AP BIO ALL UNITS PT 1

Bacteria Cell Signalling

• single celled organisms

• population density is often the key factor for signaling

• qurom sensing, uitilizing molecules called autoinducers

How does cell signaling work?

• using chemical signals (proteins or molecules produced by a sending cell) that are often secreted from the cell and released to the extracellular space, floating to neighboring cells

• The signal binds to a target cell, which has to have the right receptor for the specific signal

1. signal binds to receptor (reception)

2. receptor changes → signal transduction pathway begins, in which a sequence of molecular events and chemical reactions leads to a response, receptor changes, and causes a chain of reactions

   1. During this, a message carried by a ligand is often relayed through messengers in the cell

3. Cellular Response

Target Cells

• cells thar respond to signals for which they have receptors for

Ligand

• signal molecule that binds to a receptor

• ligand, and receptors all come in closely matched pairs, with a receptor recognizing just one specific ligand. Binding changes the receptor’s shape and activity, allowing for a response

• can enter cell: small, hydrophobic

  • steroids

  • nitric oxide

• bind outside: water-soluble, polar/charged

  • peptide ligands/proteins like insulin

  • neurotransmitters that are proteins, hydrophillic molecules, or amino acids

Autocrine signaling

A cell releases a ligand that binds to receptors on its own surface, meaning the cell is signaling to itself.

Key points:

• Helps reinforce a cell’s identity and function during development.

• Allows a cell to amplify its own signaling when needed.

• Cancer cells can exploit autocrine signaling to promote uncontrolled growth and metastasis.

Paracrine signaling

Cells that are close to each other release local regulators (ligands) that diffuse through the extracellular space to nearby target cells.

Key points:

• The ligand acts over a short distance only.

• It allows local coordination between neighboring cells.

• It helps cells differentiate and organize tissues during development (example: spinal cord patterning signals).

Sypnaptic sygnaling

• Synapse: the junction between two neurons (axon terminal of the presynaptic neuron and the dendrite/cell body of the postsynaptic neuron).

  Process:

  1. The presynaptic neuron generates an action potential that travels down the axon.

  2. When the action potential reaches the axon terminal, it opens voltage-gated calcium channels.

  3. Calcium ions (Ca²⁺) enter the terminal and cause synaptic vesicles to fuse with the membrane.

  4. Neurotransmitters are released into the synaptic cleft by exocytosis.

  5. Neurotransmitters diffuse across the cleft and bind to receptors on the postsynaptic membrane.

  6. This binding opens ion channels and produces a postsynaptic potential (can be excitatory or inhibitory depending on the neurotransmitter).

  7. To end the signal, neurotransmitters are broken down by enzymes or reabsorbed by reuptake into the presynaptic neuron.

Endocrine Signaling

used by hormones, which are signals made in one part of the body that travel through the bloodstream to reach distant target cells.

Key points:

• This is long-distance signaling.

• Specialized endocrine cells release hormones into the circulatory system.

• The blood carries these hormones to far-away target tissues that have the correct receptors.

Juxtacrine signaling

Direct Contact Signaling:
Cells communicate by physically connecting with each other, allowing signals to pass directly from one cell to another.

1. Gap junctions (animals) and plasmodesmata (plants):

• These structures directly connect the cytoplasm of two cells.

• Small molecules and ions move freely between cells.

• Large molecules (proteins, DNA, etc.) cannot pass on their own and require other mechanisms.

• This lets cells share information about their current internal state, so neighboring cells can respond to a signal that only one cell detected.

Cell-to-cell recognition (surface proteins):

• Two cells can communicate by binding complementary proteins on their membranes.

• The binding causes a shape change in the receptor protein and triggers a signal inside the cell.

• This is important in the immune system, where cell-surface markers help distinguish self cells from pathogens.

Receptors may be

Cytoplasmic receptors:

• Receptors located inside the cell (in the cytoplasm).

• They bind small, nonpolar ligands that can cross the membrane (examples: steroid hormones).

• Once the ligand binds, the receptor–ligand complex usually enters the nucleus and changes gene expression.

Membrane receptors:

• Receptors located on the cell surface (plasma membrane).

