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by Brian Lin
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About Me... and the new AP Bio test.
My name is Brian Lin, if you don’t already know me, then you sure will 70-80 pages later.
Anyways, I like playing the cello, fooling around, and complaining about things in review guides.
So have fun, learn a lot, and eat a lot (the pre-AP test breakfast is AMAZING!) However, don’t eat
so much that you end up throwing up during the test and losing time (one of my friends lol).
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proctor would tell them when to move on to the grid-in problems. So time ran out, and they didn't
do them!” -Some teacher guy
Apparently some people just didn’t do the grid-ins because… I have no idea really. Luckily, all of
us were told to work backwards on the MC, starting with the grid-ins (and the harder
normal MC) so I (at least) did not have that problem. Grid-ins are not really that hard though.
Even though you can’t guess like a MC question, there’s quite a bit of room for rounding errors
and stuff. And the math is pretty easy (though tedious).
Also, time was not an issue for me (that’s for me though, one of my friends had to throw up in
the middle and didn’t finish…). I had enough time left after the MC to check over about half of
them. On the FRQs, I was able to read through all of them (and my responses). In fact, make
sure you leave plenty of space to add stuff later since you will have time to go back and stuff
more key words in.
Also, it’s important to realize that the test has shifted away from memorization/content-based
and more towards skill/application/understanding (for example, they will have questions
where they will explain a lab/concept for you and then ask you about it). Your teachers will say
corny stuff about how understanding stuff is important (the whole Big Idea thing).
They’re actually right. Seriously, I thought it was really cheesy but it helped A LOT.
Big disclaimer here: The AP Biology test content NO LONGER coincides (completely) with
the SAT Bio test. You will have to self study around half of the material. Sucks since the
College Board makes both but haven’t updated the SAT subject test. Also, there’s a lot less
curve than physics, which sucks. Take SAT PHYSICS or CHEM! Please! (Plus Princeton
doesn’t take Bio for engineering majors). Seriously, I regret not taking SAT Physics.
Also, do not pay for test-prep books/ tutoring unless they’re based on/have actually
taken the new test. I bought the Barron’s book last year and it was a waste of money
considering entire chapters were irrelevant (and useless) and covered stuff we didn’t need to
know (all the while leaving other stuff out). Just ask someone who took the new test.
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I. Evolution
1. Evolution by Natural Selection
• Okay, let’s start off with a population (bunch of same species in same place)
• There’s going to be genetic variation. Why?
1. Random mutations. Point mutations (insert/delete/frameshift)
2. Crossing over and recombination (getting back together)
3. Law of Independent Assortment (Metaphase I ⇨ 2 dif. orientations)
4. Random fertilization
(You learn about all this stuff later, I just added it here since this is a big FRQ topic)
• These different individuals will be selected for or against by selective pressures
• Any developed traits that help you survive are known as adaptations
• Those that survive to reproduce will create offspring and change the allele frequency of the
population in favor of the ‘fit’ allele (allele = version of a gene)
• Divergent evolution⇨ branching out (becoming “more different”)
• Convergent evolution⇨ evolving similarly (explains analogous structures in 5.)
• Population ⇨ a group of individuals of same species that can interbreed and create fertile
offspring (so a herd of deer or something)
• Species ⇨ a group of populations whose members can interbreed and produce fertile offspring
(all the deer herds in the world)
2. Hardy-Weinberg
• What’s it say? Allele frequency and genotype frequency remain constant!
• But for this to apply, we’ll need 5 conditions:
1. Really big population/sample size
2. No mutations
3. Random mating
4. No natural selection
5. No migration/gene flow (ie no adding/removing organisms)
Equation 1: P + Q = 1
Equation 2: P ² + 2P Q + Q² = 1
P is the dominant allele frequency. Q is the recessive allele frequency.
So if you have mice that can either have brown hair or black hair (where hair color is the gene
with 2 different alleles). Then % brown (P) + % black (Q) = 100% (1). Should make sense.
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P² is the frequency in the population with homozygous dominant allele.
2PQ is the frequency in the population with heterozygous both alleles.
Q² is the frequency in the population with homozygous recessive allele.
Since the mice get one allele from each parent, you multiply the allele frequencies together.
Since P = chance of getting the dominant allele and Q = chance of getting the recessive allele,
you multiple P * P to get the chance of getting homozygous (2) dominant alleles and so on.
• Genotype ⇨ Set of genes it carries;; 2 alleles.
• Phenotype ⇨ Expressed traits;; characteristics. (Straight hair)
So if brown is dominant, a brown mouse can have the genotype Bb (one brown and one black)
but still have the phenotype brown since that allele takes over.
3. Microevolution
• What is microevolution? Changes in allele frequencies within a population.
• There are 4 main causes for microevolution:
1. Random mutations
2. Natural/Artificial Selection
3. Genetic drift
4. Gene flow
• Genetic drift is changing allele frequencies by changing the sample size
1. Bottleneck (natural disaster⇨random drop in gene pool, depends on survivors)
2. Founder (random group leaves and ‘founds’ new population, depends on founders)
• Gene flow and migration is when you transfer alleles from one population to another
4. Macroevolution
• What is macroevolution? Formation of a new species (speciation)
• How does this happen?
1. Start off with parent species
2. Add a reproductive barrier
3. Wait some time
4. Divergent groups can’t produce fertile offspring
5. Voilà! Macroevolution
• There are two main modes of speciation
• Allopatric speciation ⇨ geographic/physical isolation
Examples would be mountains, long distances, oceans, etc.
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• Sympatric speciation ⇨ non-physical isolation
Examples would be all the stuff in I.6: Reproductive Barriers (scroll down 1 page)
• Adaptive radiation refers to when a parent species diversifies and fills many different niches
6. Reproductive Barriers
Egg + Sperm = Zygote
• Pre-zygotic ⇨ impede mating or hinder fertilization even if mating occurs
Type 1: No mating (ie NO SEX!)
⇨ Habitat Isolation: different areas (water/land snake)
⇨ Temporal Isolation: different times (winter/summer skunk)
⇨ Behavioral Isolation: different courtship rituals (bird songs)
Type 2: No fertilization (sperm never meets egg)
⇨ Mechanical Isolation: the ‘parts don’t fit’ (use your imagination)
⇨ Gametic Isolation: sperm cannot fertilize egg (dif. color eggs in sea urchins)
• Post-zygotic ⇨ prevent the hybrid (offspring) from developing correctly
⇨ Reduced Hybrid Viability: too weak and dies
⇨ Reduced Hybrid Fertility: sterile offspring (mule)
⇨ Hybrid Breakdown: hybrid’s offspring can’t survive
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7. Modes of Selection
• Directional ⇨ favors one extreme
• Diversifying/Disruptive ⇨ favors both extremes
• Stabilizing ⇨ favors the middle
• Frequency Dependent ⇨ fitness declines if too common (ex. Google ‘scale eating fish’)
• Sexual Selection ⇨ organisms with best traits get to reproduce
⇨ Intrasexual: compete with same gender (ex. alpha lion)
⇨ Intersexual: ‘mate choice’ (choose flashy colors of peacock, etc.)
