Glossary Genetics
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Glossary - Cellbiology
1 Glossary - Cellbiology Blotting: (Blot Analysis) Widely used biochemical technique for detecting the presence of specific macromolecules (proteins, mRNAs, or DNA sequences) in a mixture. A sample first is separated on an agarose or polyacrylamide gel usually under denaturing conditions; the separated components are transferred (blotting) to a nitrocellulose sheet, which is exposed to a radiolabeled molecule that specifically binds to the macromolecule of interest, and then subjected to autoradiography. Northern B.: mRNAs are detected with a complementary DNA; Southern B.: DNA restriction fragments are detected with complementary nucleotide sequences; Western B.: Proteins are detected by specific antibodies. Cell: The fundamental unit of living organisms. Cells are bounded by a lipid-containing plasma membrane, containing the central nucleus, and the cytoplasm. Cells are generally capable of independent reproduction. More complex cells like Eukaryotes have various compartments (organelles) where special tasks essential for the survival of the cell take place. Cytoplasm: Viscous contents of a cell that are contained within the plasma membrane but, in eukaryotic cells, outside the nucleus. The part of the cytoplasm not contained in any organelle is called the Cytosol. Cytoskeleton: (Gk. ) Three dimensional network of fibrous elements, allowing precisely regulated movements of cell parts, transport organelles, and help to maintain a cell’s shape. • Actin filament: (Microfilaments) Ubiquitous eukaryotic cytoskeletal proteins (one end is attached to the cell-cortex) of two “twisted“ actin monomers; are important in the structural support and movement of cells. Each actin filament (F-actin) consists of two strands of globular subunits (G-Actin) wrapped around each other to form a polarized unit (high ionic cytoplasm lead to the formation of AF, whereas low ion-concentration disassembles AF). -
(APOCI, -C2, and -E and LDLR) and the Genes C3, PEPD, and GPI (Whole-Arm Translocation/Somatic Cell Hybrids/Genomic Clones/Gene Family/Atherosclerosis) A
Proc. Natl. Acad. Sci. USA Vol. 83, pp. 3929-3933, June 1986 Genetics Regional mapping of human chromosome 19: Organization of genes for plasma lipid transport (APOCI, -C2, and -E and LDLR) and the genes C3, PEPD, and GPI (whole-arm translocation/somatic cell hybrids/genomic clones/gene family/atherosclerosis) A. J. LUSIS*t, C. HEINZMANN*, R. S. SPARKES*, J. SCOTTt, T. J. KNOTTt, R. GELLER§, M. C. SPARKES*, AND T. MOHANDAS§ *Departments of Medicine and Microbiology, University of California School of Medicine, Center for the Health Sciences, Los Angeles, CA 90024; tMolecular Medicine, Medical Research Council Clinical Research Centre, Harrow, Middlesex HA1 3UJ, United Kingdom; and §Department of Pediatrics, Harbor Medical Center, Torrance, CA 90509 Communicated by Richard E. Dickerson, February 6, 1986 ABSTRACT We report the regional mapping of human from defects in the expression of the low density lipoprotein chromosome 19 genes for three apolipoproteins and a lipopro- (LDL) receptor and is strongly correlated with atheroscle- tein receptor as well as genes for three other markers. The rosis (15). Another relatively common dyslipoproteinemia, regional mapping was made possible by the use of a reciprocal type III hyperlipoproteinemia, is associated with a structural whole-arm translocation between the long arm of chromosome variation of apolipoprotein E (apoE) (16). Also, a variety of 19 and the short arm of chromosome 1. Examination of three rare apolipoprotein deficiencies result in gross perturbations separate somatic cell hybrids containing the long arm but not of plasma lipid transport; for example, apoCII deficiency the short arm of chromosome 19 indicated that the genes for results in high fasting levels oftriacylglycerol (17). -
A Chloroplast Gene Is Converted Into a Nucleargene
