DNA
Deoxyribonucleic Acid (DNA): A polymer made up of many monomers Sugar (pentose, deoxyribose C5H10O5): 5 carbon sugar, in a pentagon shape Nitrogenous Base: what changes between nucleotides Adenine (purine == double ring structure) Thymine (pyrimidine == single ring structure) A always bonded to T and G always bonded C DNA has two strands of nucleotides, and nitrogenous bases are held together by hydrogen bonds Antiparallel: DNA strands runs in opposite directions, one strand runs 5 to 3 and the other runs 3 to 5 (important for DNA replication) 5 Prime Side: there are five carbons (where the point of the pentose sugar points) 3 Prime Side: where three carbons at end of the pentos (fat side of the pentose points to the end) DNA Backbone: sides of the nitrogenous base ladder rung structure, made up of sugar and phosphate, keep the DNA together Double Helix: DNA twists around, made up of two strands of DNA Proteins were considered genetic information for a while before discovering DNA, bec. There were 20 amino acids, which makes more sense for complex combinations than 4 bases Frederick Griffith’s Experiment: mixed a rough strain of a disease (harmless) with a heat-killed smooth (virulent) strain and the mouse died There was a transforming factor, from the heat-killed bacteria to the rough strain → DNA Avery McCarty Macleod Experiments: wanted to discover Griffith’s transforming factor Isolated the bacterial RNA, proteins, and DNA Used enzymes that broke down each of those things until they could find out what caused the bacteria strain to transform When they broke down DNA, they found that the bacteria could no longer transform → found life was based off DNA (not definitively) Alfred Hershey and Martha Chase Blender Experiment: is it DNA or is it proteins that actually drive life (definitively)? Dyed sulfur and phosphorus in a virus that invades a bacterial cell Sulfur is found in proteins but not DNA Phosphorus found in DNA and not proteins Showed that the only one that was transforming the cell was the phosphorus → therefore DNA was hereditary material Watson and Crick: credited for discovering DNA’s structure combining Chargaff’s ATGC levels and Wilkins and Franklin’s helical structure Maurice Wilkins and Rosalind Franklin: discovered the crystallographic helical structure of DNA (basically had the data that Watson and Crick would use) Erwin Chargaff: looked at the amounts of bases: ATGC Found that A and T amounts correlated; G and C amounts correlated Must be pairs: Chargaff’s Rule DNA REPLICATION
during the S phase of interphase Semiconservative Model (of replication): original/parental strands of DNA separate, and two new strands fill in with each parental strand. Each new copy of DNA is composed of one old parental strand and one newly made strand DNA only dies if you don’t pass it down, “the immortal thread” Every new DNA molecule is made up partly of old DNA MESELSON AND STAHL Experiment: discovered semiconservative model At the time, there were two other models of DNA that were proposed: Dispersive Model: DNA was broken up, and each little DNA model was made up of old and new Conservative Model: original parental molecule was conserved, and a two new strands were formed Grew bacteria in heavy nitrogen, all DNA made in bacteria contained heavy nitrogen-15 Original bacteria has two strands of DNA both with nitrogen-15 Would have low band on centrifuge because of high density Grew bacteria in nitrogen-14, all new DNA would be made using nitrogen-14 (lighter) Two new daughter strands made using nitrogen-14 but the old strands are all originally nitrogen-15 After first round of replication, each DNA strand was half 15 and half 14 Got a medium band on the centrifuge Third Round of Replication Light Band: daughter strand of second round, paired with a new strand Medium Band: old 15 band from original paired again with another new daughter strand Never goes away because original nitrogen-15 DNA strand stays Origin of Replication “bubbles”: different in prokaryotes vs eukaryotes Where replication begins in each cell Bacterial DNA is unicircular has only one origin of replication and extends outward in both directions around the circle until completely replicated Eukaryotic DNA: multiple origins of replication with linear strands of DNA “Bubbles” at origins get bigger and bigger until they converge → multiple origins of replication make the process go faster and proves semiconservativeness Contains two replication forks: extends outward at each fork Creation of the Replication Bubble (made up of two replication forks) DNA