8. Chi-Square
X ² = Σ (O−E)²
E
• X² means “chi-squared”. DO NOT take the square root or anything.
• O means observed number
• E means expected number
• Degrees of Freedom ⇨ number of possibilities minus one (ex. rolling a die ⇨ 5 degrees of
freedom)
• P value ⇨ probability observed results are due to chance
• If P < .05 ⇨ results are NOT due to chance
• Null hypothesis ⇨ predicting that there is NO change
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9. Cladograms/Phylogenetic Trees
“Jaws, lungs, etc.” are traits that distinguish each branch.
• Clade ⇨ bunch of organisms evolved from same common ancestor
• There are different types of clades
⇨ Monophyletic: complete, all from same common ancestor (all the animals above)
⇨ Paraphyletic: incomplete, not everyone (just the chimp, mouse, and pigeon)
⇨ Polyphyletic: different common ancestor (all the animals above + a plant)
II. Biochemistry
1. Bonds
Note: Bonds are listed in order of strongest ⇨ weakest
• Intramolecular Bonds ⇨ hold a single molecule together, covalent and ionic bonds
• Covalent Bonds ⇨ a sharing of valence electrons
⇨ Nonpolar (equal b/w two of same atom): O2, H2, etc.
⇨ Polar (unequal sharing, difference in electronegativity): H2O
• Ionic Bonds ⇨ giving or taking electrons
⇨ Need a big difference in electronegativity (NaCl)
⇨ Cation donates electron, Anion receives
• Intermolecular Bonds ⇨ attraction between multiple molecules
• Hydrogen Bonds ⇨ attraction between positive (H) and negative (O) poles of water molecules
• Van der Waals ⇨ temporary dipoles from random electron movement, need to be close
together
So... Covalent>Ionic >>>>>>> Hydrogen>Van der Waals
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2. Why is Water so Special?
• Structure ⇨ polar molecule, easily forms H-bonds, hydrophilic of course
• 4 awesome properties:
1. Cohesion: Water molecules link together with H-bonds, allows for transpiration pull in plants
2. Moderation of Temperature: High specific heat ⇨ takes a lot of heat to increase
temperature, evaporative cooling (sweating), regulates the Earth’s climate
3. Freezing: ice floats on water, keeps fish and stuff alive, oceans can thaw out during
spring/summer
4. ‘Universal Solvent’: forms aqueous solution
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5. Functional Groups
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(Make sure to refresh on these before the AP test/final)
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6. Macromolecules
• Dehydration synthesis ⇨ take out a water molecule, combine two things (anabolism)
• Hydrolysis ⇨ add a water molecule, break things apart (catabolism)
• 4 groups of macromolecules ⇨ Carbohydrates, lipids, proteins, nucleic acids
• Notice that maltose does not follow the 1:2:1 ratio as it loses 2 hydrogens and 1 oxygen in the
release of a water molecule
• Carbohydrates ⇨ C, H, O ~ 1:2:1 ratio, sugars end in -ose
• Monomer ⇨ Monosaccharides
• Type of covalent bond ⇨ glycosidic linkages
For energy purposes:
⇨ Monosaccharides: single sugar (glucose, fructose, ribose, deoxyribose)
⇨ Disaccharides: double sugar
Sucrose: glucose + lactose (sucrose ⇨ table sugar)
Maltose: glucose + glucose (amylase breaks down starch ⇨ maltose)
Lactose: glucose + galactose (sugar found in milk)
⇨ Polysaccharides: multiple sugars, used for energy storage
Starch in plants (don’t move, can store energy long term as carbs)
Glycogen in animals (short term storage, fat is for long term)
For structural purposes:
⇨ Chitin: forms the exoskeleton of arthropods (crabs, bugs, etc.) and fungi cell walls
⇨ Cellulose: plant cell walls
• Lipids ⇨ insulation + long term energy storage
• Monomer ⇨ Fatty acids, glycerol, other stuff
• Type of covalent bond ⇨ Ester linkages
⇨ Saturated fats: solid at room temperature, 3 fatty acids +
glycerol
⇨ Unsaturated fats: liquid at room temperature;; 3 fatty acids
+ glycerol
⇨ Steroids: 4 carbon ring things with functional groups
⇨ Phospholipids: polar head (phosphate) and nonpolar tail
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(fatty acids)
2 fatty acids + glycerol + phosphate
Phospholipid bilayer in semi-permeable membranes
⇨ Waxes: long fatty acid + alcohol
• Proteins ⇨ do a ton of stuff
• Monomer ⇨ Amino acids (20 different)
• Type of covalent bond ⇨ Peptide bond
• Functions:
⇨ Structure (keratin, collagen)
⇨ Transport (hemoglobin)
⇨ Enzymes (amylase, lipase, polymerase, etc.)
⇨ Defense (antibodies, cytokines, etc.)
⇨ Hormones (insulin)
⇨ Motion (actin and myosin in muscles)
• 4 Levels of Protein Structure
1. Primary Structure (polypeptide chain of amino acids linked by peptide bonds)
2. Secondary Structure (folding between polypeptides, linked by Hydrogen bonds)
Forms Alpha helices and Beta pleated sheets
3. Tertiary Structure (bonds between R-groups, forms 3D shape)
Ionic bonds/ Salt bridges from acidic (-) and basic (+) R-groups
Hydrogen bonds (between -COOH and -NH2 and -OH groups on side chains)
Hydrophobic forces between non polar side groups
Disulphide bridges (strong covalent bonds b/w sulfhydryl groups in thiols)
4. Quaternary Structure (not necessary, interaction between multiple subunits)
• Nucleic Acids (Note: Nucleic acids may no longer be in this unit) ⇨ encoding, transferring,
and expressing genetic information
• Monomer ⇨ Nucleotides (phosphate + pentose + nitrogen base)
• Type of covalent bond ⇨ Phosphodiester bonds
• Two types of nucleotides:
⇨ Pyrimidines: 1 carbon ring nitrogen bases (cytosine, thymine/uracil)
⇨ Purines: 2 carbon rings nitrogen bases (adenine, guanine)
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⇨ Lock and key model: specific substrate for specific enzyme, binds to active site
⇨ Induced fit model: more accurate, the substrate induces (causes) the enzyme to align
with the substrate (not a perfect fit)
• Denaturing ⇨ temperature/salt/pH break apart bonds in secondary/tertiary structure
⇨ For example, if you have an acid such as Hydrochloric acid (HCl), it might interrupt the
H-bonds of the secondary structure, causing everything to fall apart
⇨ Also, raising the temperature can denature enzymes because of either:
1. Going beyond the optimum enzyme temperature (when enzymes are most
efficient)
2. Adding heat which raises the kinetic energy of the enzyme to the point that
bonds begin falling apart
• Cofactors ⇨ non-protein helper for enzymatic reactions
⇨ Inorganic minerals (zinc, iron, copper, etc.)
⇨ Organic coenzymes (vitamins, etc.)