Proc. Nati. Acad. Sci. USA Vol. 85, pp. 391-395, January 1988 Biochemistry Relocating a gene for herbicide tolerance: A chloroplast gene is converted into a nuclear gene (QB protein/atrazine tolerance/transit peptide) ALICE Y. CHEUNG*, LAWRENCE BOGORAD*, MARC VAN MONTAGUt, AND JEFF SCHELLt: *Department of Cellular and Developmental Biology, 16 Divinity Avenue, The Biological Laboratories, Harvard University, Cambridge, MA 02138; tLaboratorium voor Genetica, Rijksuniversiteit Ghent, B-9000 Ghent, Belgium; and TMax-Planck-Institut fur Zuchtungsforschung, D-500 Cologne 30, Federal Republic of Germany Contributed by Lawrence Bogorad, September 30, 1987 ABSTRACT The chloroplast gene psbA codes for the the gene for ribulose bisphosphate carboxylase/oxygenase photosynthetic quinone-binding membrane protein Q which can transport the protein product into chloroplasts (5). We is the target of the herbicide atrazine. This gene has been have spliced the coding region of the psbA gene isolated converted into a nuclear gene. The psbA gene from an from the chloroplast DNA of the atrazine-resistant biotype atrazine-resistant biotype of Amaranthus hybridus has been of Amaranthus to the transcriptional-control and transit- modified by fusing its coding region to transcription- peptide-encoding regions of a nuclear gene, ss3.6, for the regulation and transit-peptide-encoding sequences of a bona SSU of ribulose bisphosphate carboxylase/oxygenase of pea fide nuclear gene. The constructs were introduced into the (6). The fusion-gene constructions (designated SSU-ATR) nuclear genome of tobacco by using the Agrobacteium tumor- were introduced into tobacco plants via the Agrobacterium inducing (Ti) plasmid system, and the protein product of tumor-inducing (Ti) plasmid transformation system using the nuclear psbA has been identified in the photosynthetic mem- disarmed Ti plasmid vector pGV3850 (7). -
Intelligent Design, Abiogenesis, and Learning from History: Dennis R
Author Exchange Intelligent Design, Abiogenesis, and Learning from History: Dennis R. Venema A Reply to Meyer Dennis R. Venema Weizsäcker’s book The World View of Physics is still keeping me very busy. It has again brought home to me quite clearly how wrong it is to use God as a stop-gap for the incompleteness of our knowledge. If in fact the frontiers of knowledge are being pushed back (and that is bound to be the case), then God is being pushed back with them, and is therefore continually in retreat. We are to find God in what we know, not in what we don’t know; God wants us to realize his presence, not in unsolved problems but in those that are solved. Dietrich Bonhoeffer1 am thankful for this opportunity to nature, is the result of intelligence. More- reply to Stephen Meyer’s criticisms over, this assertion is proffered as the I 2 of my review of his book Signature logical basis for inferring design for the in the Cell (hereafter Signature). Meyer’s origin of biological information: if infor- critiques of my review fall into two gen- mation only ever arises from intelli- eral categories. First, he claims I mistook gence, then the mere presence of Signature for an argument against bio- information demonstrates design. A few logical evolution, rendering several of examples from Signature make the point my arguments superfluous. Secondly, easily: Meyer asserts that I have failed to refute … historical scientists can show that his thesis by not providing a “causally a presently acting cause must have adequate alternative explanation” for the been present in the past because the origin of life in that the few relevant cri- proposed candidate is the only known tiques I do provide are “deeply flawed.” cause of the effect in question. -
DNA Insertion Mutations Can Be Predicted by a Periodic Probability
Research article DNA insertion mutations can be predicted by a periodic probability function Tatsuaki Tsuruyama1 1Department of Pathology, Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan Running title: Probability prediction of mutation Correspondence to: Tatsuaki Tsuruyama Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan Tel.: +81-75-751-3488; Fax: +81-75-761-9591 E-mail: [email protected] 1 Abstract It is generally difficult to predict the positions of mutations in genomic DNA at the nucleotide level. Retroviral DNA insertion is one mode of mutation, resulting in host infections that are difficult to treat. This mutation process involves the integration of retroviral DNA into the host-infected cellular genomic DNA following the interaction between host DNA and a pre-integration complex consisting of