Helicase: responsible for opening DNA up and making the replication bubble → breaks hydrogen bonds of helix Topoisomerase keeps theDNA unwound and stop hydrogen bonds from reconnecting “little clamps” DNA doesn’t want to stay apart Single-strand Binding Proteins: keep the bubble open, and binds to the unpaired bases of DNA to stop them from rematching up Making new DNA strands: (S phase of interphase) Primase: not made up of DNA, made up of RNA, lays down a primerto begin DNA creation Replication happens easily in the leading strand DNA Polymerase 3: the enzyme that actually makes the new DNA, can’t start from nothing, it can only extend preexisting nucleotides, needs to go off the primase’s primer ***can only operate in one direction ONLY operates to make 5 prime to 3 prime so it starts at the 3’ side of the leading strand to make a complementary 5’ to 3’, builds a complementary strand that’s opposite prime to opposite prime, by reading the template Starts at the 3 prime side of the template original/parental strand to make DNA 5 prime to three prime Then how do you make DNA for the other parental 5 to 3 strand but polymerase 3 can only go the opposite way See DNA Replication Sheet on Drive In the lagging strand, multiple not just one like leading strand, primers are going to be laid down, and polymerase 3 operates in between the primers Okazaki Fragments: only found in the lagging strand, a segment where DNA is replicated in the opposite direction, but stops at each primer, and then moves to the left, then replicates to the right, and moves to the left… All fragments are polymerased simultaneously, so it is quicker than just two primers on the end Polymerase 1: removes the RNA primers and replaces with DNA Ligase: connects fragments of DNA together, connects Okazaki Fragments to make a continuous strand of DNA New daughter strands are IDENTICAL If there is a mutation: Polymerase 3 screwed up You get all of your materials from your food Where do Polymerases get their nucleotides? Nucleoside Triphosphate: an adenine nucleotide with two extra phosphates to which is ATP Polymerase cuts off the phosphoruses and you get Adenine Releases energy required to build DNA There are also CTP, GTP, TTP, other energy sources that when phosphorylated become all of the other nucleotides in the body. BUT, if at the very end of each DNA fragment, there’s nothing for Polymerase 1/3 to latch on to; end DNA is never replicated With every single replication of DNA, your DNA gets shorter Telomeres: contain non-coding DNA, long sequences of repetitive DNA at the end of each chromosome, it can be burned up through the process of DNA replication as to not affect your coding DNA When telomeres run up, you die because you start eating into your genes when you replicate Telomerase: enzyme found in germline cells (sperm/egg) that extend telomeres so you pass on full DNA DNA REPAIR
If a mistake/mutation occurs, Polymerase 1 or 3 is at fault, by laying down the wrong nucleotides We have enzymes that proofread our DNA and fix problems “Mismatch Repair”/ Nucleotide Excision Repair: if nucleotides are mismatched, don’t line up properly, then a protein cuts out the bad nucleotides and fixes it If this process were perfect there would never be any variation or mutations for evolution Nuclease: DNA cutting enzymes, and it cuts out the mutation Polymerase just reinserts the DNA Ligase reconnects the DNA ***bacteria and viruses lack proofreading proteins, they want and need to mutate in order to evolve and create new strains GENES AND PROTEINS
A gene is the instruction manual that creates a certain protein, each gene codes for 1 protein polypeptide
Beadle and Tatum Experiment: Studied metabolic defects in a fungus Mutated each specific gene that coded for a specific enzyme in a metabolic pathway and discovered that when a certain gene mutated a certain protein screwed up in the pathway causing a buildup of that product Discovered the 1 gene 1 enzyme (now protein and now polypeptide) hypothesis Every protein is different because it has a different sequence of amino acids TRANSCRIPTION
: takes place inside the nucleus