• They bind large or polar ligands that cannot cross the membrane (examples: peptide hormones, neurotransmitters).

• Binding triggers a signal transduction pathway inside the cell.

Plasmodesmata specialized junctions

• Plant cells cannot touch directly through their plasma membranes because cell walls sit between them.

• Plasmodesmata are small channels punched through the cell wall that allow cytoplasm to move between cells.

• Each channel is lined with plasma membrane, continuous between the two connected cells.

• A thin strand of cytoplasm, including a narrow piece of endoplasmic reticulum (the desmotubule), runs through the channel.

• Small molecules and ions can passively diffuse through plasmodesmata, although the size limit varies among plants.

• Plasmodesmata can open wider when needed to allow larger molecules to pass.

Gap Junctions

• Channels that connect neighboring animal cells, allowing ions, water, and small molecules to move directly from one cell’s cytoplasm to the other.

• In vertebrates, each gap junction channel is formed when six membrane proteins called connexins assemble into a connexon.

• When a connexon from one cell aligns with a connexon from the adjacent cell, they form a continuous intercellular channel.

• This allows very fast communication and helps tissues coordinate activity (example: heart muscle contraction).

Tight Junction

• Form a watertight seal between neighboring cells.

• Prevent substances from leaking between cells; forces materials to pass through cells instead of between them.

• Made of many proteins called claudins.

• Claudins on one cell’s membrane bind tightly to claudins on the adjacent cell, creating a continuous, sealed barrier.

• Important in tissues like the intestines and kidneys, where controlled transport is essential.

Desmosomes

• Act like spot welds that hold cells together in strong sheets.

• Cadherins (adhesion proteins) extend from each cell’s membrane and bind to cadherins from the neighboring cell.

• Inside the cell, cadherins attach to a cytoplasmic plaque, which connects to intermediate filaments.

• This anchoring system gives tissues strength and flexibility, allowing them to withstand stretching (important in skin and muscle).

Membrane receptors

• Integral membrane proteins that let cells sense and respond to signals in the external environment.

• An extracellular signaling molecule (ligand) binds to the receptor, forming a ligand–receptor complex that triggers a specific cellular response.

• Each receptor is highly specific and binds only one type of ligand.

• Many drugs work by activating or blocking these receptors.

• These receptors help cells specialize and carry out the correct functions.

• Binding often follows the lock-and-key or induced-fit model.

• ligand doesn’t have to pass the membranes

• Membrane receptors have three main regions: an extracellular ligand-binding domain, a hydrophobic transmembrane region, and an intracellular domain that transmits the signal.

Major types:

• Ligand-gated ion channels: ligand binding opens an ion channel allowing ions to flow in/out of the cell.

• G-protein–coupled receptors (GPCRs): ligand binding activates a G-protein, leading to a second-messenger signaling pathway.

• Enzyme-linked receptors (e.g., receptor tyrosine kinases): ligand binding activates an intracellular enzyme, usually leading to phosphorylation cascades.

Intracellular (cytoplasmic) receptors and hydrophobic ligands

• Hydrophobic signaling molecules (such as steroid hormones) can diffuse across the plasma membrane because they are nonpolar.

• These ligands bind to intracellular receptors located in the cytoplasm or nucleus.

• Most intracellular receptors act as transcription factors. After the ligand binds, the receptor–ligand complex enters the nucleus and binds directly to DNA, altering gene transcription.

• This causes direct changes in gene expression inside the cell.

• Only small, hydrophobic ligands can use this pathway because they must cross the lipid membrane.

Small hydrophobic ligands

• hormones

• Small hydrophobic ligands

  • Steroid hormones have similar chemical structures to their precursor, cholesterol.

  • Unlike water soluble ligands which typically bind to cell-surface receptors, steroid hormones can diffuse directly across the plasma membrane into the cell, where they interact with internal receptors.

There are also gas ligands (e.g., nitric oxide)

Ligand-gated channel receptors

• Ion-channel receptors are membrane proteins that open or close in response to ligand binding.

• When activated, they allow specific ions to flow across the plasma membrane.

• The resulting change in ion concentration inside the cell generates a cellular response.