retroviral DNA and integrase. Here, we report that retroviral insertion sites around a hotspot within the Zfp521 and N-myc genes can be predicted by a periodic function that is deduced using the diffraction lattice model. In conclusion, the mutagenesis process is described by a biophysical model for DNA–DNA interactions. Keywords: Insertion, mutagenesis, palindromic sequence, retroviral DNA 2 Text Introduction Extensive research has examined retroviral insertions to further our understanding of DNA mutations. Retrovirus-related diseases, including leukemia/lymphoma and AIDS, develop after retroviral genome insertion into the genomic DNA of the infected host cell. Retroviral DNA insertion is one of the modes of insertional mutation. After reverse-transcription of the retroviral genomic RNA into DNA, the retroviral DNA forms a pre-insertion complex (PIC) with the integrase enzyme, which catalyzes the insertion reaction. -
Paul Modrich Howard Hughes Medical Institute and Department of Biochemistry, Duke University Medical Center, Durham, North Carolina, USA
Mechanisms in E. coli and Human Mismatch Repair Nobel Lecture, December 8, 2015 by Paul Modrich Howard Hughes Medical Institute and Department of Biochemistry, Duke University Medical Center, Durham, North Carolina, USA. he idea that mismatched base pairs occur in cells and that such lesions trig- T ger their own repair was suggested 50 years ago by Robin Holliday in the context of genetic recombination [1]. Breakage and rejoining of DNA helices was known to occur during this process [2], with precision of rejoining attributed to formation of a heteroduplex joint, a region of helix where the two strands are derived from the diferent recombining partners. Holliday pointed out that if this heteroduplex region should span a genetic diference between the two DNAs, then it will contain one or more mismatched base pairs. He invoked processing of such mismatches to explain the recombination-associated phenomenon of gene conversion [1], noting that “If there are enzymes which can repair points of damage in DNA, it would seem possible that the same enzymes could recognize the abnormality of base pairing, and by exchange reactions rectify this.” Direct evidence that mismatches provoke a repair reaction was provided by bacterial transformation experiments [3–5], and our interest in this efect was prompted by the Escherichia coli (E. coli) work done in Matt Meselson’s lab at Harvard. Using artifcially constructed heteroduplex DNAs containing multiple mismatched base pairs, Wagner and Meselson [6] demonstrated that mismatches elicit a repair reaction upon introduction into the E. coli cell. Tey also showed that closely spaced mismatches, mismatches separated by a 1000 base pairs or so, are usually repaired on the same DNA strand. -
DNA Sequence Insertion and Evolutionary Variation in Gene Regulation (Mobile Elements/Long Terminal Repeats/Alu Sequences/Factor-Binding Sites) Roy J
Proc. Natl. Acad. Sci. USA Vol. 93, pp. 9374-9377, September 1996 Colloquium Paper This paper was presented at a colloquium entitled "Biology of Developmental Transcription Control, " organized by Eric H. Davidson, Roy J. Britten, and Gary Felsenfeld, held October 26-28, 1995, at the National Academy of Sciences in Irvine, CA. DNA sequence insertion and evolutionary variation in gene regulation (mobile elements/long terminal repeats/Alu sequences/factor-binding sites) RoY J. BRITrEN Division of Biology, California Institute of Technology, 101 Dahlia Avenue, Corona del Mar, CA 92625 ABSTRACT Current evidence on the long-term evolution- 3 and 4). Sequence change, obscuring the original structure, ary effect of insertion of sequence elements into gene regions has occurred in the long history, and the underlying rate of is reviewed, restricted to cases where a sequence derived from base substitution that is responsible is known (5). a past insertion participates in the regulation of expression of The requirements for a convincing example are: (i) that a useful gene. Ten such examples in eukaryotes demonstrate there be a trace of a known class of elements present in gene that segments of repetitive DNA or mobile elements have been region; (ii) that there is evidence that it has been there long inserted in the past in gene regions, have been preserved, enough to not just be a transient mutation; (iii) that some sometimes modified by selection, and now affect control of sequence residue of the mobile element or repeat participates transcription ofthe adjacent gene. Included are only examples in regulation of expression of the gene; (iv) that the gene have in which transcription control was modified by the insert. -