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• Enzyme regulation ⇨ in addition to active site, enzymes also have allosteric sites
III. Cells, Membranes, and Transport
1. Surface Area to Volume Ratio
• The greater the SA:V ratio is ⇨ more efficient because more ‘stuff’ can pass through
• Smaller the cell ⇨ higher the SA:V ratio ⇨ better
2. Cell Organelles
• Eukaryotes can have ⇨ golgi apparatus, mitochondria, vacuole, chloroplast (plants only), cell
wall (plants, fungi, etc.), nucleus, ribosomes, endoplasmic reticulum, cytoplasm, cytoskeleton,
plasma membrane
• Prokaryotes can have ⇨ ribosomes, cytoplasm, nucleoid, plasma membrane, cell wall, capsule
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3. Organelle Interaction
• Let’s follow a protein pathway. For our purposes, the protein has already been synthesized.
The process of protein synthesis will be covered in VIII: Protein Synthesis
• Proteins are synthesized in ribosomes. Free ribosomes are found floating around in the
cytoplasm while bound ribosomes are stuck to the rough endoplasmic reticulum.
• Rough-ER bound ribosomes
⇨ Protein is synthesized in ribosome
⇨ Enters lumen (area within the entire ER)
⇨ Chaperonin (protein) folds new protein in secondary and tertiary structure
⇨ Protein travels to Smooth-ER (parts of ER without ribosomes)
⇨ Buds off in a transport vesicle towards the Golgi
⇨ Within the Golgi, travels in cis to trans direction
⇨ At cis end, enzymes will begin modifying protein by phosphorylation or glycosylation
⇨ Glycosylation adds/removes sugars. This decides where the protein will go
⇨ At trans end, the finished protein will exit the Golgi in secretory vesicles
⇨ If the vesicles fuse with lysosomes, the proteins will be for digestion of stuff
Protein examples: Nuclease, lipase, protease, etc.
Stuff examples: Food, antigens, screwed up organelles, etc.
⇨ These vesicles can also carry the proteins out or to other organelles
⇨ The proteins will leave the cell and enter the bloodstream via exocytosis
⇨ Examples of RER proteins include: hormones (insulin) and digestive enzymes (lipase)
• Free ribosomes
⇨ Protein is synthesized in ribosome
⇨ Receive little amount of modification (compared to RER proteins)
⇨ Still fold into tertiary structure by chaperonin in the cytosol
⇨ Cytosol: glycolytic enzymes, Actin for microfilaments (in cytoskeleton, muscles, etc.)
⇨ Nucleus: histones, transcription factors, etc. very important!
⇨ Mitochondria and Chloroplast
These organelles actually have their own genome and protein factories
Still import most integral proteins (electron transport chain, etc.) from cytosol
⇨ Always inside the cell it was produced in!
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4. Prokaryotic vs. Eukaryotic Cells
• Prokaryotes ⇨ include domains Archaea and Bacteria (E. coli, mold, etc.)
• Eukaryotes ⇨ include domain Eukarya (echinoderms, chordates, plants, etc.)
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• Peripheral proteins ⇨ located on the hydrophilic surface of membrane, responsible for
regulating cell signaling, interaction, and other events
• Integral proteins ⇨ embedded within membrane, serve as pumps, channels, and electron
transport chains
• Cholesterol ⇨ located within the hydrophobic regions, maintains membrane stability when
warm, maintains fluidity when cool
• Glycolipids ⇨ carbohydrate (glyco-) bound directly to membrane (lipid), provides energy,
cellular recognition,
• Glycoproteins ⇨ carbohydrate (glyco-) bound to a membrane protein (usually peripheral), cell
signaling, determine blood type, recognition of self vs. nonself
Glycolipids + Glycoproteins = Glycocalyx
⇨ Immune system can recognize and attack foreign (nonself) organisms
⇨ Immune system can recognize and attack cancerous cells
⇨ Transplant issues
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8. Types of Passive Transport
• Concentration Gradient ⇨ substances, molecules, ions, etc. will naturally travel from high
concentrations to low concentrations
• Diffusion ⇨ simply going down the concentration gradient
• Osmosis ⇨ the diffusion of water down its concentration gradient (from high water potential to
low water potential)
• Facilitated Diffusion ⇨ still going down the concentration gradient, but traveling through an
integral protein channel (ex. ‘leak’ channels for K+ ions)
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IV. DNA Replication and Cell Cycle
1. Scientists and DNA
• Griffith Experiment
1. Live smooth bacteria + mouse ⇨ mouse dead
2. Live rough bacteria (no protective coat) + mouse ⇨ mouse alive
3. Heat killed smooth bacteria + mouse ⇨ mouse alive
4. Heat killed smooth bacteria + live rough bacteria + mouse ⇨ mouse dead
⇨ Genetic material for coat passed between bacteria ⇨ transformation
• Avery Experiment: what is the genetic material?
⇨ Same bacteria as Griffith experiment
⇨ Isolate potential genetic materials (DNA, RNA, and proteins)
⇨ Turns out to be DNA!
• Hershey and Chase: what is the genetic material?
⇨ Bacteriophage: virus which injects its own genetic material into bacteria
⇨ Protein labeled with radioactive sulfur
⇨ DNA labeled with radioactive phosphorus
⇨ Process: infection (phage attaches) ⇨ blending (break phage off) ⇨ centrifuge
⇨ Results: proteins stays in phage, DNA enters the bacteria!
• Chargaff’s Rules: what is the ratio between nucleotide bases?
⇨ Ratio of T
A = C = 1
G
• Watson and Crick: what is DNA’s structure?
⇨ Rosalind Franklin: x-ray crystallography (picture of double helix)
⇨ 1953: W&C publish article in Nature magazine
⇨ Double helix model
2. Nucleotides
• Nucleotide ⇨ phosphate + sugar + nitrogen base
• Phosphate creates negatively charged ‘phosphate backbone’
• Purines ⇨ double ringed bases, adenine and guanine “AG is pur 2”
• Pyrimidines ⇨ single ringed bases, cytosine and thymine
• Hydrogen bonds (the ‘ladder rungs’) formed between 1 pyrimidine and 1 purine (bases)
• Phosphodiester bonds ⇨ (covalent) connect nucleotides
• A&T ⇨ 2 hydrogen bonds
• C&G ⇨ 3 hydrogen bonds (C ⇨ 3rd letter of the alphabet)
• Nitrogen bases are hexagonal. Sugars are pentagonal.
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• RNA is older than DNA (think RNA world thing)
• RNA is multipurpose (mRNA sends messages, rRNA composes ribosomes, tRNA carries
proteins, ribozymes catalyze reactions)
3. DNA Structure
• OH ⇨ 3’ end
• Phosphate backbone is negatively charged
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Prokaryotes Eukaryotes
5. DNA Replication
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6. DNA Replication and Repair
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7. Mitosis
• Let’s keep a chromosome count!