• In some cases, ligand binding closes the ion channel instead of opening it.

Phosphorylation

• A phosphate group (PO₄³⁻) is added to the amino acids serine, threonine, or tyrosine, which all have –OH groups.

• This reaction is catalyzed by kinases, enzymes that transfer phosphate groups to proteins.

• Phosphorylation often acts as a molecular switch, sometimes activating a protein and sometimes inhibiting it or marking it for breakdown.

• Phosphatases remove phosphate groups, reversing the signal.

MAP Kinase Signaling Cascade

• ERK is a MAP kinase that becomes active only when it is phosphorylated.

• Activated ERK phosphorylates MNK1, and MNK1 then phosphorylates eIF-4E.

• When eIF-4E is phosphorylated, the mRNA structure unfolds, allowing translation to begin.

• This links cell signaling → phosphorylation cascade → gene expression/protein synthesis.

Example pathway: Epidermal Growth Factor (EGF):

• EGF binds to its receptor, causing two receptors to pair (dimerize).

• The paired receptors phosphorylate each other’s intracellular tails (autophosphorylation).

• This begins a phosphorylation cascade:

  • The receptor activates RAF.

  • RAF phosphorylates MEK.

  • MEK phosphorylates ERK.

  • ERK phosphorylates target molecules, leading to changes in gene expression.

This is a classic MAP kinase pathway, showing how phosphorylation amplifies a signal and produces a long-term cellular response.

Protein Kinase Receptor

• Ligand binding causes the receptor to change shape and activate its protein kinase domain.

• The receptor phosphorylates itself or other proteins, starting a phosphorylation cascade.

• Example: Receptor tyrosine kinases (RTKs) like the EGF receptor.

Enzyme linked receptor

• Ligand binding triggers a conformational change, and the receptor either acts as an enzyme or activates an associated enzyme.

• Not all enzyme-linked receptors are kinases; some activate different enzymes on the intracellular side.

• These receptors initiate various signaling pathways that lead to cellular responses.

G Protein-linked receptor

• GPCRs are a large family of receptors with seven transmembrane segments that transmit signals inside the cell through a G protein.

• Before the ligand binds, both the G protein and the effector protein are inactive, and the G protein (attached to the plasma membrane) holds GDP.

• When a ligand binds to the GPCR, the receptor becomes active and causes the G protein to exchange GDP for GTP, turning it on.

• The G protein then splits into two parts (the α subunit and the β/γ complex), β/γ leave the receptor and interact with other proteins, including the effector protein.

• The activated effector protein produces many molecules of a second messenger, creating signal amplification that leads to a single cellular response.

• Eventually, the α subunit hydrolyzes GTP to GDP, which turns the G protein off and ends the production of second messengers; the subunits then recombine and return to the inactive state.

Tyrosine-Kinase Receptors

• Ligand binding causes two RTKs to come together and dimerize.

• The paired receptors use ATP to autophosphorylate tyrosine residues on each other’s intracellular domains.

• RTKs specifically transfer phosphate groups to tyrosines, which activates the receptor.

• The phosphorylated tyrosines act as docking platforms for many intracellular proteins that have special binding domains.

• Because many different proteins can bind at once, RTKs can activate multiple signaling pathways simultaneously (common in growth and differentiation signals).

• RTKs have one transmembrane region with extracellular and intracellular domains.

• After activation triggers downstream cascades, phosphatases remove the phosphates to terminate the signal.

• Many growth factors (such as EGF and PDGF) use RTKs to regulate cell growth, survival, and division.

Second messengers

• Second messengers allow the cell to respond to a single membrane event with many events inside the cell—they distribute the signal. 

  They amplify the signal by activating more than one enzyme target. 

• small non protein molecuels that pass along a signal initiated by binding ligand

Calcium ions as second messengers

a. calcium ions

• in msot cells, calcium concentration incytosol is low, as ion pumps remove it

• calcium is stored in the ER for signaling purposes

• upstream signaling release ligand that binds to and open ligand gated calcium channels which allow calcium to flow into cytoplasm down its concentration gradient and raises cytoplasmic calcium concentration

cAMP as second messengers

• A small second messenger made from ATP.

