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LIFE 102 Final Exam Study Guide

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by: Bailey Sniffin

LIFE 102 Final Exam Study Guide LIFE 102-220

Marketplace > Colorado State University > Biology > LIFE 102-220 > LIFE 102 Final Exam Study Guide
Bailey Sniffin
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This is the study guide for my final exam last semester in LIFE 102.
Attributes of Living Systems (Honors)
Dr. Patricia Bedinger
Study Guide
Science, Biology, final, exam, Studyguide, study, guide, LIFE102, honors, drbedinger, patriciabedinger
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This 9 page Study Guide was uploaded by Bailey Sniffin on Sunday April 17, 2016. The Study Guide belongs to LIFE 102-220 at Colorado State University taught by Dr. Patricia Bedinger in Fall 2015. Since its upload, it has received 105 views. For similar materials see Attributes of Living Systems (Honors) in Biology at Colorado State University.


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Date Created: 04/17/16
STUDY GUIDE FOR EXAM IV (FINAL) The final will be worth 130 points, 90 from new material, 30 cumulative (see below) and  10 about stem cells GENES TO PROTEINS– CHAPTER 17 Translation all phases: ­ A charged tRNA binds to the A site ­ A peptide bond forms ­ mRNA shifts relative to the ribosome (translocation) ­ Uncharged tRNA is released ­ 1. Initiation: (formation of the initiation complex) o mRNA o Special initiator tRNA  in the P site o Ribosomal subunits o Requires Initiation Factors and GTP hydrolysis ­ 2. Elongation: o A charged tRNA enter the A (amino acid) site, the anticodon H­bonds with the  codon of the mRNA o A peptide bond forms between aa at P site and aa at A site o Translocation: mRNA, with tRNA with attached polypeptide shifts to the P site,  “naked” tRNA at P site moves to E, exits site and leaves ­ 3. Termination: o Stop codon is reached in the mRNA  There is no charged tRNA that recognizes it o A release factor binds, releases protein, and disrupts the complex Po/ly(ribo)somes: ­ On any single mRNA, there are usually many ribosomes translating at one time Mutagens: ­ Agents that increase mutation frequency ­ Is an agent (light, chemical, radiation) that causes mutations Types and notations of mutations; silent, missense, nonsense, frameshift, deletions, insertions: ­ Mutation: a heritable change in a gene = DNA ­ Can be inherited by offspring or arises in a somatic cell o May or may not cause problems ­ Occur because: o Errors made during DNA replication (wrong base pairs)  Very rare o Errors during repair  Mutagens ­ Point mutations: o Not chromosomal arrangements o NT substitutions: silent (often third base) o Missense (substitution of aa) o Nonsense (a stop codon is produced so premature termination of the protein) o Nucleotide insertions or deletions cause a frame­shift  Unless it’s 3 or multiples of 3 ­ Sickle Cell Anemia: o The 6  amino acid is usually Glu but the mutation causes a substitution of Val Getting proteins into the endomembrane system on the RER: ­ The first few aa are very specific and are recognized as a “signal” by a Signal  Recognition Particle o SRP, a protein­RNA complex ­ SRP attaches the translation complex to the RER and the growing peptide is “fed” into  the center (cisternal space) of the RER o The “signal” is clipped off How DNA repair can cause mutations ­ Mutagens are agents that increase mutation frequency REGULATION OF GENE EXPRESSION – CHAPTER 18 What is a gene? ­ A segment of DNA that is transcribed to produce a functional RNA product Operons in bacteria – polycistronic mRNAs ­ ­ Genes are clustered and transcribed together in operon Operon: multiple gene, single promoter o Functioning unit of genomic DNA containing a cluster of genes under the control ­ of a single promoter Lactose: o The repressor of transcription is inactivated o RNA polymerase will bind to the promoter and transcribe all 3 genes in a  polycistronic mRNA containing three start codons for 3 separate proteins  Can encode more than one polypeptide separately within the same RNA  molecule   Usually bacterial mRNA Chromatin modification/epigenetics (histone modification and DNA methylation): ­ DNA can be methylated: o Affects its expression o Involved in genomic imprinting, X­inactivation o Prevents transcription ­ DNA can be acetylated:  o Chromatin is looser o Easier to transcribe ­ Chromatin modification: o Histone proteins can be acetylated or methylated Enhancers: ­ Often tissue­specific, so whether or not a gene gets transcribed often depends  on whether the enhancer­binding transcription factors are present in the cell ­ A typical eukaryotic gene has enhancers + promoters ­ Promoter = on DNA ­ Enhancer = can be far away from DNA strand Transcription factors: ­ Proteins that bind to promoters and enhancers o Allows RNA polymerase to “load” onto a gene and begin transcription Alternative splicing: ­ >92% of human genes ­ A regulated process during gene expression that results in a single gene  coding for multiple proteins MicroRNAs, what are they, how do they work to inhibit gene expression: ­ miRNA, siRNA, RNAi ­ Small non­coding (nc) that can interfere with gene expression by inhibiting  translation or causing degradation of target mRNAs Cell fate, determination, differentiation, morphogenesis, and Morphogen: ­  Differentiation: cells become specialized o Structurally and biochemically  ­ Cell fate: final differentiated state of a cell ­ Determination: a cell has become committed to a cell fate o Stem cells are NOT determined ­ Morphogenesis: the creation of form o The shape of an organism ­ Morphogen: a factor that influences morphogenesis Importance of transcription factors: ­ Proteins that bind DNA and influence transcription Homeotic genes and mutations (what do mutants look like?) ­ Homeotic genes discovered in Drosophila encode transcription factors that  determine the structures in different body segments ­ Fly with legs for eyes o Organs in the wrong place Cytoplasmic determinants in development, example: ­ Factors that are asymmetrically distributed in the cytoplasm and influence  development ­ Ex. Body plan in drosophila (fruit fly) Induction in development, example: ­ Process by which one cell influences the development of a neighboring cell ­ Ex. Stem cell connection ­ A neighboring cell may emit signals differently to one daughter cell that will  influence its cell fate o A cell­cell signaling during development Apoptosis, example in development: ­ Cell suicide ­ Ex: webbed hands in fetus Cancer causes: viruses and mutations: ­ Viruses: Have transcription factors that transcribe where it shouldn’t ­ Most cancers are caused by mutations in genomes of somatic cells o More rarely: occur in cells that will produce gametes  Can then be inherited ­ About 15% of human cancers are genital warts Difference between sporadic vs. inherited cancer: ­ Sporadic: mutation occurs in somatic cells o 2 normal copies of the gene in every cell  one copy mutated in cell  (acquired)  second copy mutated in cell (also acquired) ­ Inherited: one of the 2 homologous genes is already mutated in gametes o The first mutational “hit” is already present at birth o The second “hit” sometimes called “loss of heterozygosity” can occur  to another mutation, a deletion, or epigenetic silencing  Resulting in cancer at a younger age Oncogenes; what is their normal function, what goes wrong when mutated, example: ­ Normal, non­mutated version: proto­oncogene: promote cell division/growth;  lthe “gas pedal” of the cell cycle ­ Oncogenes are dominant mutations in proto­oncogenes o Gas pedal gets stuck ­ Ex. Ras What causes a proto­oncogene to become an oncogene? ­ Figure on page 15 of notes ­ Translocation or transposition: gene is moved to a new locus and under new  controls ­ Gene amplification: multiple copies of the gene ­ Point mutation within a control element  oncogene  Tumor Suppressor Genes – what is their normal function, what goes wrong when  mutated, example ­ Normal function: inhibit cell division – “brakes” on the cell cycle o Cell cycle checkpoints ­ Recessive mutations: no gene product or dysfunctional gene product = “loss  of function” ­ In order to see effect, BOTH alleles must be mutated ­ Ex. p53 Additional issues in cancer; multiple mutations, apoptosis, angiogenesis, telomeres,  metastasis: ­ At the molecular level of cancer: multiple mutations ­ The next mutation may be in a more “general” proto­oncogene like