1. G1 phase ⇨ somatic cell has 46 chromosomes in 23 pairs of 2
2. S phase ⇨ 46 chromosomes with 92 sister chromatids
3. Anaphase/Telophase ⇨ 2 new sets, each has 46 chromatids/chromosomes
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• This is what happens during S phase to duplicate the chromosomes:
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cell division, oncogenes (mutated) are the equivalent of a “stuck accelerator”
V. Ecology
1. Ecological Levels
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3. Survivorship Curves
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4. Logistic and Exponential Growth Graphs
• Density-dependent factors ⇨ factors that increase as density increases
ex. Competition for food, predation, waste buildup, disease
• Density-independent factors ⇨ factors whose occurrence is unrelated to density
ex. Floods, forest fire, hurricane
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5. Relationships
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6. Behavior
• Operant Conditioning ⇨ behavior depends on consequences (reward/punish)
ex. Don’t get straight A’s. Asian parents yell at you.
• Classical Conditioning ⇨ associate two things together
ex. Pavlov’s Dogs (ring bell ⇨ dog salivates)
• Fixed Action Pattern/ Sign Stimulus ⇨ organism has to follow through with response
⇨ Receive stimulus or signal (ex. Goose sees egg-shaped ball outside nest)
⇨ Action or response (ex. Goose retrieves ball and places it into the nest)
⇨ Once started, this behavior cannot stop
• Imprinting ⇨ parents pass on characteristics or behavior to offspring
⇨ Can only occur within a short critical period
• Taxis ⇨ directional movement
⇨ Move towards a positive stimulus
⇨ Move away from a negative stimulus
• Kinesis ⇨ non-directional movement
⇨ Move in random direction
⇨ Movement slows down or stops once in the presence of a positive stimulus
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7. Biogeochemical Cycles
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VI. Plants and Photosynthesis
1. Photosynthetic Pigments
• Each pigment has its own absorption spectrum
• Having a greater variety of pigments (and wider absorption spectrum) allows plant to harvest
more energy
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2. Light Dependent Reactions
• Stroma ⇨ the ‘cytoplasm’ of a chloroplast (fluid)
• Thylakoid ⇨ one of the poker chip things
• Thylakoid space ⇨ space inside a poker chip
• Granum ⇨ a stack of poker chips
• Photosystem ⇨ integral protein complex, conducts both light
harvesting, light reaction, and electron transfer, located in the
thylakoid membrane
• Photosystem II ⇨ discovered second, but starts first
⇨ Wavelength p680
⇨ Water is split ⇨ donates electrons(2) to PSII, protons for gradient, oxygen released
⇨ Released energy (electrons) travel down electron transport chain
⇨ Primary electron acceptor is plastoquinone
⇨ Cytochrome complex pumps H+ ions from stroma (out) to thylakoid space (in)
⇨ Creates chemiosmotic (H+) gradient ⇨ H+ have to leave through ATP synthase
⇨ Photophosphorylation adds phosphate to ADP to make ATP
• Photosystem I ⇨ discovered first, starts second
⇨ Wavelength p700
⇨ Receives electrons from PSII
⇨ Released energy (electrons) travel down another electron transport chain
⇨ Primary electron acceptor is ferredoxin
⇨ Enzyme NADP+ reductase combines NADP+ and H+ to make NADPH
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3. Electron Flow Comparisons
• In non-cyclic / linear electron flow ⇨ goal is making NADPH with some ATP along the way
⇨ Process is described in detail above
⇨ Reactants: light, water
⇨ Products: ATP, NADPH, O2 (waste product from splitting water)
• In cyclic electron flow ⇨ goal is making ATP
⇨ Only uses Photosystem I
⇨ Recycles electrons
⇨ Cytochrome complex, chemiosmosis, and phosphorylation work same way as above
5. Paper Chromatography
• You have a pigment and a solvent
• Pigments that are soluble in the solvent will travel farther up the paper strip
• Pigments that have lower molecular mass will also travel farther up the paper strip
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6. Calvin Cycle (Light Independent Reactions)
• What was the purpose of the light reactions?
⇨ Make a little bit of ATP
⇨ Make NADPH (energy ‘truck’) for the Calvin cycle
• The Calvin cycle does not require light to occur
• The Calvin cycle takes place within the stroma of the chloroplast
• Carbon dioxide first enters the plant by diffusing through the stomata
• 3 carbon dioxides (1C) are ‘fixed’ to 3 RuBP molecules (5C)
• This is catalyzed by the enzyme rubisco and creates a 6 carbon compound, which quickly
breaks into two 3-phosphoglycerate (3C)
• Next, ATP and NADPH allow for reduction to G3P (3C), which is a sugar
• Once you collect 2 G3P molecules, you can form glucose and other sugars
• More ATP is used to regenerate the RuBP to accommodate more carbon dioxides
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• Now that we understand what’s going on, let’s take a look at the math:
3 Carbon Dioxide + 9 ATP + 6 NADPH ⇨ 1 G3P + 9 ADP + 6 NADP+
Note: Double all coefficients if you want to produce a glucose molecule
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7. C3 Plants in Hot and Dry Weather
• C3 ⇨ 3 carbons, carbon dioxide creates a 3 carbon molecule (3-phosphoglycerate)
• C3 plants like warm moist climates. Hot and dry weather is bad.
• It’s hot and dry ⇨ the plant wants to save water!
• Where does the water evaporate from? ⇨ Stomata (openings in the leaves)
• So, C3 plants respond to hot and dry weather by closing the stomata
• Unfortunately, this also traps O2 in (waste from LR) and CO2 out (what plants like)
• Remember rubisco, the enzyme from before? It can also bind to O2.
• Now, the plant goes through the process of photorespiration in order to get rid of the O2
• Photorespiration uses up the carbon stores of the plant, wastes energy, and doesn’t do
anything
• This is bad. That’s why plants in hot and dry climates have evolved ways to cope (they join
support groups)
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8. C4 Plants in Hot and Dry Weather
• C4 plants have evolved to spend a bit more energy to limit water loss in arid conditions
• C4 ⇨ 4 carbon compound
• There is spatial separation between mesophyll and bundle sheath cells
• Rubisco is replaced by PEP Carboxylase (only binds to carbon dioxide, not oxygen)
• 3-phosphoglycerate is replaced by Oxaloacetate (are 4 carbon compound)
• This is then stored as malate / malic acid
• Now we move from the mesophyll to the bundle and sheath cells for the Calvin cycle
• Pyruvate is recycled while CO2 can now go into the normal Calvin cycle
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9. CAM Plants in Hot and Dry Weather
• CAM plants have temporal separation ⇨ time (night and day)
• Same thing as C4 plants with oxaloacetate and everything, but instead of separating by cell,
CAM plants separate by time
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11. Adhesion-Cohesion-Transpiration Mechanism
• Water Potential = Solute Potential +
Pressure Potential
• Pressure potential ⇨ pressure exerted by
the cell wall against its contents
• Solute potential ⇨ more solute means a
lower solute potential
• More solute added ⇨ solute potential
becomes more negative ⇨ water potential
also becomes more negative
• Water moves from high water potential ⇨
low water potential
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A Comprehensive Guide to AP Biology (cont’d)
by Brian Lin
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Anaerobic: don’t need oxygen present to occur
Takes place in the cytoplasm
Since we’re going from big molecule (glucose) to small molecule (pyruvate), this is a
catabolic reaction.
