila (http://www.ceolas.org/VL/fly/) The Berkeley Drosophila Genome Project (http://www.fruitfly.org/) FlyMove (http://flymove.uni-muenster.de/) The Interactive Fly A guide to Drosophila genes and their roles in development (http://www.sdbonline.org/ fly/aimain/1aahome.htm) Drosophila Nomenclature naming of genes (http://www.flynome.com/index.html)
Drosophila melanogaster Make Your Own Fruit Fly Trap (http://lancaster.unl.edu/pest/resources/FruitFlyTrap.shtml) Illustrates a simple to make non-toxic Vinegar fly trap (http://ohioline.osu.edu/hyg-fact/2000/2109.html) Measurement of Courtship Behavior in Drosophila melanogaster (http://www.cshprotocols.org/cgi/content/ full/2007/20/pdb.prot4847) Maintenance of a Drosophila Laboratory: General Procedures (http://www.cshprotocols.org/cgi/content/full/ 2007/6/pdb.ip35) Transcript In Situ Hybridization of Whole-Mount Embryos for Phenotype Analysis of RNAi-Treated Drosophila (http://www.cshprotocols.org/cgi/content/full/2006/21/pdb.prot4519) Injection of dsRNA into Drosophila Embryos for RNA Interference (RNAi) (http://www.cshprotocols.org/cgi/ content/full/2008/3/pdb.prot4918)
12
13
License
Creative Commons Attribution-Share Alike 3.0 Unported //creativecommons.org/licenses/by-sa/3.0/