• The enzyme adenylyl cyclase converts ATP into cAMP by removing two phosphates and linking the remaining phosphate to the sugar in a ring structure.

• cAMP activates protein kinase A (PKA), which then phosphorylates specific target proteins to pass the signal.

• Each cell has different PKA targets, so cAMP produces different responses in different cell types.

• cAMP is turned off by phosphodiesterases, which break the ring and convert cAMP into AMP.

Phosphates

• Certain membrane phospholipids, especially phosphatidylinositol (PIP₂), can be phosphorylated and then split into fragments that act as second messengers.

• The enzyme phospholipase C (PLC) cuts PIP₂ into DAG and IP₃, both of which function as second messengers.

DAG (diacylglycerol):

• Stays in the plasma membrane.

• Activates protein kinase C (PKC), which then phosphorylates target proteins.

IP₃ (inositol trisphosphate):

• Diffuses into the cytoplasm.

• Binds to ligand-gated Ca²⁺ channels on the smooth ER, causing calcium ions to be released.

• The increase in cytoplasmic Ca²⁺ acts as an additional second messenger inside the cell.

Epineprhine

• Epinephrine binds to its GPCR on the cell membrane.

• The activated receptor stimulates a G protein, which activates adenylyl cyclase.

• Adenylyl cyclase converts ATP into cAMP, a second messenger.

• cAMP activates protein kinase A (PKA).

• PKA phosphorylates two metabolic enzymes, producing opposite effects:

Activation pathway:

• PKA phosphorylates and activates phosphorylase kinase.

• Activated phosphorylase kinase then activates glycogen phosphorylase.

• Glycogen phosphorylase breaks down glycogen, liberating glucose molecules.

Inhibition pathway:

• PKA phosphorylates and inactivates glycogen synthase, preventing glycogen synthesis and blocking glucose storage.

Overall effect:
Epinephrine causes a coordinated response: stop storing glucose and start releasing glucose by breaking down glycogen.

Amplification

• One signaling molecule can trigger activation of many downstream molecules.

• Each step in the pathway can activate multiple copies of the next protein.

• Results in a large cellular response from a small initial signal.

• Common in hormone signaling (e.g., adrenaline).

• Makes cell responses fast and powerful even with low signal concentration.

Primary messenger

• steroids/thyroid hormones that can pass cell membrane and bind to intravellular receptors, which can affect transcription of protein activated hormones

EGFR

• The epidermal growth factor (EGF) receptor (EGFR) is a tyrosine kinase receptor involved in the regulation of cell growth, wound healing, and tissue repair. 

• When EGF binds to the EGFR, a cascade of downstream events causes the cell to grow and divide. 

• If EGFR is activated at inappropriate times, uncontrolled cell growth (cancer) may occur.

How cells alter balance of enzymes

Cells can alter the balance of enzymes in two ways:

• Synthesis or breakdown of the enzyme

• Activation or inhibition of the enzymes by other molecules

• through balancing active and inactive forms, the cell controls or regulates its response to a signal molecule

Cell functions change in response to environmental signals:

Cell functions change in response to environmental signals:

• Opening of ion channels

• Alterations in gene expression

• Alteration of enzyme activities

• Trigger apoptosis

Quorom sensing

• Bacteria release small chemical signaling molecules into the environment.

• As the population grows, the concentration of these signals increases.

• When the signal reaches a threshold, all bacteria detect it and change their behavior simultaneously (ex: biofilm formation, virulence, bioluminescence).

Symbiosis example: Aliivibrio fischeri and the Hawaiian bobtail squid:

• The squid has a light organ where A. fischeri form dense bacterial colonies.

• The squid provides the bacteria with nutrients.

• In return, the bacteria produce bioluminescence, helping the squid camouflage from predators at night (counter-illumination).

• A. fischeri only glow inside the squid, not when free-living in the ocean, because quorum sensing requires high population density; glowing alone would waste energy without benefiting the bacteria.

Mechanism of quorom sensing

• Bacteria release autoinducers, signaling molecules that let them sense population density and coordinate behavior.

• When there are few cells, autoinducer (AHL in Gram-negative bacteria) diffuses away, so its internal concentration stays low.