Show me the math:
x1 Glucose (6C) ⇨ x2 Pyruvate (3C)
x2 ATP ⇨ x4 ATP (+2 ATP Net)
x2 NAD+ ⇨ x2 NADH
Phosphofructokinase (enzyme): lots of ATP ⇨ ATP binds allosterically to phosphofructokinase
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⇨ shuts phosphofructokinase down (feedback inhibition of an enzyme)
No oxygen? Diagram below. Yes oxygen? Next page.
What’s the point of anaerobic fermentation?
It empties the energy trucks (2 NADH ⇨ 2 NAD+) while creating a little bit of energy (ATP)
(Note: You CANNOT do glycolysis without the empty energy trucks)
This is OKAY for yeast and other little organisms who can live off the +2 ATP. However, big
things have to use aerobic respiration to get enough energy out of glucose +26-28 ATP.
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Okay, so we got some pyruvate. That still has lots of energy inside.
But first, we need some more energy trucks (NADH and FADH2)
The Krebs will do that, but we need to make pyruvate ready for Krebs.
That’s the Bridge Reaction.
Bridge Math
Pyruvate (3C) + Coenzyme A ⇨
Acetyl CoA (2C) + CO2 (1C)
NAD+ ⇨ NADH
*Multiply by 2 for both pyruvate molecules
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Citric Acid/Krebs occurs in the mitochondrial matrix (random space inside cistae)
Goal: Create tons of energy trucks (NADH + FADH2)
Krebs Math
Acetyl CoA (2C) ⇨ x2 CO2 (1C)
x3 NAD+ ⇨ x3 NADH
FAD ⇨ FADH2
6
Aerobic: need oxygen or won’t happen
We’re going through a series of redox reactions in which we are oxidizing and reducing
molecules, ending with oxygen, the final electron acceptor.
Note: Lose electron oxidize
Gain electron reduce
“LEO says GER”
1. NADH and FADH2 arrive at the mitochondrial membrane (top row of circles is the outer
bottom is the inner)
2. NADH arrives higher up in the electron transport chain. Therefore, it can pump more H+
across the membrane, effectively synthesizing 3 ATP.
3 FADH2 arrives lower down the electron transport chain. Therefore, it can pump ⅓ less H+
across the membrane, effectively synthesizing 2 ATP.
4. Pumping H+ across the membrane creates a chemiosmotic gradient. Because charged
ions cannot simply diffuse across the membrane, they must diffuse across ATP synthase
(integral protein) via facilitated diffusion.
5. This drives the reaction ADP + P ⇨ ATP
The electron transport chain creates a lot of ATP. Around 26-28 molecules of ATP.
If you don’t like my crummy drawing, go to the next page for a diagram.
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AMP (a cell resp. reactant) stimulates glycolysis
ATP/Citrate (cell resp. products) inhibit glycolysis
Next page has some general overviews of where all the
products and reactants come from and go to.
8
9
VIII. Protein Synthesis
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1. Central Dogma
DNA ⇨ (transcription) ⇨ RNA ⇨ (translation) ⇨ Protein ⇨ (processing)
DNA strand is always read in the 3’ to 5’ direction.
Thus, RNA polymerase builds mRNA in the 5’ to 3’ direction.
AUG is the start codon (methionine)
Codon: a 3 nucleotide sequence (note: Uracil replaces Thymine in RNA sequences)
Bottom strand of DNA is called the template strand
Top strand of DNA is called the coding strand
mRNA: messenger RNA that leaves the nucleus for a ribosome in order to code for a
polypeptide
tRNA: transport RNA that carries amino acids from cytoplasm to ribosome, has complimentary
anti-codon to the mRNA
rRNA: ribosomal RNA that makes up the ribosome’s subunits
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2. Why is Redundancy Important in
Codons?
As you can see in the diagram, there are usually 4 different
codon sequences that can code for the exact same thing.
This means that a point mutation (substitution) from ACU to
ACC won’t screw you up. This is known as a silent mutation
because you don’t notice any change.
That variation in the 3rd base pair is known as wobble.
Of course, some codons such as AUG (start) do not exhibit
any redundancy and this can be problematic.
3. Transcription
Once again, transcription involves us copying DNA to mRNA within the nucleus.
There are 3 main steps to transcription:
1. Initiation
Before DNA can be copied, the copier, RNA Polymerase must bind to the DNA strand at the
promoter region (specifically at the TATA box).
In order for RNA Polymerase to bind, you need a bunch of transcription factors. This provides an
effective means for gene regulation (please see X. Gene Regulation for further detail)
2. Elongation
DNA is unwound by transcription factors. RNA Polymerase then transcribes a single strand of
mRNA complementary to the template DNA strand.
3. Termination
RNA Polymerase and completed mRNA disconnect from the DNA strand upon reaching the
termination sequence.
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Ok, so at this point, we got a complete mRNA strand. However, we only want the parts of it that
are important- the coding regions (known as exons). The non-coding regions are introns.
So, how are we going to cut the introns out? mRNA editing
Spliceosome (a complex of SNRPs) cuts introns out
A poly-Adenine tail is added (to 3’ end)
A 5’ methylated cap is added
4. Translation
1. Initiation
Assemble ribosomal subunits out of rRNA
AUG is the start codon
2 subunits: large on top, small on bottom
5’ end enters first
2. Elongation
Amino acids added to tRNA by Aminoacyl-tRNA synthetase (an enzyme)
Amino acid chain assembled out of the P-site
New amino acids carried by tRNA join to the complementary codon on the A-site
tRNA and mRNA exits via the E-site
3. Termination
Stop codons (UGA, UAA, UAG) signal the ribosomal subunits to break apart, releasing the
completed polypeptide (string of amino acids)
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5. Post-Translational Protein Editing
• Rough-ER bound ribosomes
⇨ Protein is synthesized in ribosome
⇨ Enters lumen (area within the entire ER)
⇨ Chaperonin (protein) folds new protein in secondary and tertiary structure
⇨ Protein travels to Smooth-ER (parts of ER without ribosomes)
⇨ Buds off in a transport vesicle towards the Golgi
⇨ Within the Golgi, travels in cis to trans direction
⇨ At cis end, enzymes will begin modifying protein by phosphorylation or glycosylation
⇨ Glycosylation adds/removes sugars. This decides where the protein will go
⇨ At trans end, the finished protein will exit the Golgi in secretory vesicles
⇨ If the vesicles fuse with lysosomes, the proteins will be for digestion of stuff
Protein examples: Nuclease, lipase, protease, etc.
Stuff examples: Food, antigens, screwed up organelles, etc.
⇨ These vesicles can also carry the proteins out or to other organelles
⇨ The proteins will leave the cell and enter the bloodstream via exocytosis
⇨ Examples of RER proteins include: hormones (insulin) and digestive enzymes (lipase)
• Free ribosomes
⇨ Protein is synthesized in ribosome
⇨ Receive little amount of modification (compared to RER proteins)
⇨ Still fold into tertiary structure by chaperonin in the cytosol
⇨ Cytosol: glycolytic enzymes, Actin for microfilaments (in cytoskeleton, muscles, etc.)
