Study Guides (234,319)
Canada (113,098)
Biology (1,377)
Tom Haffie (146)

lecture outcomes second half
lecture outcomes second half

21 Pages
93 Views
Unlock Document

School
Western University
Department
Biology
Course
Biology 1002B
Professor
Tom Haffie
Semester
Winter

Description
Major Outcomes L2-11  General mechanisms by which vaccines protect against diseases - Vaccines pre-expose an individual to a disease, allowing the body to produce antibodies in advance to fight off the disease once it is actually incorporated into the system - The “incorporation” of a small dose of the disease ahead of time in order to help the body prepare for when it actually happens  Why is developing a vaccine against HIV challenging compared to other diseases? - HIV has a very high rate of mutation - HIV is a virus, antiviral drugs need to be used (which may do more harm than good, as host cells need to be targeted) - HIV destroys cells that fight off invaders in the process of its own replication (taking control of the cell, bursting cells via lysis)  Why are people encouraged to get a flu vaccine yearly? - The flu vaccine every year is a “cocktail” that protects against more than one strain of flu - Prominent strains of the flu are predicted yearly and change on a yearly basis. Being immunized for a previous year’s strain of flu will do no good against the current prominent strain.  General temporal trends in HIV infection rates - Most prominent in sub-SaharanAfrica (60% of the world’s population living with HIV resides in sub-SaharanAfrica) - 90% of the world’s HIV+ children live in sub-SaharanAfrica - Less than 0.5% in NorthAmerica and Europe  General temporal trends in HIV infection rates - Similar to the distribution of the disease, most prominent in sub-Saharan Africa (through inheritance as well) - The pandemic: 20.9-24.9M of the world’s 33M infected with HIV reside in sub-Saharan Africa  Why is there no universal cure or vaccine with respect to the treatment of HIV? - HIV mutates constantly and very fast - There could be issues with companies that believe vaccines will not generate money  Why are viruses not considered to be “alive?” - Viruses need to take control of a host to use its own cellular machinery for biological processes such as metabolism, synthesis of DNA… - Viruses are “obligate cellular parasites”  viruses cannot carry out biological processes on their own  Why do anti-viral drugs often have serious side effects? - Anti-viral drugs target viruses which inhabit the host’s own cells - Targeting these viruses means that the host’s own cells will have to be targeted as a result - This can result in more harm than good  cells will often have to be destroyed for the extermination of viruses  Major steps in the life cycle of HIV - After a person has been infected with HIV, HIV cells go towards the host’s own body cells and penetrate the membranes - HIV incorporates itself into the nuclear DNA from there, transcription and translation occurs as it usually does (though the products are viral RNAand protein) - The cell works as a factory for these viral products until they leave the cell via lysis (resulting the in the destruction of the cell)  Roles of integrase and reverse transcriptase in the retroviral life cycle - Integrase splices (integrates) viral DNAinto the DNAof the host cell - Reverse transcriptase reverse transcribes viral RNAinto viral DNA(hence reverse transcriptase) once the virus is incorporated into the host cell  Mechanism of action of AZT - AZT is a drug that mimics thymidine  very similar chemically - During the process of the reverse transcription of viral DNA, the enzyme reverse transcriptase may accidentally grab a molecule ofAZT as opposed to a thymidine, thus stopping the production of the growing viral DNAchain  Reasons why the effectiveness ofAZT decreases over time - AZT loses effectiveness over time (6 mo. – 1 year) - The presence ofAZT introduces selection pressure  the HIV virus is more likely to develop resistance to the drug as time goes on - AZT effectively gets rid of all of the susceptible virions, leaving only the ones that have resistance - Virions containing resistance toAZT are left to reproduce, the offspring effectively inherit thisAZT resistance and in time, the entire population will have becomeAZT-resistant - Note that mutations that conferAZT-resistance can still occur in the absence of AZT itself  Rationale for the “drug-cocktail” approach in treating viral infections - Viruses are likely to produce resistance to just one drug, but the likelihood of developing resistance drops as more types of drugs are used - The introduction of a drug introduces selection pressure and inevitably the virus will confer resistance to all the drugs in the cocktail - The cocktail consists of various drugs that work at various stages of the virus’s lifecycle (i.e, entrance inhibitors, integrase inhibitors…)  The evolution of HIV - Variation: Mutates rapidly, almost never the same in certain points of its lifecycle. This variation is a major issue when it comes to developing a vaccine - Heritability: The offspring of individuals with HIV will inherit the virus - Reproduction, change in genotype:As selection pressure is introduced, susceptible virions die off, leaving only the ones showing resistance alive. The ones that confer drug resistance will effectively reproduce until the entire population is found to contain the resistance.  