• As the population grows, more AHL is produced, raising its concentration inside and outside the cells.

• When AHL reaches a threshold level, it binds to and activates a receptor protein inside each cell.

• The activated receptor functions as a transcription factor, binding DNA and changing gene expression in all cells at the same time.

• This creates an amplifying positive-feedback loop, making the response synchronized across the population.

• Some autoinducers can be detected by multiple bacterial species, allowing cross-species communication.

Yeast Cell Signaling

• Haploid yeast (a and α types) can fuse to form a diploid cell.

• Diploid cell can undergo meiosis → haploid spores with new genetic combos.

Mating Factor Pathway

• Haploid yeast secrete mating factors to find a compatible mate.

• Only opposite mating type has the correct receptor.

• Mating factor binding triggers a signal transduction cascade.

Cell Response

• Cell cycle pauses to prepare for fusion.

• Cell produces an outgrowth (shmoo) that grows toward the mating partner.

• Two haploid cells fuse → form diploid zygote.

Signal relay pathways

• Binding of a signal molecule initiates a signaling pathway.

• When reception occurs, the receptor’s intracellular domain changes shape.

• This activates the receptor (as an enzyme or by allowing it to bind other molecules).

• Activation triggers a series of signaling events → changes the cell’s behavior.

• Upstream: earlier steps in the signaling chain.

• Downstream: later steps in the signaling chain.

Signal Amplification: Pathways often amplify the signal → one molecule can activate many downstream targets.

• Proteins typically relay signals.

• Ions and phospholipids can also serve as important signaling molecules.

Types of cellular response

Gene Expression

• Gene expression = using the information in a gene to make a functional product.

• Changes in gene expression = turning genes on or off.

• Transcription: DNA → RNA.

• Translation: RNA → protein.

• Example: growth factors can activate pathways that turn on specific genes.

Cellular Metabolism

• Signaling can cause metabolic responses.

• Metabolic enzymes may become activated or inactivated.

• Example: adrenaline (epinephrine) triggers liver cells to break down glycogen → releases glucose.

Large-Scale Cellular Responses

• One signal can trigger big outcomes (“1 signal → amplified response”).

• Cells may undergo:

  • Cell migration

  • Changes in cell identity/differentiation

  • Apoptosis (programmed cell death)

Cell division

Serves as a means of asexual reproduction in unicellular organisms

Allows for growth and tissue repair in multicellular organisms

Reproduction

Reproduction

can be asexual resulting in clones

genetic changes may occur due to mutations

Prokaryotes – binary fission

Eukaryotes – mitotic cell division (mitosis)

can be sexual resulting in offspring showing genetic variation that results from mutations as well as processes in meiosis

union of two gametes (reproductive cells) form a zygote

Binary Fission

• Binary fission is the asexual reproduction method of prokaryotes (bacteria and archaea).

• It produces two genetically identical daughter cells, unless mutations occur.

• It is simpler and faster than mitosis because prokaryotes do not have a nucleus and have only one circular chromosome.

Key Steps (AP Bio–appropriate detail)

1. DNA Replication

   • The single circular chromosome is copied starting at the origin of replication.

2. Chromosome Segregation

   • As replication continues, the two DNA molecules attach to different parts of the cell membrane and move apart as the cell elongates.

3. Cell Growth

   • The cell increases in size, pushing the chromosomes toward opposite ends.

4. Cytokinesis

   • A septum (new cell wall) forms in the middle.

   • The cell splits into two identical cells

DNA and Genomes

• When a cell divides, it passes an identical copy of its DNA to each daughter cell.

• In sexual reproduction, DNA from two parents combines when sperm and egg fuse.

• Genes contain the instructions for making proteins, which determine cell structure and function.

• In eukaryotes, most DNA is found in the nucleus, but mitochondria and chloroplasts also contain small circular DNA molecules.

• A genome is the complete set of DNA in a cell or organism; each species has its own characteristic genome.

Chromatin

• DNA is organized by specialized proteins that help package it and regulate gene activity.

• Histones are positively charged proteins that act like spools; negatively charged DNA wraps around them, creating a more compact structure.

• The combination of DNA + histones + other organizing proteins is called chromatin.