DNA Microarrays (Gene Chips) and Cancer
DNA Microarrays (Gene Chips) and Cancer Cancer Education Project University of Rochester DNA Microarrays (Gene Chips) and Cancer http://www.biosci.utexas.edu/graduate/plantbio/images/spot/microarray.jpg http://www.affymetrix.com Part 1 Gene Expression and Cancer Nucleus Proteins DNA RNA Cell membrane All your cells have the same DNA Sperm Embryo Egg Fertilized Egg - Zygote How do cells that have the same DNA (genes) end up having different structures and functions? DNA in the nucleus Genes Different genes are turned on in different cells. DIFFERENTIAL GENE EXPRESSION GENE EXPRESSION (Genes are “on”) Transcription Translation DNA mRNA protein cell structure (Gene) and function Converts the DNA (gene) code into cell structure and function Differential Gene Expression Different genes Different genes are turned on in different cells make different mRNA’s Differential Gene Expression Different genes are turned Different genes Different mRNA’s on in different cells make different mRNA’s make different Proteins An example of differential gene expression White blood cell Stem Cell Platelet Red blood cell Bone marrow stem cells differentiate into specialized blood cells because different genes are expressed during development. Normal Differential Gene Expression Genes mRNA mRNA Expression of different genes results in the cell developing into a red blood cell or a white blood cell Cancer and Differential Gene Expression mRNA Genes But some times….. Mutations can lead to CANCER CELL some genes being Abnormal gene expression more or less may result -
Genetic Code
AccessScience from McGraw-Hill Education Page 1 of 9 www.accessscience.com Genetic code Contributed by: P. Schimmel, K. Ewalt Publication year: 2014 The rules by which the base sequences of deoxyribonucleic acid (DNA) are translated into the amino acid sequences of proteins. Each sequence of DNA that codes for a protein is transcribed or copied ( Fig. 1 ) into messenger ribonucleic acid (mRNA). Following the rules of the code, discrete elements in the mRNA, known as codons, specify each of the 20 different amino acids that are the constituents of proteins. In a process called translation, the cell decodes the message in mRNA. During translation ( Fig. 2 ), another class of RNAs, called transfer RNAs (tRNAs), are coupled to amino acids, bind to the mRNA, and in a step-by-step fashion provide the amino acids that are linked together in the order called for by the mRNA sequence. The specific attachment of each amino acid to the appropriate tRNA, and the precise pairing of tRNAs via their anticodons to the correct codons in the mRNA, form the basis of the genetic code. See also: DEOXYRIBONUCLEIC ACID (DNA) ; PROTEIN ; RIBONUCLEIC ACID (RNA) . Universal genetic code The genetic information in DNA is found in the sequence or order of four bases that are linked together to form each strand of the two-stranded DNA molecule. The bases of DNA are adenine, guanine, thymine, and cytosine, which are abbreviated A, G, T, and C. Chemically, A and G are purines, and C and T are pyrimidines. The two strands of DNA are wound about each other in a double helix that looks like a twisted ladder (Fig. -
Dna the Code of Life Worksheet
Dna The Code Of Life Worksheet blinds.Forrest Jowled titter well Giffy as misrepresentsrecapitulatory Hughvery nomadically rubberized herwhile isodomum Leonerd exhumedremains leftist forbiddenly. and sketchable. Everett clem invincibly if arithmetical Dawson reinterrogated or Rewriting the Code of Life holding for Genetics and Society. C A process look a genetic code found in DNA is copied and converted into value chain of. They may negatively impact of dna worksheet answers when published by other. Cracking the Code of saw The Biotechnology Institute. DNA lesson plans mRNA tRNA labs mutation activities protein synthesis worksheets and biotechnology