The CCR5-delta32 mutation - ~18% in Western Europe granting individuals with HIV resistance (either partial or full resistance) - The mutation could have happened by chance or it could have been due to past selection pressures in Europe (plague, smallpox…) - Virtually nonexistent in other parts of the world  Characteristics shared by all life - Genetic basis composed of DNA(similar biochemical characteristics) - Use ofATP, growth and development and glucose/glycolysis - Abide by the “central dogma” DNA RNA protein - Have lipids, common system of protein assembly  How are properties of life “emergent”? 1. Living things display order (i.e. flowers) 2. Harness/utilize energy (use energy to maintain ordered state) 3. Reproduce 4. Respond to stimuli (make adjustments to structure, function in response to changes in the external environment) 5. Exhibit homeostasis (the regulation of the organism’s internal environment) 6. Growth and development 7. Evolve (change over generations to become better adapted to their environment)  Characteristics of the “habitable zone” - Water must be present (seen as the prerequisite for life) - Temperatures that would allow for liquid water - Access to energy from a natural source (stars)  Conditions of a primitive Earth - Consisted of a reducing atmosphere (allowed for complex organic molecules to form)  abundance of water vapor, large quantities of Hydrogen gas, Carbon Dioxide gas,Ammonia, Methane (almost no oxygen) - Reducing atmosphere was due to the concentration of ammonia, hydrogen and methane  Products of the Miller-Urey experiment - Organic compounds (urea, amino acids, lactic, formic, aceteic acids) were synthesized - These were constituents (monomers) of more complex biological polymers (proteins…)  Importance of liposomes in the evolution of first cells - Liposomes provided a membrane sealed compartment that allowed internal conditions to be different than that of the outside environment - This allowed for many reactions to occur that would have otherwise not been possible  Characteristics of a mimivirus suggesting that its alive - Mimiviruses have protein coding genes that allow it to perform many of the functions that living cells can do - Can code for some nucleotides and amino acids though it lacks ribosomal proteins  it depends on the host cell for protein/energy synthesis  Characteristics of a Virophage - Infects other viruses  uses the machinery of other viruses to inhibit the replication of that virus itself - Uses mamavirus proteins to make copies of itself - Impairs a mamavirus’viral factory, leading to deformed versions of the mamavirus  Age of the Earth - 4.6 Bya  Start of life on Earth - 3.5 – 4 Bya  Domains of Life - 3 Kingdom system  eubacteria, archaea, eukaryotes - Five kingdom  Prokaryotes, protists, fungi, plants, animals - Two kingdom  Plantae, animalia  Characteristics of LUCAand those shared by all life - Basis for the biochemical characteristics of all living things - DNAas genetic material,ATP for growth/development/energy, RNA(central dogma), liposoimes - Basis for cprotein assembly,ATP  glucose/glycolysis  Why is the term “prokaryote” inappropriate? - Prokaryote suggests directionality (simple to more complex evolution which is not true) - Not evidence that eukaryotes didn’t come before prokaryotes, or prokaroytes after eukaryotes - Could have evolved from being a “protoeukaryote” to become more efficient, reproduce faster, etc…  Reductive evolution ▯ bacteria and archaea - Bacteria and archaea could have “reductively evolved” from a protoeukaryote - This could have been due to the desire to become more energy efficient, reproduce faster, and in the case of archaea, live in extreme environments (extremeophiles)  Relationship between homochirality and life - Life is homochiral  we only use one form of the two homochiral partners (i.e. L amino acids and D sugars) - Miller-Urey experiment produced racemic (50/50 of each homochiral partner) - No underlying reason behind why one of the two is accepted. They are identical chemically but we only have receptors that allow for us to accept one or the other  Why do scientists believe RNA was the first of the central dogma to evolve? - DNAneeds RNAto replicate although RNA can replicate itself - RNAhas catalytic properties (ribozymes) and to replicate itself it must have had to catalyze the process - DNAis more complex than RNAstructurally (i.e. thymine is methylated uracil)  Force that drives RNAto fold - RNAfolds into 3D structures through base pairing and hydrogen bonding. Once folded, RNAacts as an enzyme  Characteristics of a ribozyme and cleaving ability, amino transferase - 2/3 RNA, 1/3 protein - Able to catalyze reactions but not nearly as fast as regular enzymes - Mainly used in the transfer of amino acids to the growing peptide chain (peptididyl transferase activity) - Able to cleave the 5’end of a tRNA(adding of a nucleotide to the growing strand) - Also responsible for intron excision and mRNAprocessing - Amino transferase activity (peptididyl transferase) uses ribozymes (and enzymes) to cleave the 5’end and add a base pair to the growing