DNA in chromosomes is too long and condensed, must use mRNA to leave through nuclear pores Genes tell the ribosome what order to put amino acids in One specific gene is read and used to make a sequential copy called mRNA (messenger RNA) mRNA is a transcript/copy of a gene and goes to the ribosome Gene DNA is read in triplets of bases called the reading frame TEMPLATE STRAND IS ALWAYS 3’ to 5’, the COPIED RNA CODING STRAND IS 5’ to 3’ RNA Polymerase 2: reads the template strand of DNA makes an RNA coding strand, which is complementarybut where there’s an A in the DNA, polymerase puts a U (uracil) in place of a T The result is mRNA which in triplets has codons each codon corresponds to a specific amino acid Determination of Structure/Function: ultimately the DNA determines protein structure Sequence of DNA → mRNA (codons) → amino acids → protein structure → protein function Proteins in different shapes perform different functions AUG (start codon): codes for amino acid methionine, ALWAYS the first codon, and methionine is always the starting amino acid in every protein Therefore, in DNA, the beginning of every gene is TAC There are also stop codons, each gene always starts with a start codon and ends with a stop codon Noncoding DNA: DNA that does not correspond to coding for a protein, it acts as a buffer, only 1% of DNA actually codes for proteins, the majority is noncoding Most noncoding DNA is used to regulate our genes, Promoter: region right before the gene of noncoding DNA where RNA polymerase binds to after transcription factor binds to TATA. Never transcribed as part of mRNA, only part of DNA. TURNING ON A GENE: TATA Box: first four nucleotides of promoter (TATA) When a transcription factor binds to the TATA Box, begins the process of transcription.The transcription factors (steroid hormones) are what turn genes on. Steroid hormones control the process of protein synthesis Terminator Sequence (AUAAA): a sequence that causes the RNA polymerase to stop transcription and send off the mRNA mRNA transcription starts at the promoter and ends at the terminator sequence Before mRNA can leave the nucleus, the Pre-mRNA must go under RNA Processing: stuff added to the Pre-mRNA before leaving the nucleus 5 Prime Cap: made out of GTP, how the ribosome knows what part of the mRNA is the front Poly A tail: long string of adenine, that protects against degradation (back of mRNA) Exon: parts of the RNA are coding, each exon corresponds to a location in a polypeptide called a domain Intron: part of RNA, that is noncoding Alternative Splicing: why have introns when you could just have exons? 23,000 genes can actually code for more than 23,000 proteins One piece of mRNA can code for multiple proteins in the body by switching the exon and intron parts Spliceosome: cuts out the introns and splices together the exons so only coding mRNA is left TRANSLATION
: comes after transcription in ribosome
Ribosome receives and reads the mRNA and reads it, puts together a sequence of amino acids Redundancy of codons: if a mutation takes place you may not put down the wrong amino acid, protection against mutations Multiple codons can code for the same amino acid Silent Mutation: mutation that doesn’t do anything, doesn’t change the amino acid it codes for, because of redundancy tRNA: (transfer RNA) bottom part of the tRNA is a complementary, anticodon that is complementary to the codon (STILL USES URACIL) and carries an amino acid on the top. tRNAs can be recycled, just attach new amino acids to build a protein Each has a specific anticodon and amino acid Aminoacyl-tRNA-synthetase: enzyme that attaches tRNA to new amino acids, using ATP (get amino acids from food) Ribosome Structure: (GTP powers everything) CONVEYOR BELT Small Subunit: scans mRNA for the start codon, the mRNA lays on top of the subunit and tRNA attaches Large Subunit: (Left to Right: Environmental Protection Agency) attaches on top of small subunit E Site: exit site, where the used tRNA leaves P site: first tRNA enters Works like a conveyor belt, tRNA attaches to the codon SEE THE ANIMATION ON GOOGLE CLASSROOM Release Factor: carries water and performs hydrolysis, enters the A site instead of another tRNA and stops the building of a protein GTP used to dehydration synthesize the amino acids, creating peptide bonds and GDP Polyribosomes: Since it’s a conveyor belt, you have multiple ribosomes working on the same strand of mRNA, speeds up the rate of protein production Primary Structure: linear sequence of amino acids peptide bonded together Protein folding takes place in the endoplasmic reticulum Secondary Protein Structure: hydrogen bonding creates beta pleated sheets and alpha helices Tertiary Protein Structure: Hydrophobic bonds, ionic bonding, disulfide bridges, etc. creates one polypeptide subunit Quaternary Protein Structure: multiple polypeptides come together to form a complex protein Wobble: for each amino acid, there is only ONE tRNA that carries it, even though there are multiple codons that code for a single amino acid (redundancy), only the first two nucleotides of codon and anticodon fit together, the last one doesn’t usually matter, so the tRNA and mRNA fit wobbles, not perfectly together to save energy Relaxation in the base pairing rules for the third nucleotide Eukaryotes vs. Prokaryotes: RNA processing only takes place in Eukaryotic cells (prokaryotes don’t have spliceosomes) Prokaryotes don’t have a nucleus MUTATIONS