• Chromatin structure helps determine which genes are active, because tightly packed regions are harder for transcription machinery to access.

• For most of the cell cycle, chromatin is decondensed, allowing the cell to grow and express genes.

• When the cell prepares to divide, chromatin becomes highly condensed, forming visible chromosomes.

Chromosomes

• Each chromosome consists of a single, long DNA molecule with associated proteins.

• Somatic cells contain two sets of chromosomes (diploid), arranged in homologous pairs.

• The two chromosomes in a homologous pair have the same size, shape, and gene locations, but they may carry different versions (alleles) of those genes.

• Gametes (sperm and egg) are haploid, meaning they contain one chromosome from each homologous pair.

• When sperm and egg fuse during fertilization, the resulting zygote becomes diploid again.

• Sex chromosomes (X and Y) determine biological sex.

  • XX = female, XY = male.

  • X and Y are not true homologous chromosomes because they carry different genes, although they pair during meiosis.

DNA behavior

The number of DNA molecules (chromosomes) in the cell nucleus varies among species 

Within a species, chromosome number is consistent, but may vary with developmental stage or specific cell type

Gametes, haploid, fertilization, diploid

Gametes contain only one set of chromosomes—one homolog from each pair.

Haploid cell—Number of chromosomes = n

• fungi spend most of their lives as haploids

Fertilization—Two haploid gametes (female egg and male sperm) fuse to form a zygote.

Chromosome number in zygote = 2n, and cells are diploid.

• Chromosomes (homologs) that pair in the reproduction of diploid cells are described as homologous

• Some genomes have pairs that don’t match, for example X and Y chromosomes in humans

• These are heterologous pairs

Chromosomes and cell division

• When a chromosome is replicated, the two identical copies are called sister chromatids.

• They are held together by proteins called cohesins, with the tightest attachment at the centromere, which is essential for proper separation later.

• As long as the sister chromatids remain attached, they count as one chromosome; once they separate, each chromatid becomes its own chromosome.

• This ensures that, during cell division, each daughter cell receives exactly one copy of every chromosome.

Why sexual reproduction

• The essence of sexual reproduction is that it allows the random selection of half the diploid chromosome set. 

• This forms a haploid gamete that fuses with another to make a diploid cell (zygote).

• Thus, no two individuals (who aren’t identical twins) have exactly the same genetic makeup.

Eukaryotic DNA must be condensed into compact chromosomes to fit into the nucleus

Short stretches of DNA wrap around a core of 8 histone proteins –like a string of beads

This combination of DNA and Proteins is called chromatin

The histone-DNA complex (the bead) is called a nucleosome

This structure coils to form a chromatin fiber

Fibrous proteins further pack each chromosome

Four events must occur for cell division:

Four events must occur for cell division:

• Reproductive signal—to initiate cell division

• Replication of DNA

• Segregation—distribution of the DNA into the two new cells

• Cytokinesis—division of the cytoplasm and separation of the two new cells

Cell cycle

• to divide cells must grow, copy DNA, and split to 2 daughter cells

• in eukaryotic cells; stages are: interphase, mitotic phase

Interphase

• G₁ phase: the cell grows, copies organelles, and produces molecular building blocks needed for DNA replication and later steps.

• S phase: the cell synthesizes a complete copy of its DNA in the nucleus and duplicates the centrosomes, which help organize the mitotic spindle.

• G₂ phase: the cell continues to grow and produces the proteins and organelles needed for mitosis; it also begins reorganizing its contents for cell division.

Key points:

• A cell spends most of its life in interphase.

• Chromosomes are not condensed; they remain in the loosely packed chromatin form.

• The centrosome serves as the microtubule-organizing center and is duplicated before mitosis begins.

Prophase

• Chromosomes condense, making them easier to move.

• The mitotic spindle begins to form from microtubules as the centrosomes move apart.

• The nucleolus disappears.

Late prophase (prometaphase):

• Chromosomes are fully condensed.

• The nuclear envelope breaks down, allowing spindle microtubules to interact with chromosomes.

• Kinetochore microtubules attach to the chromosomes at the kinetochore, a protein structure at the centromere.