nucleotide strand  Why are ribosomes also considered to be ribozymes? - Ribozymes have catalytic enyzyme-like properties - Ribozymes can carry out enzyme functions but are also 2/3 RNA - Ribozymes usually function in operations that deal with ribosomes  Role of cell cycle checkpoints - Cell cycle checkpoints ensure that the cell is ready to proceed into the next stage of growth - i.e. metaphase is the mitotic checkpoint for cells. The cell waits for all chromosomes to be attached to spindle before metaphase (mitosis) proceeds to ensure that chromosomes are all brought to their respective poles - G1 checkpoint: ensures that all DNAis repaired before replication occurs  Implications for cell division with malfunctioning components (no microtubule polymerization?) - Cell must pass through checkpoints during cell division (G1, G2, mitosis) - In this example due to the malfunctioning of microtubules (spindle formation), the cell would not pass the mitotic checkpoint of metaphase (no spindles attaching to the chromosomes)  Mechanism of proofreading, result of proofreading defects - Proofreading allows for mismatched base pairs to be repaired to prevent future damage leading to mutation - Defects in the ability to proofread may increase the number of mutations in the future - Ins/del mutations caused by the “shifting” of the new or old strand (as a result of many repeated base pairs on the DNAstrand) - DNApolymerases responsible for proofreading  they have 3’-5’exonuclease ability and are able to move back and excise mismatched pairs, replacing them with the correct base  Mechanism of mismatch repair - Mismatched pairs are detected by DNApolymerase and are removed by the polymerase’s deoxyribonuclease (using 3’ 5’exonuclease function) - Deoxyribonuclease breaks the DNAbackbone to remove the mismatched pair, DNAPIII then adds the correct pair  Insertion Sequences vs. Transposons vs. Retrotransposons (+ structure) - Insertion sequences are a type of transposable element that codes for its own movement (transposase). Insertion sequences are repeating sequences that surround that transposase gene - Transposons are also known as jumping genes. They move via “cut and paste” or “copy and paste” method. Genes in the central region that are enclosed by two insertion sequences usually code for antibiotic resistance and the movement of these transposons provide antibiotic resistance to many cells - Retrotransposons are transposons which move via RNA. They start off with an intermediate RNAcopy use reverse transcription to create a DNAcopy (which is transposed to a target site where it is integrated into DNAat that location). The original copy stays where it is. - Retroviruses start at RNA reverse transcribes to viral DNA  Implications of insertions of mobile elements into DNA - Mobile elements are big source of variation in the genome - Sometimes these variations can be h armful  alu-elements are retroviruses that disrupt the functions from within genes - Transposable elements are biological mutagens that are able to increase or decrease certain gene expression - In general they may cause DNArearrangements (ins/del/transloc) and may alter DNAsequences that impair gene expression  Why are transposons not actually “jumping genes”? - Transposition requires contact between the transposable element and the target site  Types of genomic variation among humans - ~1.2 million variants - ¼ single nucleotide polymorphism (differing between one base pair in individuals) - ¾ due to copy number variations (~1000 affecting 35% of genes) - ~300 variants in insertion of retroelements  Evidence that might suggest how long a human genome has been infected by any mobile element - Compare genome to other (relatively related) species to see if the element is prevalent in those other than humans - Look at the frequency of which the element has shown up in the genome in the past  Mechanism of tautomeric shifts leading to alternative base pairing - Sometimes a tautomeric shift can occur in one of the bases, where instead of accepting its respective purine/pyrimidine it instead accepts the other one (that it is not usually matched up with) - This happens by chance and does not inhibit DNA’s ability to form a double helix (a purine and pyrimidine are still bonding)  Tautomeric shifts causing mutations - i.e.Adenine attaches to Cytosine (opposite pyrimidine to thymine) - This causes “damage” that will eventually lead to a mutation in the next generation - In the next generation, the Cytosine would call a Guanine (though there would be a mutation)  Why are incorrect tautomers not recognized as mismatches? - Incorrect tautomers do not distort the DNAdouble helix - Tautomers are still bonds between purines and pyrimidines  Mutagenic mechanism of action of base analogues such as 5-Bromouracil - 5-Bromouracil is a tautomerically unstable base analogue - 5-Bromouracil closely matches the structure of thymine - 5-Bromouracil can be mistakenly added to the elongating chain, producing negative effects after it is incorporated into the DNA(contains a bromine group instead of a methyl group on thymine)  Mutagenic mechanism of UV radiation and damage repair - Thymine rings can absorb UV light which reorganizes electrons and bond formation, hooking thymine’s