⇨ Nucleus: histones, transcription factors, etc. very important!
⇨ Mitochondria and Chloroplast
These organelles actually have their own genome and protein factories
Still import most integral proteins (electron transport chain, etc.) from cytosol
⇨ Always inside the cell it was produced in!
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6. Mutations
Mutation: a change in DNA during DNA replication, allows for methods of evolution
Evolution: a change in allele/gene frequency
Mutations arise from 1. DNA replication copying errors or 2. External factors (ie mutagens)
There are 2 categories of mutations, point mutations and chromosomal mutations
Point: (1 base pair)
Substitution
Silent (Redundancy)
Missense (Wrong amino acid)
Nonsense (Stop codon)
Insertion or Deletion
Adding in/ removing amino acids
Can lead to a frameshift
Chromosomal: (change in entire chromosome)
This can be a change in structure (losing part of it) or number (monosomy, etc.)
7. Universal Genome
All domains of life share central genetic code (DNA).
All domains of life share similar metabolic pathways.
Just read Big Idea #1.
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● Creates all of your non-sex body cells ● Creates gametes for sexual
(for example, new skin cells) reproduction
● Genetically identical offspring ● Allows for genetic variation
(basically clones) ● (In humans) chromosome number is
● Note: Due to random mutation, there halved from diploid to haploid
may still be very slight genetic
variation
● Chromosome number remains
constant
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Mendel’s Laws
● Law of Segregation ⇒ Each gamete (sex cell) carries one allele (version of a gene).
Each offspring then gets 1 allele from each parent for a total of 2 alleles (such as
dominant brown hair from dad and recessive blonde hair from mom).
● Law of Independent Assortment ⇒ Separate traits are inherited independently from
each other. For example, your height and your eye color are coded for by different genes.
● Law of Dominance ⇒ A dominant allele will take priority/override a recessive allele.
You should also know how to do Punnett Squares and Family Trees/Pedigrees/etc.
This is some pretty basic stuff really. So pay attention in class and practice as much as you
can. There aren’t any ‘tricks’ really, so I’ll leave you on your own here.
Basically, I didn’t take notes for this part of the unit. And I’m not about to do so now, in
August, when I have much better things to do. So once again, you’re on your own for this.
Seriously, it’s not hard. Just pay attention in class and do your work.
Okay fine. Even though I still refuse to put more effort into this, I happen to still have some
examples that I can share with you. Also, some very important terms to know and definitely
not to confuse (such as incomplete dominance and co-dominance).
Here’s the quiz (on dominance, I believe). Not only is it embarrassing but very silly and
immature as well. Have fun. Don’t say I didn’t warn you. And no, there are no answers. That’s
because you must take pride in your learning (ie I lost the answer key or there never was one).
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their parents, Sally and Bob.
4. Fill in the blanks!
H = dominant
h = recessive
5. The ultimate question: The members of the Chen family are affected by both hair color and
Hokey-Pokey disease (dominant). The father, Phat Dadda “Pkash” Money (the original Bile-o-G
gangsta), has fluorescent purple hair (dominant) but does not express any alleles for
Hokey-Pokey disease. The mother, Val Mart-Agupta, has normal brown hair (recessive) but has
the dominant allele for Hokey-Pokey disease. What is the probability that their new child, Alfred
the Undulator, will have both purple hair and hokey-pokey disease?
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X. Gene Expression
Once again, written by Chris Yao, edited by me.
In Vivo Cloning
● In vivo (use dat spanish) = cloning within a living organism (in our case, using a bacteria
as a ‘factory’ of sorts to produce specific proteins!)
○ Compare to In Vitro, which is cloning within a glass test tube (the Polymerase
Chain Reaction stuff you learned about)
● Class example = AMP experiment
● Isolate mRNA for desired gene... since it’s mRNA, there are no exons.
● Use reverse transcriptase to create cDNA from the mRNA template.
● Use a restriction enzyme to cut the plasmid once and the ends of the gene of interest
twice.
● Combine plasmid and gene of interest. They will be attracted to each other since the
sticky ends (cut by the restriction enzyme) will be complementary.
● Ligase will seal with covalent bonds (phosphodiester).
● Now that our gene has been successfully introduced into the bacteria’s plasmid (a
chromosome), the bacteria will start producing whatever we wanted it to!
Microarrays
● Using reverse transcriptase and DNA polymerase cDNA is synthesized from a RNA
template (typically mRNA from the cells of interest), binds with certain ssRNA in the
microarray, the ones that bind glow under the fluorescence detector, indicating that these
are the genes expressed.
Operons
● Promoter is like a door knob, promoters of many operons are similar, like a keyhole
because only a specific regulatory protein binds it.
● Co-repressor ⇒ binds to repressor to help prevent transcription of the gene
● Repressor ⇒ prevents transcription of the gene by blocking the attachment of RNA
polymerase
● Activator ⇒ protein that increases gene transcription
Types of Regulation
Please just use your class notes (ppt. slides) + diagrams for this... SO MUCH easier.
Inducible (lactose)
● The system begins as off. However, it can be induced (aka turned on).
● Repressor starts off attached to the operator (that’s why it’s off).
● Under certain conditions, the repressor will be removed, turning the system on.
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Repressible (tryptophan)
● The system begins on. However, it can be repressed (turned off).
● When the levels of the expressed gene exceed the needs of the cell, the repressor
activates and inhibits expression.
● When trp levels are high enough (and you therefore need to get rid of it), activators bind
to the repressor to get it off.
Positive
● cAMP accumulates when glucose is scarse used to activate CAP
● CAP is a regulatory protein ⇒ activator
● when cAMP is low cap stops activating
Methylation
● Addition of methyl caps to histones prevent expression
Histone Acetylation
● Add more space, make expression more likely to happen
RNAi
● siRNA- Small interfering RNA that degrade a specific mRNA upon recognition (RISC )
● siRNA made from dsRNA using a dicer, which dices the dsRNA into siRNA
● RNAi can abolish gene function of specific genes, because they are created in vitro
(shRNA/siRNA), RNAi allows us to control timing
● Applications include gene therapy,
● Problems include stability, delivery, toxicity, off target
● miRNA is like siRNA but longer, made using dicers and takes out homologous mRNA
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causing vasodilation
○ Vasodilation⇒blood vessels and capillaries increase in diameter allowing
phagocytes easier access to the infected cells, this causes swelling and redness
○ Phagocytes⇒Neutrophils, eosinophils and Macrophages all are phagocytes that
eat infected cells
○ Cytokines ⇒ chemicals released by cells for cell to cell communication, ie) Helper
T Cells release Cytokines to activate B cells.
○ Pyrogens ⇒ chemicals released by phagocytes that cause fevers in an attempt to
denature invaders through heat
○ Interferons ⇒ infected cells also release interferons which are the cytokines that
Third Level of Defense⇨ specific immune response
○ Macrophages, after eating infected cells, uses MHC to present antigen fragments
on their surface
○ Helper t-cells become activated if they recognize the antigen fragments
○ Helper t-cells activate the killer T cells (AKA Cytotoxic T Cells) and B cells
● Humoral Response
○ Plasma B cells (activated B cells) produce antibodies which bind onto their
respective antigen (specific)
○ Antibodies are Y shaped proteins that bind onto an antigen, they then either mark
the antigen for destruction (via killer t-cells for example) or they can block the
pathogen from further spreading.
