Unit 6: Gene Expression and Regulation

Deoxyribonucleic Acid (DNA):
A polymer made up of many monomers
Nucleotide: (monomer)
Sugar (pentose, deoxyribose C5H10O5): 5 carbon sugar, in a pentagon shape
A ribose minus an oxygen
Phosphate Group (PO3)
Nitrogenous Base: what changes between nucleotides
Cing Tut == pyrimidines
Adenine (purine == double ring structure)
Thymine (pyrimidine == single ring structure)
Guanine (purine)
Cytosine (pyrimidine)
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
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
Centrifuge results:
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
5 to 3 == leading strand
Replication happens easily in the leading strand
3 to 5 == lagging 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…
P→ P→ P→
Overall direction: ←
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
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
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
: 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)
RNA Splicing:
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
: 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
Binding sites:
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
A Site: next tRNA enters
Works like a conveyor belt, tRNA attaches to the codon
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
Bound Ribosomes:
Protein Structure:
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 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)
Insertion & Deletion:
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
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)
Turning on genes causes:
Create different proteins
Create different cells
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
Happens in the womb
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
Trp (tryptophan) Operon
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 Genome:
70% of the genome occurs only once 1% is actually coding the other 69% is used to regulate your genes
30% is repetitive
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
Transcription Factors:
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
MicroRNA (miRNAs)
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
Histone modifications
Acetylate histones: expands chromatin by attaching acetyl groups to the histones
Creates euchromatin (active)
Methylate DNA:
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
Epigenetic Inheritance:
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
Bacteria is considered alive but viruses aren because they aren’t cells
Size: animal cell > bacterium > virus
VIRUSES: aggregate of nucleic acids and proteins
All viruses have
Capsid: Outer coat of proteins called capsomeres
Give virus it’s shape
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
Virus goal: Replication
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)
Unicellular organisms
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
“Male bacteria”
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
Caused by:
Physical tissue damage
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”
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.
Active Immunity:
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
Effector T’s:
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
Memory T’s:
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
Memory B’s
Self vs. Nonself:
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
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