Mutations take place during the process of DNA replication (polymerases screw up) Point Mutation: single base modification causes a nucleotide base change, insertion, deletions, substitutions, etc. Substitution: one nucleotide is substituted for another (Sickle Cell Anemia) Changes only one amino acid in a protein, can radically change the shape of a protein (change takes place in the primary structure, and all other structures, etc.) Tay Sachs: lipase in the brain (breaks down lipids) mutates so lipids in the brain build up and kill the baby Missense: when you have the wrong nucleotide and it changes the amino acid Nonsense: when the mutation creates a premature stop codon (bigger effect on the protein than missense) Silent Mutation: change at a point that doesn’t change the amino acid because of redundancy (third nucleotide usually doesn’t matter) If a nucleotide is put in where it shouldn’t or if a nucleotide is removed. Causes a shift in the reading frame, causes all triplets to be screwed up Frameshift: all reading frames moves Affect every amino acid after that mutation CONTROL OF GENE EXPRESSION
Not all genes are turned on all of the time, else you would be making all of your proteins constantly which would waste resources and energy. Cells regulate genes to control the production of proteins in the body using hormones (mainly steroids) Create different proteins Development (changes that take place during your lifetime, puberty especially) If a gene is being expressed it means its being transcribed or turned on Cell Differentiation: Different types of cells (heart cells, skin cells, etc.) are created by turning on and off certain genes even tho every cell has the same code Stem Cell: a cell that has not yet differentiated Differential Gene Expression: having certain genes on or off Internal and External Factors can affect gene expression Operons and other structures herein are only found in prokaryotes, not eukaryotes, a simplified model Operon: a region consisting of the operator, genes, and promoter Operator: only in prokaryotes, sits in front of RNA polymerase before gene and after promoter, controls whether or not genes are turned on or off Regulatory Gene (way before operon): codes for the repressor protein which can bind to the operator, if the repressor binds to the operator, RNA polymerase cannot get to the genes → turns off the genes/inhibits gene expression or transcription Repressible Operon: normally turned on but can be turned off EXAMPLE: Leads to the production of tryptophan proteins The bacterium will turn off the tryptophan if it consumes enough of it The repressor is normally the wrong shape so it cannot bind to the operator to shut off the gene, so tryptophan acts as a corepressor, binds to the repressor changing its shape. The new structure can now bind to the operator and shut off production of that gene → don’t waste energy making more of the protein when you have enough Turned back on when you run out of tryptophan because the repressor turns back into its inactive shape Inducible Operon: normally turned off but can be turned on The lac operon (stands for lactose sugar found in milk) Produces lactase enzymes needed to break down lactose Only want to produce these enzymes when you ingest lots of lactose/milk The repressor is normally bound to the operator, RNA polymerase normally does not have access to the genes → turned off most of the time Lactose is an inducer changes the shape of the repressor to release it from the operator, and makes it inactive If there’s no more lactose it would shut off the gene EUKARYOTIC GENE CONTROL
