AP Biology Notes

Unit 1: Chemistry of Life

Unit 2: Cell Structure and Function

Unit 3: Cellular Energetics

Unit 4: Cell Communication and Cell Cycle

Unit 5: Heredity

Unit 6: Gene Expression and Regulation

Unit 7: Natural Selection

Unit 8: Ecology

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Unit 4: Cell Communication and Cell Cycle

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CELL COMMUNICATION + APOPTOSIS

Cells communicate with each other via chemical signals

Intro to nervous and endocrine systems

Cell-to-cell communication is essential for all organisms

E.g. flight or fight response is triggered by a signaling molecule (epinephrine)

Signal Transduction Pathway: series of steps that take place when a signal binds to a cell (message delivered) and converts it into a specific cellular response

Ligand binds to receptor → induces series of reactions for cell response

Pathway similarities suggest that ancestral signaling molecules evolved in prokaryotes and were modified later in eukaryotes

Ligand - things that bind to receptors and trigger signal transduction pathways

Neurotransmitters: SYNAPTIC SIGNALING nervous system ligands, how nerves communicate with target cells thru a synapse, enter synapse through exocytosis, doesn’t travel a far distance in synaptic cleft (ergo local)

Bind to receptors like GPCR (epinephrine), RTK (growth factors), or ligand gated

Hormones: ONLY LONG DISTANCE, sent thru bloodstream

Growth Factors: most important ligand PARACRINE SIGNALING trigger cell division, cause growth and repair. Don’t travel a far distance. Fix damaged parts of the body. Large role if cancer occurs

Local Signaling: animal cells may communicate by direct contact, or cell-cell recognition, info not sent very far

Gap junctions: cells are tightly bound and act as one unit (heart pumping)

Plasmodesmata: rigid cell walls make diffusion difficult between plant cells, they have plasmodesmata tubes instead

Cell-to-Cell Recognition: can determine if self or nonself using glycoproteins

Synaptic signaling- use neurotransmitters for neurons to communicate to target cells

Paracrine signaling- use growth factors, can repair wounds

Affect nearby cells, do not enter bloodstream

Long-distance Signaling:

Released in the bloodstream by endocrine system (hormones)

Every cell in body is exposed to hormone, only cells with receptors respond to the hormone

Target cell is the cell being communicated wit

Growth hormone: grow a lot of cells, growth factors only affect nearby cells, hormones in the bloodstream

RECEPTION

Receptors: specific membrane proteins that receive the ligands and trigger transduction, ligands that bind to ion channel, GPCR, RTK has to be polar

(G protein-coupled receptors) GPCR Receptors: largest family of cell surface receptors, include epinephrine

G-protein normally an inactive protein but activated when ligand binds to it (epinephrine and using GTP), sent on a mission by receptor to trigger a cell response

(Receptor tyrosine kinases) RTK Receptors: Growth factors, any broken receptors associated with cancer

Responds to ligands like growth factors

Causes cell division

Malfunctioning RTKs causes cancer

Phosphorylates relay proteins

Ligand-gated ion channel: acts as a gate when the receptor changes shape, e.g. neurotransmitters

In nervous system: e.g. sodium & calcium channels

Have a gate, and the only way to open it is to have a ligand bind to it, K+, Ca+ or Na+ can enter/leave the cell

Intracellular receptors: proteins found in the cytosol or nucleus of target cells, receives NONPOLAR hormones

Small or hydrophobic chemical messengers can readily cross the membrane and activate receptors

E.g. testosterone, or estrogen (steroids)

Binds to protein in nuclear envelope and initiates transcription

Activated hormone-receptor complex can act as a transcription factor, turning on specific genes

TRANSDUCTION

Protein Kinase: 2nd messengers perform transduction where message is relayed throughout the cell. Proteins that are specialized activated thru phosphorylation “Passing the baton” (relay message), causes a chain

Phosphorylation Cascade: series of activated protein kinases that receive and transport the relay molecule (using ATP) often involving 2nd messengers

Message relayed throughout the cell, prompting a cell response

Using a series of protein kinases using phosphorylation

Responsible for passing the message through the cell using a phosphorylation cascade , passing the relay message as a baton

Second Messenger: anything not a protein kinase that performs transduction/relay the message; water-soluble molecules or ions that spread throughout a cell by diffusion. Participate in pathways initiated by GPCR and RTK.