• Other microtubules connect to microtubules from the opposite side to stabilize the spindle, and some extend outward from each centrosome to the cell edge, forming asters.

metaphase

• The spindle has captured all chromosomes and aligned them in the center of the cell.

• Chromosomes line up at the metaphase plate.

• The two kinetochores of each chromosome must be attached to microtubules from opposite spindle poles.

• Before moving to anaphase, the cell performs the spindle checkpoint, ensuring every chromosome is properly attached and aligned.

• If a problem is detected, the cell halts division until the attachment error is corrected, preventing uneven chromosome distribution.

Anaphase

• Sister chromatids separate as the cohesin proteins holding them together are broken down.

• Once separated, each chromatid is considered its own chromosome and is pulled toward opposite poles.

• Motor proteins at the kinetochores (such as cytoplasmic dynein) use ATP to move chromosomes along the microtubules toward the spindle poles.

• Non-kinetochore microtubules (those not attached to chromosomes) elongate, pushing the poles farther apart and lengthening the cell.

• These movements are driven by motor proteins acting on both the chromosomes and the microtubules.

Telophase

• cell nearly done dividing

• reestablish normal structures

• mitotic spindle breaks down to its building blocks

• 2 new nuclei form, nuclear membranes and ncleoli reappear

• chromosomes decondense

Cytokinesis

Cytokinesis (AP Bio standard):

• The cytoplasm divides, producing two separate daughter cells.

• Cytokinesis overlaps with the end of mitosis and usually begins during anaphase or telophase.

In animal cells:

• A contractile ring made of actin filaments tightens to pinch the cell in two.

• This creates the cleavage furrow, which deepens until the cells separate.

In plant cells:

• A cell plate forms in the middle of the cell because the rigid cell wall prevents pinching.

• Vesicles from the Golgi fuse at the center to build the cell plate, which becomes a new cell wall separating the two daughter cells.

Why mitosis?

• populates cells

• replaces old cells

• can be a forom of reproduction in unicellular eukaryotes

• ensure each daughter cells get perfect, full set of chromosomes

Important factors about mitosis

After cytokinesis:

Each daughter cell contains all of the components of a complete cell.

Chromosomes are precisely distributed, but organelles are not always evenly distributed.

The orientation of cell division is important to development.

G1 checkpoint

• Occurs between G₁ and S phase and is the main decision point for the cell.

• The cell decides whether to proceed with division or not.

• Once it passes this checkpoint, the cell is irreversibly committed to DNA replication and division.

• The checkpoint evaluates internal and external conditions, including:

  • Nutrient availability

  • Cell size

  • Growth factor signals

  • DNA integrity

• If conditions are not adequate, the cell does not pass and may enter G₀, a non-dividing state.

• Some cells can re-enter the cycle from G₀ if conditions improve.

G2 checkpoint

• Occurs between G₂ and M phase.

• Ensures that DNA replication is complete and that the DNA is undamaged.

• If replication errors or DNA damage are detected, the cell halts the cycle to finish replication or repair the DNA.

• If the damage cannot be repaired, the cell undergoes apoptosis to prevent faulty division.

Spindle checkpoint/ M checkpoint

• Occurs between metaphase and anaphase.

• Ensures that all sister chromatids are correctly attached to spindle microtubules at their kinetochores.

• The cell will not proceed to anaphase until every chromosome is properly attached and aligned.

• The checkpoint detects any misattached or “straggler” chromosomes that are not in the correct position.

• If a chromosome is misplaced, the cell pauses mitosis until the spindle fibers successfully attach and correct the error.

Cell cycle regulators

• A group of related proteins that control progression through the cell cycle

• The main regulators are cyclins

• Four basic types: G1 cyclins, G1/S cyclins, S-phase cyclins, M-phase cyclins

• Cyclin levels stay low for most of the cycle and rise sharply only when needed to activate CDKs

Cyclin-dependent kinases (Cdk)

• A protein kinase that catalyzes phosphorylation, transferring a phosphate from ATP to target proteins.

• Phosphorylation changes a protein’s shape and function by altering its charge.

• CDKs drive the cell cycle but are inactive on their own.