70% of the genome occurs only once 1% is actually coding the other 69% is used to regulate your genes Control Elements: regions where transcription factors (steroids or growth hormones NOT just roids, etc.) bind, noncoding regions Proximal Control Elements: close to promoter Distal Control Elements (enhancers): far from promoter Activators: turn genes on Usually bind to the enhancer/distal region Repressors: turn genes off *Can delay/stop the process of protein production is to not process the Pre-mRNA Noncoding RNAs: used to slow or stop the production of proteins by blocking or destroying mRNA before they get to the ribosome, instead of turning off the gene → regulate protein synthesis Coding RNAs are rRNA tRNA and mRNA used to make proteins Small interfering RNAs (siRNAs) Interference: prevents mRNA from hitting the ribosome put in a holding pattern Degradation: destroy mRNA Proteases break down extra proteins in a proteasome to purely destroy unneeded proteins Modifications to Chromatin Structure Control whether genes are on or off by changing chromatin structure Either loosen or contract DNA to expose or hide genes for replication, if hidden, polymerase cannot get to the DNA Acetylate histones: expands chromatin by attaching acetyl groups to the histones Creates euchromatin (active) Add a methyl group (CH4) to the DNA, to condense the chromatin making DNA inaccessible Creates heterochromatin (silent) Regions like centromere or telomeres are made up of heterochromatin cuz they are noncoding and you don’t need them unwound During mitosis no genes are turned on because chromatin is condensed Traits are much more than just DNA It’s about what genes are on or off Studying inheritance abt what genes are on or off Outside factors, like lifestyle MICROBIAL GENETICS
Bacteria is considered alive but viruses aren because they aren’t cells Size: animal cell > bacterium > virus VIRUSES: aggregate of nucleic acids and proteins Capsid: Outer coat of proteins called capsomeres Some viruses use DNA, RNA and single/double stranded variations Viral Envelope made up of cell membrane and glycoproteins Only SOME viruses have this because cells steal it from the host cell Tobacco Mosaic Virus: infects tobacco plants most common viral model Adenovirus: causes meningitis, common cold, stomach bug, etc. (incl. Rhino viruses) Influenza Virus: has a viral envelop, flu Bacteriophage (phage): viruses that only infect bacteria, look like a space moon lander Like a parasite, hurts specific host cells and hurts us for benefit → can’t reproduce on their own Does not contain enzymes or ribosomes → cannot make own DNA or proteins → uses a host cell ***all viruses have some mechanism to get information into the host cell, takes over organelles + enzymes to make virus components Have existed since the very first cells, viruses evolved to exploit them Viruses self assemble in host cells, lyse the cell when there’s enough Viruses don’t intend to kill you, they want to get you sick enough to spread the viruses around Vaccines: you receive a component of the virus (viral proteins, genes, heat-killed virus, live virus) to trigger an immune response and antibodies to defend against a real attack Lytic Cycle: used by virulent viruses → KILLS HOST CELL Hydrolyzes host cells DNA Injects viral DNA and builds new viral parts Used by phages, bust out of the cell and lyse it Lysogenic Cycle: used by temperate viruses DOES NOT KILL HOST CELL Prophage: viral genes inserted into a bacteria Provirus: viral genes inserted into an animal cell Viral DNA incorporates into the cell’s genome When cell reproduces, builds viral proteins and replicates the bad DNA If the cell is stressed, it causes the phage to be released from cell → NO LONGER DORMANT, will enter the lytic cycle (e.g. shingles) Stays dormant until there are optimal conditions, then releases to create an infection in the lytic cycle Viral envelope surrounds capsid containing RNA (used by retroviruses) Retrovirus: has RNA for its genetic information Reverse Transcriptase: undoes transcription, takes RNA and makes DNA for host cell Enters Helper-T cells thru endocytosis, that's why envelop so important Then capsid appears and makes DNA to incorporate in the cell → provirus that’s dormant in lysogenic cycle Why HIV appears years after infection Drugs keep the provirus a provirus, keep it dormant HIV LEAVES THRU EXOCYTOSIS → makes a viral envelope Over time the the cell’s membrane would be destroyed because it's eaten up ***cell no longer functional wipes out the core of the immune system Why the virus is bad → virus badness depends on which type of host cell is affected Even simpler infectious agents: Viroids: infect plants, just floaty RNA Prion: infectious misfolded proteins (mad cow disease in humans) BACTERIA