Cyclic AMP (cAMP)

Most common 2nd messenger

Created using Adenylyl cyclase by taking ATP and cutting off two phosphates (becomes adenosine monophosphate)

E.g. epinephrine binds to GPCR and G protein phosphorylates adenylyl cyclase and makes cAMP and cAMP activates a protein kinase

Ca+++ (calcium ions)

Cell can tightly regulate Ca concentration (active transport) in ER and mitochondria

Can activate IP3 or DAG

IP3

Diacylglycerol (DAG)

RESPONSE

Cell Response: depends on the pathway within the cell leads to regulation of transcription or cytoplasmic activities or “output response”

Many signaling pathways regulate the synthesis of enzymes or other proteins usually by turning genes on or off in the nucleus

Other pathways regulate the activity of enzymes rather than their synthesis

Signal pathways can also affect the overall behavior of a cell, for example, changes in a cell shape

Initiate transcription: begin production of proteins within the cell, control what happens in the cell

E.g. testosterone, estrogen, progesterone

Change cell behavior: tell the cell to do something

E.g. yeast (fungus) cells mating (making shmoos, induce change in cell shape) produce actin microfilaments (for cell movement and shape) to form cortex for changing cell shape (shmoo)

Muscle contractions

Pheromones: externally released ligands for organism-to-organism communication

Activate enzymes: control what chemical reactions the cell is able to perform

Apoptosis (1. DNA mutation, 2. Misfolded protein, 3. Death signal)

Active or suppress genes: triggered by growth factors and hormones

Fine-Tuning of the Response

Amplification of the Signal (and response): enzyme cascades amplify the cell’s response the number of activated products is much greater than in the preceding step

Small amount of ligand create a large response

All of the proteins relaying the message can amplify the response, can activate many enzymes

Specificity of the Response: pathway within the cell dictates the response given from that ligand

Cell can only respond if they have the receptor but the pathway determines what that response is

Efficiency of the Response: increased using scaffolding proteins hold many relay proteins in one location. Have proteins associated with pathway close together to make pathway faster

Termination of the Signal: unbound receptors revert to an inactive state

Specific Responses

Apoptosis: controlled cell death using lysosomes’ hydrolytic proteins (proteases, amylases [carbs], nucleases, etc.) cells in a vesicle the vesicles are taken in by white blood cells and digested

Lysosomal enzymes are released in the cell and break everything down, package everything into vesicles and WBC phagocytosis consumes the vesicles

Release of “death-signal” binds to receptor initiation of phosphorylation cascade and activates nucleases (nucleic acids) and proteases (protein) that break down the cell

Activate enzymes mainly caspase

Reasons: normal development, selectively killing particular cells (finger webbing removal, more space between digits) embryonic development

Triggered by DNA damage (mutation) in the nucleus

Extracellular death ligands (signals)

Protein misfolding in the nucleus (e.g. alzheimer's, parkinson's)

Mutations cause cancer and disease so it’s better to destroy the cell → when things go awry apoptosis is the safeguard

Evolved in early animal evolution and is essential for development and maintenance of all animals

Interference with apoptosis may cause cancer

Caspases are the main proteases (enzymes that cut up proteins that carry out apoptosis)

CELL CYCLE

Interphase: any time the cell is not dividing

G1 (Growth 1): cell spends the bulk of its time, the cell grows and begins normal processes

S (Synthesis): cell begins to prepare for division. DNA replicatescritical to mitosis so both new daughtercells get a full set of DNA

****The chromosomes make copies and are held together by a centromere band, the two copies held are called sister chromatids, those chromatids are identical to each other and are still considered one chromosome, one mitotic chromosome, when the cell divides, the sister chromatids separate and are now separate chromosomes, both daughter cells get one copy and have the same chromosomes as the parent.

If DNA replicates it has to divide, a critical point to decide whether or not it will divide

G2 (Growth 2): undergoes more growth, the cell prepares more for division, organelles begin to replicate

Mitosis: process of cell division, occurs after the G2 phase, technically only when the nucleus divides

The two daughter cells are identical does not produce variation, purpose = cloning

Cytokinesis: when the rest of the cell (cytosol) divides after mitosis nuclei divide

In animal cells:

Cleavage furrow (groove in cell) is formed using a ring of actin microfilaments (for movement)the ring gets tighter until it cuts through the cytoplasm into two daughter cells

In plant cells:

Can’t pinch plant cells into two because of the rigid cell wall

Creates cell plates (produces new membrane and cell wall) the vesicles containing new material form a plate and build new structures to be separated in two through growth

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REGULATION

Checkpoints: points at which the cell checks its function to determine if it will undergo mitosis or not, using analysis of internal conditions

If things go wrong at these checkpoints, the cell will undergo apoptosis

If something goes wrong and goes unregulated/undetected, cell will divide out of control, and this is cancer