experiments for open school property school biology. DNA the code for life FutureLearn. Cracked the genetic code to DNA cloning twins and Dolly the sheep. Dna are being turned into consideration the code life? DNA The Master Molecule of Life CDN. This window or use when he has been copied to a substantial role in a qualified healthcare professional journals as dna the pace that the class before scientists have learned. Explore the Human Genome Project within us Learn about DNA and genomics role in medicine and excellent at the Smithsonian National Museum of Natural. DNA The Double Helix. Most enzymes create a dna the code of life worksheet is getting the. Worksheet that describes the structure of DNA students color the model according to instructions Includes a. Biology Materials Handout MA-H2 Microarray Virtual Lab Activity Worksheet. This user has, worksheet the dna code of life, which proteins are carried on. Notes that scientists have worked 10 years to disappoint the manner human genome explains that DNA is a chemical message that began more data four billion years ago. -
Resistance to HIV (Exercise)
1 Evolution in fast motion – Resistance to HIV (Exercise) Resistance to HIV In the early 1990s, a number of studies revealed that some people – although they had repeatedly contact with HIV – did not become carriers of HIV or, in the case of a confirmed HIV-infection, showed a delayed onset of the disease (AIDS) (a delay of several years was reported). First attempts to explain these phenomena were observed a few years later, when scientists identified important co-receptor molecules on the surface of the host cells, which are essential for HIV to infect the host cell. Scientists assumed that resistant persons may carry an aberrant version of the co-receptor molecule, which makes it impossible for the virus to enter the host cell. Such a co-receptor is the chemokine co-receptor CCR5, which is normally involved in the host’s immune answer (Dean & O’Brien, 1998). In order to test their hypothesis, the scientists sequenced the genes which code for the co- receptor CCR5. They investigated more than 700 samples from HIV-infected patients and compared them with the CCR5-sequences from more than 700 healthy persons. The results of the DNA-sequencing revealed mutations in the CCR5-gene in HIV-infected persons with a delayed onset of AIDS, as well as in some samples of healthy persons (but not in HIV- patients with typical onset of AIDS) (Samson et al., 1996). Exercises 1. In material 1, you can find two CCR5-gene-sequences selected from the data set of the scientists. Compare the sequences and a. find out where the mutation is (identify the position and label it in both! sequences). -
GENOME GENERATION Glossary
GENOME GENERATION Glossary Chromosome An organism’s DNA is packaged into chromosomes. Humans have 23 pairs of chromosomesincluding one pair of sex chromosomes. Women have two X chromosomes and men have one X and one Y chromosome. Dominant (see also recessive) Genes come in pairs. A dominant form of a gene is the “stronger” version that will be expressed. Therefore if someone has one dominant and one recessive form of a gene, only the characteristics of the dominant form will appear. DNA DNA is the long molecule that contains the genetic instructions for nearly all living things. Two strands of DNA are twisted together into a double helix. The DNA code is made up of four chemical letters (A, C, G and T) which are commonly referred to as bases or nucleotides. Gene A gene is a section of DNA that is the code for a specific biological component, usually a protein. Each gene may have several alternative forms. Each of us has two copies of most of our genes, one copy inherited from each parent. Most of our traits are the result of the combined effects of a number of different genes. Very few traits are the result of just one gene. Genetic sequence The precise order of letters (bases) in a section of DNA. Genome A genome is the complete DNA instructions for an organism. The human genome contains 3 billion DNA letters and approximately 23,000 genes. Genomics Genomics is the study of genomes. This includes not only the DNA sequence itself, but also an understanding of the function and regulation of genes both individually and in combination.