Binary Fission (mitosis for bacteria): asexual reproduction (w/o a partner) Doesn’t produce any genetic variation → asexual W/o genetic variation you can’t have evolution not able to evolve so you need another way to produce genetic variation High rate of mutation → lack proofreading enzymes, the primary method of creating variation Bacteria have a single circular chromosome and no nucleus (just nucleoid region), one origin of replication Plasmid: extra small circular pieces of DNA, that has a relatively small number of genes on it (3-7 genes) Can be exchanged with other bacteria Can cause increased genetic variation R(resistance)-plasmid: contain genes for resistance, in particular, antibiotic resistance, used in labs, not usually in natural bacteria Genetic Recombination: mixing up all of the genes to increase the amount of variation Transformation: (most common) when a bacteria takes in plasmids from their environment (Griffith experiment), new genes make new proteins, increases genetic variation In order to make the bacteria accept the plasmids, you must induce competency, using a process known as heat-shocking (expose to cold-hot-cold to open bacteria to take in plasmid) Transduction: transfer of DNA through phages When a virus accidentally transfers DNA from one bacteria to another When a host cell assembles viruses, sometimes bacterial DNA will be packaged into one of the virus capsids This virus infects another cell, and inserts the host cell’s bacteria Conjugation (‘bacterial mating’): direct transfer of genetic material between bacteria pairs F-plasmid: allows bacteria to form a cytoplasmic bridge (mating bridge/sex pili) outside the cellcan only make this if the bacteria has the F-plasmid The sex pili can be attached to a “female bacteria” and transfer plasmids, (including the F-plasmid, change the bacterial sex of the female) Can copy the plasmid over, cannot lose a plasmid, so once it’s male it stays male
Nonspecific Defense (innate immunity) GENERAL Your body targets everything the same, it doesn’t adapt to things, everyone has the same nonspecific defense 1st line of defense: prevents stuff from entering the body Skin: protects body from external world Skin is pH acidic, creates bad, antibiotic environment for bacteria Mucous: lines the holes/orifices in your body Acidic to repel bacteria and contains lysozymes: which break down and destroy bacteria This is why licking a wound helps because of the pH of the mouth and the enzymes of the saliva 2nd line of defense: if stuff enters the body Phagocytic White Blood Cells: large cells that perform phagocytosis (endocytosis) and destroy invaders, all target slightly different things, encapsulates the invader in a vesicle and the vesicle travels to the lysosome and performs hydrolysis. Doesn’t matter if the invaders are viruses or bacteria, eat em anyway Natural Killers (NKs): target tumors (cancer) and virus-infected body cells (only highly specific WBC) Eosinophils: specialized for worms Macrophage (most important, but still nonspecific): eats everything Antimicrobial Proteins: float around in the bloodstream and destroy or lyse microbial invader cells Part of the Complement System Interferons: (chemical messenger) secreted by virus-infected cells and cause all nearby cells to change their cell membrane, to prevent them from being infected. Prevent virus spread from cell-to-cell. Lymphatic System:has a bunch of macrophages and transports using vessels usually for bacterial infections Pathogens enter the lymphatic system through the intestinal fluids bathing the cells Has a bunch of vessels (in green) that are around your veins, interconnected with your bloodstream, has a whole lot of macrophages Everything in blood except blood cells enter the lymphatic system in lymph fluid Spleen: also where macrophages are produced (not as much) Lymph Nodes: where macrophages get activated, if you have an infection, lymph nodes swell because they are filled with macrophage WBCs. Lymph: fluid in lymphatic vessels, also goes thru veins collected from veins Inflammation: redness, swelling, and warmth → caused by #1. Increased blood flow makes it warm and red and #2. Swelling caused by blood vessels leaking fluid into that area Infection: entry of a microorganism Histamine: released when a tissue damage or infection occurs (chem. msger) CAUSED INFLAMMATION Increased blood flow increased/speedy transport of things you need More macrophages get to that area Blood vessels get much more permeable so things can leave the blood vessels (large phagocytes) easily Hypersensitivity: things that cause inflammation when they shouldn’t e.g. allergies Allergies: swollen sinuses cause a runny nose, by fluid draining out of nose Can be assuaged by antihistamines Specific Defense/Immunity (ADAPTIVE): Adapts to each specific antigen that enters your body, your actual “immune system” Antigen: ANY MOLECULE THAT TRIGGERS THE RELEASE OF ANTIBODIES AND AN IMMUNE RESPONSE T-dependent: originally goes through the helper T cell to produce antibodies T-independent: antigen originally went to the B-cell to produce antibodies Passive Immunity: antibodies provided the mother guard against pathogens that have never infected the newborn Breastfeeding passes her antibodies to the baby so the baby is immune to everything the mom was, so the vulnerable newborn is protected. Antibodies go away after the mother stops breastfeeding. Primary Immune Response: when your body first encounters the antigen Secondary Immune Response: when your body is exposed to the antigen in the future (ANTIBODIES PART OF SECONDARY IMMUNE RESPONSE) Epitope: part of the antigen that a B or T cell goes into the cell’s receptors for the T and B cells to recognize the antigen Lymphocytes: major WBCs, made in the bone marrow just like rest of blood ***both made in bone but mature in different places ***respond to specific antigens, every single B/T cell has unique receptors for any type of antigen and gets more thru genetic recombination You have receptors for antigens that may not even have evolved yet, so anything that enters your body can be countered If an antigen is received by a lymphocyte’s specific receptor, that WBC clones itself a lot in order to combat the antigen Clonal Selection: create a lot more of that lymphocyte to combat the antigen Half of the cells produced become: Effector Cells: short lived cells, immediate response and take care of the problem initially Memory Cells: stick around for weeks, years, etc. in case there is a recent second exposure, so you can’t catch the same cold again, but don’t stay with you forever T-cells: mature in the Thymus Cytotoxic T’s (w/ memory T’s part of the CELL-MEDIATED RESPONSE) : “soldiers of the immune system” attacks infected cells in the body, does not kill the antigen directly, do not produce antibodies Perforin: a protein that forms pores in the target cell’s membrane → causes cell to lyse and die Respond to tumor antigens that are involved in cancer formation ***Helper T’s: "the core of the immune system” Responds to Class II MHC from WBCs Activates both B-cells and T-cells using cytokinins B-cells: mature in the Bone HUMORAL RESPONSE Effector B’s (Plasma Cells): produces ANTIBODIES which remain in your bloodstream for the rest of your life so you can’t get it again Immunoglobulin (Igs/antibody formal name):quaternary protein made of multiple polypeptides, in a “Y” shape 2 purple subunits: heavy chains 2 blue subunits: light chains Used in the SECONDARY immune response The two top tips of the “Y”are where antigens would attach to the antigen Neutralization: can’t kill a virus but antibody covers entire surface of virus, to prevent it from infecting any other body cells MAC (Membrane Attack Complex): only happens to bacteria, when antibody punctures holes in bacteria, and lyses the bacteria Glycoprotein (MHC, Major Histocompatibility Complex): every person and every cell has a glycoprotein unique to the body for cell-to-cell recognition Class I: found on all normal body cells with nuclei Class II: found on white blood cells Also used for antigen presentation: holding out a piece of the antigen for T-cells from infected cells so they can come kill that cell Cytotoxic T’s respond to Class I MHC Helper T’s respond to Class II MHC on WBCs Vaccinations: try to trigger a primary immune response Inactivated bacterial toxins, heat-killed pathogens, parts of pathogens, genes coding for microbial proteins → injected with antigen material If you trigger a primary immune response you build antibodies to prevent an actual attack from a disease Autoimmune Diseases: loss of self tolerance, body attacks part of self because it doesn’t recognize it Lupus: attacks histones and DNA Rheumatoid Arthritis: cartilage and bones in joints are attacked Multiple Sclerosis: CNS and schwann cells are targeted Diabetes Mellitus (Type I): pancreatic cells are targeted Immunodeficiency Diseases: defective or absent immune system SCID (Severe Combined Immunodeficiency): treated with gene therapy, born without an immune system Hodgkin’s: (lymphoma, and cancers): lymphocytes in the body are cancerous → cancers form in the lymph nodes AIDS: (Acquired Immunodeficiency Syndrome) targets Helper T-cells using HIV, will destroy the immune system HIV+ just means you have the HIV virus AIDS is when a certain percent of the immune system has been wiped out → shuts down cell-mediated and humoral responses Can’t die of AIDS, because you die of simple infections because you don’t have normal defenses 
Unit 6: Gene Expression and Regulation