G1 “Restriction Point”: to replicate or not replicate DNA, ultimatum either to divide or not divide

If the signal is not reached at the restriction point for the go-ahead, the cell enters:

G0 Stage: a perpetual state of G1, like neurons and heart cells

In order to enter the S Stage, the restriction point go-ahead needs to be reached using the chemical ligand of growth factors

After checkpoint you are committed to divide

G2 Checkpoint: point at which cell decides if they should leave interphase

Uses internal factors ; chemical messengers in side of the cell

Cyclin: levels increase and decrease in a cycle, but at G2, its levels are at its highest and combines with CDK

Cyclin-dependent Kinase (CDK): levels remain constant

Cyclin + CDK come together and form the Maturation Promoting Factor (MPF) which triggers the end of interphase

M Checkpoint (Metaphase Checkpoint): checks if all of the chromosomes are lined up in the middle of the cell, if they aren’t lined up properly, causes apoptosis

Conditions: detected using proteins

Anchorage Dependence: in order for a cell to divide it needs to be attached to something

Density-dependent Inhibition: if cells get crowded, they stop dividing

***cancer cells do not exhibit either of these conditions, that’s why they keep dividing out of control.

CANCER

Cells are unable to regulate mechanisms going thru the process of the cell cycle

→ cells divide out of control

Cancer: unregulated and uncontrolled cell division

Cancer cells do not require growth factors to grow and divide

They can make their own growth factors

Convey a growth factor signal without the presence of a growth factor

***Abnormal cell cycle control mechanism

CDK, cyclin, receptors, growth factors, condition proteins, are all proteins, which are created using DNA, which codes specifically for proteins

If a gene mutates, the protein changes, and when you change a shape of a protein you change its function, and improper regulation begins

Proto-oncogenes: genes that code for all of the proteins used in the cell cycle

If a gene mutates it causes transformation: proto-oncogenes become, oncogenes which are cancerous

Causes proteins to change shape and no longer work

One oncogene is not enough to cause cancer, need 6-9 genes to get cancer

Cannot directly inherit cancer, can’t pass down 7 oncogenes, but could pass down a couple oncogenes, so you’re predisposed

Tumor suppressor genes: group of genes that stop cancer from developing, can also mutate

Can code for proteins that correct mutations and proofread DNA

*P53 Gene: codes for p53 protein which triggers apoptosis

If the gene mutates, bad cells cannot be stopped from living

We normally undergo many mutations on a daily basis, P53 gene prevents these cells from manifesting

50% of cancers involve a mutation to the P53 gene

BRCA1 and BRCA2 genes: genes related to ovarian cancer and breast cancer

HER2 gene: codes for growth factor receptors in breast tissue, if it mutates, cells would divide out of control

Found in high concentration in breast/ovarian cancer patients

Ras gene: codes for G-protein which relays the signal from growth factors

Carcinogens: cause proto-oncogenes to mutate (radiation (x-ray), UV light, Nicotine, e.g.)

***Each cancer is caused by a different set of mutated genes, so there is no possible cure-all

Can only treat certain cancers using specific methods, they have to be tailored to that specific type of cancer

Tumors:

Major difference between the two is a number mutations

Benign: have 5 mutations about, generate a mass but do not spread stays at original site, abnormal cells but are not cancerous

Malignant: impairs the functioning of whatever organ it’s in, this is cancerous so about 7 mutations,

can metastasize: part breaks off, enters the bloodstream, divides and creates a tumor elsewhere in the body

Release their own growth factors, and cause blood vessels to grow towards it so it can nourish and spread

Radiation: high dosage of energy generated to a specific part of the body (lasers) to kill tumor at location (using an MRI)

Usually done in part of chemotherapy

Chemotherapy: toxin that kills all dividing cells

Destroys the spindle fibers that make cells split

Negative Feedback

Set point: an original amount or condition, set by hypothalamus, desired condition

Fever: hypothalamus changes set point to a high temperature to run immune system on hyperdrive (speed reactions) to fight illness

Stimulus: causes you to move away from the set point

Response: attempt to reach back to the set point

NOT FEEDBACK INHIBITION, feedback inhibition is where the final product stops the metabolic pathway, uses allosteric enzymes to control reactions

Negative feedback regulates much larger things (blood-sugar levels, and body temperature)

Positive Feedback

Does not maintain homeostasis

Like cooperativity, where one enzyme binds activating more enzymes

A stimulus pulls you away from the set point, and then your body keeps going away from set point

E.g. breastfeeding, or uterine contractions

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