together in an unusual way - Athymine dimer is formed as a result  dimers distort the DNAhelix and it is hard for DNApolymerase to get through - DNApolymerase, as a result, has to relax its pairing mechanisms in order to get through the dimer (i.e. adding any kind of base to the dimer regardless of what it is). This creates damage and possible further mutations - Photolyase breaks bonds and puts thymine back into order (which happens through the absorption of white light) - Because mammals do not have photolyase, usually excision repair happens through the breaking of the DNAbackbone on both sides of the dimer  Mutagenic mechanism of in/del damage - The loss or gain of base pairs during replication - This happens during a long stretch of repeated DNA a “shift” occurs in either the top or bottom strand without the polymerase adding to the strand noticing - This “slippage” will result in the insertion or deletion of base pairs  Mutagenic mechanism of ionizing radation - Ionizing radiation is usually form the decay of a radioactive species (i.e. radioactive iodine) - ROS: reactive oxygen species’are generated  they look for electrons and can be devastating to the structure and functioning of DNA - ROS are able to break the backbones of DNAand when the backbone breaks, the chromosome also “breaks”  Chromosomal rearrangement when trying to repair double stranded breaks - Deletion/Duplication: When repairing double stranded breaks, deletion or duplication can occur (self explanatory) of certain genes (i.e. they may be left out of may be duplicated twice) - Inversion/Translocation: The genes can successfully recovered although they may appear in a different, inverted order. When genes are translocated they are basically rearranged, i.e.ABCDEFG  ABEFGCD  Possible advantages of gene duplication - Two times the amount of the same gene means two times the amount of the protein that it can code for  you get twice the amount of “stuff” - You have a backup gene in the case that one of them stops being functional - It’s possible for one of the genes to diverge and be able to perform a new function  General use of gene families to create phylogenic trees - Gene families reflect evolutionary relatedness - i.e. our hypothetical common ancestor shares genes on the same places of the chromosome with other species (mice, drosphilia…) - These species all have genes in the same order  changes in copy number variations allows for the divergence in these genes  Products of meiosis in plants, animals, fungi, algae - In animals: Meiosis produces gametes (the only situation in which gametes are produced by meiosis) - In plants: Meiosis produces spores (gametophytes) which divides via mitosis to produce gametes - In algae/fungi: Meiosis produces spores (gametophytes) which divides via mitosis to produce gametes. The single celled cycle in fungi/algae and plants is haploid  Timing of meiosis in vertebrate life cycles - Homologues pair and undergo genetic recombination in prophase of Meiosis I (the recombination of DNAfrom both parents in the same cell - This crossing over generates new collections of alleles - Recombination is driven by enzymes  backbone is cut and pasted to the opposite backbone - Recombination is a mutation - Males are always undergoing genetic recombination whereas females underwent genetic recombination as a fetus (only completes meiosis once an egg becomes fertilized)  Main differences between meiosis and mitosis - Meiosis: Product (in humans) is four gametes. Genetic recombination occurs in Prophase I between homologues. Undergoes two separate phases (I and II) which are called the reductional division and equational phase respectively (reduction from diploid to haploid, by the separation of chromosomes, and equational division where chromatids are split and four daughter cells are formed) - Mitosis: Only one phase, two daughter cells are formed from the one, no genetic recombination happens, diploid throughout the entire event  Characteristics of homologous chromosomes - Chromosomes of approximately the same length containing genes corresponding to specific characteristics at the same loci (i.e. class example with two people undergoing sexual recombination  their waists, feet, eyes etc. are around the same place with respect to their similarly sized bodies)  Reasons why meiosis I is reductional and meiosis II is equational - meiosis I is called “reductional” because the chromosome number in the first phase is reduced from diploid to haploid - meiosis II is equational because the chromosome number does not change but the amount of DNAdoes (reduced)  Changes in C and n during meiosis - Meiosis I: Before Meiosis I you have 2n and 4C.After meiosis I, you have n and 2C (the number of chromosomes is reduced from diploid to haploid, but the amount of DNAis the same at 2C) - Meiosis II: n and C. Chromatids are separated and thus the amount of DNAin each cell is reduced (half of what it originally was)  Mechanism of recombination during prophase - In Prophase I of meiosis, homologues pair up and crossing over occurs - Recombination is driven by enzymes and occurs via the cutting of DNA backbones and p
More Less

Related notes for Biology 1002B

Log In


OR

Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.

Submit