ras (in  about 25% of all human tumors) or loss of a “general” tumor suppressor gene  like p53 or RB (in about 50% of all human tumors) ­ Apoptosis: last lines of defense – even if a cell acquires a series of mutations  in cancer genes, DNA damage can trigger cell suicide ­ Angiogenesis: development of new blood vessels o Tumor size is limited unless blood vessels develop in tumor ­ Metastasis: secondary site of tumor ­ If a cell escapes apoptosis, there is normally still a “shut­off” system for cell  division = shortening of telomeres causes cells to stop after 20­60 divisions BIOTECHNOLOGY – CHAPTER 20 DNA cloning (recombinant DNA) as opposed to organism cloning: ­ Recombinant DNA: 2 molecules of DNA (vector and insert DNA) that  combine ­ DNA cloning:  o Restriction enzyme cuts sugar­phosphate backbones  Produces sticky ends o DNA fragment added from another molecule cut by same enzyme.  Base pairing occurs o DNA ligase seals strands covalently ­ Organism cloning: o Organisms that receive recombinant DNA are GMO  Dolly was a cloned organism, but not a GMO Restriction enzymes – be able to recognize sticky ends: ­ Enzymes that cut double­stranded DNA at a specific DNA sequence ­ These and DNA ligase make it possible to recombine DNA in the lab Insert, vector, plasmid, recombinant DNA, transformation, transgenic or GM organisms: ­ Insert: can be from any kind of organism; the vector DNA mixes with insert  DNA ­ Vector: can replicate in bacterial cells o A smaller circular plasmid or viral DNA o Has 3 things:  Bacterial replication origin  A cloning site for the insert DNA  A “selectable marker” gene that allows bacteria to grow only if ­ they contain the vector Transformation: getting the recombinant DNA into the cells ­ Transgenic: DNA from a separate organism has been introduced o Gene therapy is a transient (so far) kind of genetic modification  Bubble boy = gene therapy is being used Applications of recombinant DNA technology including GMOs and gene therapy: ­ Bubble boy ­ Bone marrow transplants PCR – how is it done (including steps and ingredients) and what are applications? ­ Denatures  anneals (primers attach)  elongation (RNA polymerase) GENOMES – Chapter 21 Approximate # genes are found in prokaryotes vs. multicellular eukaryotes like humans: ­ 2,000 – 4,000 genes in bacteria ­ 20,000 – 40,000 genes in multicellular eukaryotes How much of the human genome sequence consists of exons (encodes proteins or  functional RNAs)? ­ 1.5% exons o Encodes proteins/functional RNA ­ 22% introns ­ 15%psueudogenes ­ 15% SSR (simple sequence repeats) ­ 44% transposons What are transposons? ­ “Jumping genes” ­ Transposable elements ­ Occur in all major life forms What other kinds of sequences are found in the human genome? ­ More “junk” DNA ­ Simple sequence repeats (SSRs) of 1­13 bases ­ ~19,000 pseudogenes (mutated nonfunctional genes) DESCENT WITH MODIFICATION — Chapter 22 4 common misconceptions about the Theory of Evolution: ­ Evolution is “just a theory” ­ Evolution is about the origins of life ­ Evolution means atheism ­ “Survival of the fittest” What is Intelligent Design? ­  No natural explanation, life form is caused by an intelligent power Historic views of the relationships of organisms: Aristotle, Lamarck (how did it differ  from Darwin’s?) ­ Aristotle: great chain of being o Primitive to complex organisms in a chain  Humans at the top  No interactions of the rings of the chains ­ Lamarck: father of evolution o Evolution is sporadic o No exchange between generations ­ Darwin: naturalist for the captain o Galapagos islands o Darwin and his journey, Wallace as co­discoverer Darwin’s “context”: taxonomy (role of Linnaeus), fossils, geology/uniformitarianism,  and artificial selection ­ Grouped by common characteristics ­ Artificial selection: o Breeding types of crops, etc. Two postulates of Darwinian Evolution ­ Natural selection ­ Descent with modification Adaptation ­ Being fit for the environment Fitness (what is the equation?) ­ Survival + reproductive success What two conditions are necessary for natural selection to work? ­ Genetic variation in a population ­ Limits to survival How does each of these support Darwinian Evolution: Biogeography (what is this), Fossil  Record, Comparative