● Cell Mediated Response
○ Cytotoxic t cells
○ Helper t cell binds to macrophages presenting a virus on its mhc
○ Activates cytotoxic t cell for that specific infection, finds all cells with that infection
and kills them using perforin
● Humoral vs Cell Mediated- What’s the Difference?
○ Cell mediated is a direct attack versus humoral which marks for an attack later
○ both produce memory cells which remain for second incidence
○ part of acquired immunity
Passive Immunity
■ Natural: Transfer of antibodies from mom to child during pregnancy
■ Artificial: Addition of antibodies through some other means to an individual
who cannot create the necessary antibodies
Active Immunity
■ Natural: Exposure to a pathogen and going through b cells/t cells
■ Artificial: Being ‘infected’ through a vaccine which stimulates the body to
create the necessary antibodies/memory cells for future attacks
The thing you just read (passive/active) confuses a lot of people. Let me (Brian) elaborate a little.
Passive immunity means that you get antibodies.
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Active immunity means that you make antibodies.
Here’s an analogy: Passive immunity is like getting $100 for your birthday as a gift whereas
active immunity would be like getting a job so that you can continually make money.
Natural means that no voodoo science stuff is going on. Artificial means that we ‘use science’
(whatever that means) to create the immunity (such as getting a shot).
HIV
● Destroys the body’s ability to fight disease by disabling helper t cells.
Blood Type
● People can only take in specific blood types that match with their own
● Each blood type has a specific antigen on their surface and antibodies around them.
○ ex. Type A blood is marked with ‘a’ antigens but has antibodies that destroy stuff
marked with ‘b’.
● AB is a universal receptor, O is a universal donor.
○ If you have both A and B blood, then you’ll recognize everything. If you have type
O, you can only recognize type O blood.
Allergies
● Body detects non-self (such as some pollen) and releases histamine to fight something
that’s not even dangerous.
○ This causes inflammation and all the other typical allergy symptoms.
Organ Transplantation
● Organs need to be accepted by the host, otherwise they will be destroyed as non-self.
● Body uses the MHC to identify self vs non-self.
Autoimmune Disorders
● Body somehow confuses self with non-self and begins destroying self cells.
XII. Cellular Signaling
Content courtesy of Pulkit. However, I could tell that he copied it from somewhere else because
the formatting was absolutely atrocious. In order to attest to this, I’m leaving it as is so you all can
suffer unnecessarily. Hahaha. But seriously, I’m not about to spend an hour fixing this mess so
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pay attention in class and make your own notes lol. I tried fixing this page (added the bullet
points, the original picture was absolute crap since you couldn’t read any words, but then I
realized that this stuff is basically worse than the textbook so I’m reaching out to you guys for
help here).
● Long Distance Neurons = Electrical signals (chem for short paths), used for regulation
and information
● Dendrites- branched extensions that receive signals
● Axon- extension that transmits signals to other cells (information);; branched at one end,
hillock at other
● Cell Body- where neurons organelles are located
● Axon Hillock- signals that are transferred down the Axon generated here
● Synaptic Terminals- Branched ends of the axon, neurotransmitters transmit information
from the axon to the receiving cell from here;; the cell sending the signal is presynaptic,
postsynaptic is the cell that receives. Dendrite conc.= synapse conc. Electrical
synapses are rare but serve for really fast reactions. Usually chemical reactions.
Presynaptic neuron packages and transports its neurotransmitters in synaptic vesicles
towards the terminals of the recipient neuron. This change in action potential causes the
neurons membrane to become permeable because it depolarizes which in turn means
Ca+2 concentration goes up and then that causes some vesicles to fuse and dump their
contents in the receiving neuron
Myelinated neuron- sheets that surround axons (produced by oligodendrocytes) -> electrical
insulation, space eficient
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Unmyelinated neuron- slower, travels in waves
Sensory Neurons- transmit information from eyes and other sensors that detect external
stimulation (light, sound, touch, heat, smell, taste)
Motor output- necessitates nerves (bundles of neurons) to make muscles function properly
CNS- brain and longitudinal nerve cord, integration up here (analyzing and interpreting the
sensory information)
Peripheral- send and take out information from the CNS
Brian edit: What is going on here?
Neurotransmitters have more than a dozen diff. receptors
Sodium-Potassium pumps are used for the maintenance of resting potential. They send out NA+
and bring in K+. Clusters of proteins make ion channels. These ion channels are selectively
permeable to NA+ or K+ depending on the channel. K+ is taken out , leaving a negative charge
behind, and NA+ comes in, the movement of these charges causes the generation of potential.
The buildup of negative charge behind the movement of K helps create the membrane potential
Eion = 62 mV ( log ([ion outside]/ [ion inside] ))
Gated Ion channels open or close in response to stimuli when neurons are active. This in turn
means that membrane potential changes (and permeability changes). Ex. Resting neurons k+
ion channels open up again, making it more negative, polarity goes up (hyperpolarization->
increases the outflow of positive or in flow of negative ions, either way end result is a negative
inside). Depolarization- reduction of membrane potential by opening gated sodium channels,
these are graded potentials a bigger stimuli = bigger change. These have a major effect on the
generation of nerve signals. Voltage gated ion channels open or close to a change in the
membrane potential. If depolarization opens voltage-gated sodium channels, then the resulting
flow of Na+ causes more depolarization which opens more gates which in turn opens more
gates and all of this changes the membrane potential , called an action potential. Action
potentials are transmitted along the axon, occur whenever membrane voltage gets to the
threshold, act independently of stimuli and are an all-or nothing (happen or do not happen).
During this period, the sodium channels close up till after the undershoot. Therefore if a stimuli
occurs during the undershoot period no action potential will occur, this is called the refractory
period. When an action potential is generated, it can only move towards the synaptic terminals
because the area behind the generation point (the hillock) prevents another potential from being
formed. Action potentials go as far as the synpases which allow the current to flow from one
neuron to another
Synaptic Terminals- Branched ends of the axon, neurotransmitters transmit information from the
axon to the receiving cell from here;; the cell sending the signal is presynaptic, post synaptic is
the cell that receives. Dendrite conc.= synapse conc. Electrical synapses are rare but serve for
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really fast reactions. Usually chemical reactions. Presynaptic neuron packages and transports
its neurotransmitters in synaptic vesicles towards the terminals of the recipient neuron. This
change in action potential causes the neurons membrance to become permeable because it
depolarizes which in turn means Ca+2 concentration goes up and then that causes some
vesicles to fuse and dump their contents in the receiving neuron
Ligand gated ion channels are clustered in the membrane of the post synaptic cell, binding of the
neurotransmitter to a particular part allows specific ions to diffuse across the membrane.