Morphology, Molecular Biology, Direct observation (examples): ­ Biogeography: where you are located o Might not be the same species but they seem alike ­ Fossil record: species past vs. now ­ Comparative morphology: comparing bones from then vs. now ­ Molecular biology: looking at genes ­ Direct observation: observing What are fossils and how are they produced ­ Preserved remnants of a life form o Form when something interferes with the natural process of decomposition The evolutionary relationship of apes and humans ­ Humans are not descendants of modern apes EVOLUTION OF POPULATIONS – CHAPTER 23 Modern synthesis ­ Genetics as applied to populations Locus, gene, allele, gene pool, population, species, microevolution ­ Locus: position on a gene ­ Gene: a segment of DNA that encodes a functional protein or functional RNA  ­ product Gene pool: ALL of the alleles of ALL of the genes of ALL the individuals in a  population ­ Population: a localized group of freely interbreeding individuals of the same species ­ Species: according to the biological species concept: a group that freely interbreeds  and produces fertile offspring in a natural setting and is reproductively isolated  from other groups ­ Microevolution: changes in a gene pool which = changes in allele frequencies =  evolution of populations Hardy­Weinberg Theorem, be able to do simple calculations of allele and genotype  frequencies, e.g. frequency of all genotypes if know frequency of recessive trait (homozygous  recessive genotype) ­ Genotype frequency: p  and q 2 ­ Allele frequency: p and q What conditions need to exist for Hardy­Weinberg to apply to a population? ­ Not changing, not evolving ­ Allele frequencies do not change 3 things that can cause microevolution; genetic drift (bottleneck and founder effect), gene flow, natural selection (how do each of these increase or decrease alleles in a  population?) ­ Bottleneck: catastrophe  decreased alleles ­ Founder effect: some break off and move somewhere else  decrease alleles ­ Gene flow: immigration – introduction of new alleles o Increases gene pool ­ Natural selection: gene pool decreases o But more fit o Remaining alleles are adaptive ORIGIN OF SPECIES­CHAPTER 24 Macroevolution, speciation ­ Macro: the origin of new groups, such as species, genera, families, etc. ­ Speciation: formation of new species Biological species concept: ­ A group that freely interbreeds and produces fertile offspring in a natural setting  and is reproductively isolated from other groups Examples of pre­ and postzygotic barriers: ­ Pre: habitat, temporal, behavioral, mechanical, Gametic ­ Post: reduced hybrid viability, hybrid breakdown, reduced hybrid fertility Allopatric vs sympatric speciation, examples ­ Allopatric: An original group becomes separated by formation of geographical barriers or by migration of a splinter group o Peripheral isolate ­ Sympatric: new species can arise within an original population at the same  location o Especially well documented in plants STEM CELLS (10 points)  What are 2 ways to get stem cells to differentiate? ­ 1. Get embryonic stem cells to grow and then differentiate in culture o Different treatments with small peptide growth factors cause the cells  to divide and differentiate ­ o Remember cell division and cell communication and induction 2. Inject the undifferentiated stem cells into an organism and let the other cells within the body cause the embryonic stem cells to differentiate by induction,  just like in normal development What are potential uses for stem cells, know at least one for both disease/age and injury: ­ Regenerative medicine: or cell­based medicine to replace dead or injured cells ­ Help with Parkinson’s, diabetes, osteoarthritis, blindness, heart disease,  stroke, spinal cord injuries, burns How are stem cells being used in research for human genetic diseases? ­ Can make iPCs from people with a genetic disease including  neurodegenerative diseases o Including Alzheimer’s o Can use for drug discovery Cumulative (40 points): Summary figures; Cell structure, Respiration (equation,  locations, steps with inputs and outputs), and Photosynthesis (equation, steps with inputs  and outputs), Transcription vs. Translation


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