Post Synapatic Potentials- vary depending on the concentration of neurotransmitter sent, the
potential degenerates as it gets farther from the synapse. ESPS is too small to effectively
generate a reaction
Temporal summation- two ESPS occur at once almost (one happens and then another
happens before first done) – same synapse
Spatial summation- different synapses- but made simultaneously
Excitatory - bringing membrane potential closer to threshold (cap)
Inhibitory- taking away from threshold (cap);;
It’s almost like a cycle. One neuron sends a signal via neurotransmitters to another neuron. The
connection of neutransmitters to the post synaptic cell’s membrane causes channels to open
that depolarize the cell, this depolarization causes excitatory postsynaptic potential which brings
the cells potential up to the threshold. When this happens to twice in one synapse, its called
temporal separation and can cause an action potential to be generated. When this happens with
two different synpases at the same time, an action potential is generated. The generation of an
action potential then gets the axon hillock to transmit it down the axon to the synpases which in
turn starts the cycle all
over again with another cell, ISPS (hyper polarization) can lower the threshold and balance out
with the ESPS.
REFLEX ARC
Reflexes- the body’s automatic response to certain stimuli, produced by spinal cord
Ex: touching a hot stove, knee buckling, hitting knee w/ hammer
How knee-jerk reflex response works:
1) Muscle is tapped
2) Sensory Neurons detect a sudden stretch in quadriceps muscle
3) Information is conveyed by these sensory neurons back to the spinal cord (white matter)
4) Motor neurons, thanks to this information, signal the quadriceps to contract
5) In the meanwhile, sensory neurons are also communicating with inter neurons to prevent
inhibition of the reflex
Spinal Cord runs to and fro the brain, therefore it generates basic patterns of
locomotion/movement
CNS/PNS
Describe how the nervous system components work together to maintain homeostasis.
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Define the functions of the CNS and PNS (include the following: brain, spinal cord,
autonomic nervous system, somatic nervous system, interneurons, sensory
neurons).
Brain- contains white matter on the inside, used predominantly for signaling, sensory
information processing, feeling emotions, generating commands, and gray matter
consists mainly of neuron cell bodies, dendrites, and unmyelinated axons. Integrates
sensory neuron information;;
Spinal Cord- white matter on the outside, used for transmitting information from CNS to
sensory/motor neurons of the PNS;; generates basic patterns of locomotion (reflexes too)
Astrocytes- Provide structural support for neurons and regulate the extracellular
concentrations and neurotransmitters. Astrocytes cause blood vessels to dilate which
increases the flow of oxygen to neurons, they create the blood-brain barrier, radial gilia
help move the new neurons from the neural tube
Cranial nerves- connect the brain with locations in organs of head/upper body, some are
afferent only i.e. the one for smell (Peripheral)
Spinal nerves- run between spinal cord and parts of the body below head (Peripheral)
Afferent- The Sensory neurons that tell the CNS whats going on, Efferent = the neurons
that tell the muscles what to do (motor)
Motor System (Somatic) - consists of neurons that carry signals to skeletal muscles,
mainly in response to external stimuli, it is voluntary since we can consciously control it,
but there is also a major reflex aspect to it.
Autonomic nervous system- regulates internal environment by controlling smooth and
cardiac muscles ;; Controls the organs of the digestive, cardiovasulcar, excretory, and
endocrine systems;; involuntary control, three divisions- sympathetic, parasympathetic,
and enteric-
Sympathetic division—energy generation (“fight or flight” response- heart beats faster,
digestion is inhibited, liver converts glycogen to glucose, adrenaline.
parasympathetic division- calming, return to self- maintenance functions (rest and digest)
**need relation to homeostasis**
T6- Hypothalamus- endocrine gland in brain;; receives information from nerves throughout
the body and from other parts of the brain. It initiates endocrine signaling appropriate to
environmental conditions;;
Pituitary Gland- a gland located at base of hypothalamus, size and shape of lima bean,
two parts (posterior and anterior).
Posterior- Extension of hypothalamus that grows downward towards the
mouth, stores and secretes two hormones made by the hypothalamus;; releases oxytocin
and antidiuretic hormone;; hormones released travel along the axon’s of the
neurosecretory cells to the posterior pitiuary. Impulse stimulates a neurosecretory cell to
release neurohormone which diffuses into bloodstream. (nerve impulse from
hypothalamus making oxytocin get released).oxytocin- regulate milk release;;
Anterior- regulated by hormones secreted by the hypothalamus;; Anterior pituitary
hormones are all controlled by some hypothalamus hormonone which determines their
release (the hormones from the hypothalamus are released near the base by capillaries
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which in turn go into portal vessels which then go into another layer of capillaries by the
anterior pituitary.
Brian edit: WTF is with this picture? Why would you stretch it out to the point
where no one can read it?
.
T7-
Long distance regulators:
Animal hormones are cheimcal signals that are secreted into the circulatory system and
commnicate regulatory msgs within the body
hormons reach all parts of body, but only target cells have receptors of that hormo
What Is a hormone- secreted cells that serveto maintain homeostasis, mediate
responses to environmental stimuli, regulate growth, development, and reproduction.
Hormones coordinate the body’sr esponse t ostress, dehydration, low blood glucose;;
control appearances. COME FROM ENDOCRINE SYSTEM!!
Insulin- Hormone. Polypeptide. Cleavage of longer protein chain forms insulin;;
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Epinephrine & Thyroxine are amine hormones which come from an amino acid;;
Cortisol- lipids that contain four fused carbon rings
Polypeptide/Amine hormones are water soluble while Steroids are lipid soluble
(membranes are hydrophobic so they let the steroids diffuse through but don’t let the
polypeptides through)
Protein Hormones:
-Receptors on the outside, on the plasma membrane
- Secreted by exocytosis, bind to the receptor on the outside, and initiate a
change in gene transcription (serve as transcription factors for the mRNA, allow it to
translate
- signal transduction: converting the extra-cellular signal (the binding of the hormone to
the receptor) to a intracellular response (change in transcription etc.)
-second messenger: ex. cAMP, activates protein Kinase A which leads to activation of an
enzyme required for glycogen A breakdown and inhibits the synthesis of more glycogen
which in turn releases more glucose via the liver into the blood which helps you chase
the bus (example provided based on hormone epinephrine)
Hormone binds to G protein coupled receptorà releases G protein(uses GTP for
transport)-à gets to Adenylyl Cyclaseà bind and w/ help of ATP make cAMPà activates
protein kinase Aà (in the case of epinephrine) activates the inhibition of glycogen
synthesis & the promotion of glycogen breakdown
Steroid Hormones:
-Receptors are located within the cell
-bind to intracellular receptors, cause gene transcription changes, go through
the plasma membrane
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- hormone binds to receptor, this directly activates cell response (directly
regulate gene expression usually), bind to DNA (in nucleus) and transcribe certain parts
of mRna i.e. binding of estradiol leads to the transcription and translation of Vitellogenin
which goes to the reproductive system in birds for egg yolk production
NEED: SHORT DISTANCE (WATER SOLUBLE) + LONG DISTANCE (LIPID SOLUBLE)
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