• They become active only when bound to a cyclin, which both activates the CDK and directs it to the correct target proteins for that stage of the cycle.

• Cyclin levels fluctuate (low most of the cycle, rising when needed), while CDK levels stay constant; CDK activity depends on cyclin availability.

• CDKs require activating phosphorylation at a specific site, but phosphorylation at other sites or binding of inhibitory proteins can block or reduce activity.

ex) RB normally inhibits the cell cycle, but when phosphorylated by G1-S cyclin-Cdk, RB becomes inactive and no longer blocks the cell cycle.

Maturation promoting growth factor

• M cyclin stays at low levels through most of the cycle and accumulates approaching the G2/M transition.

• As M cyclin builds up, it binds its CDK partner to form MPF (Maturation-Promoting Factor).

• MPF becomes fully active after receiving a final activating phosphorylation and then triggers entry into M phase.

• MPF phosphorylates proteins in the nuclear envelope, causing it to break down.

• MPF also activates proteins that promote chromosome condensation and other mitotic steps.

APC/C (Anaphase-Promoting Complex/Cyclosome)

• MPF activates APC/C in M phase, starting at anaphase.

• APC/C triggers the destruction of M cyclins, pushing the cell out of mitosis and into G1.

• APC/C is an enzyme that adds ubiquitin tags to target proteins, marking them for destruction by the proteasome.

• Targets include M cyclins and securin (which normally inhibits separase).

• When securin is destroyed, separase becomes active.

• Separase cleaves cohesin, the protein glue holding sister chromatids together.

• This allows sister chromatids to separate and move to opposite poles in anaphase.

checkpoints and regulators

Cell Cycle Control: Internal and External Cues

• Cells respond to external and internal signals.

• These cues influence the activity of cell-cycle regulators to decide whether the cell should advance through the cycle.

• Positive cues: increase cyclin and CDK activity, pushing the cycle forward.

• Negative cues: decrease or block CDK–cyclin activity to stop progression.

• Example of a negative cue: DNA damage.

p53 (DNA-Damage Checkpoint Protein)

• p53 ensures that cells do not pass damaged DNA through the cycle.

• When DNA damage is detected, p53 halts the cell cycle at the G1 checkpoint.

• It does this by triggering CDK inhibitor proteins, which bind and block CDK–cyclin complexes.

• p53 activates DNA repair enzymes to fix the damage.

• If the damage cannot be repaired, p53 triggers apoptosis (programmed cell death).

• Without functional p53, cells can continue dividing with mutations, leading to cancer development.

Cell death

Cell death occurs in two ways:

1. Necrosis - the cell is damaged or starved for oxygen or nutrients. The cell swells and bursts.

 Cell contents are released to the extracellular environment and can cause inflammation.

2. Apoptosis is genetically programmed cell death. Two possible reasons:

The cell is no longer needed, e.g., the connective tissue between the fingers of a fetus.

Old cells may be prone to genetic damage that can lead to cancer—blood cells and epithelial cells die after days or weeks.

Events of apoptosis

Cell death occurs in two ways:

1. Necrosis - the cell is damaged or starved for oxygen or nutrients. The cell swells and bursts.

 Cell contents are released to the extracellular environment and can cause inflammation.

2. Apoptosis is genetically programmed cell death. Two possible reasons:

The cell is no longer needed, e.g., the connective tissue between the fingers of a fetus.

Old cells may be prone to genetic damage that can lead to cancer—blood cells and epithelial cells die after days or weeks.

Cell death cycle is controlled by signals:

• Lack of a mitotic signal (growth factor)

• Recognition of damaged DNA

• External signals cause membrane proteins to change shape and activate enzymes called caspases, hydrolyze proteins of membranes.

Cancer

• Can divide without added growth factors.

• May produce their own growth factors, keep growth factors stuck on their receptors, or trick nearby cells into producing growth factors for them.

• Ignore inhibitory signals that normally stop cell division.

• Show loss of contact inhibition: continue dividing even when crowded.

• Have replicative immortality, meaning they divide far more times than normal cells.

• Often express telomerase, which prevents shortening of chromosome ends and supports unlimited division.

• Can undergo metastasis, allowing them to spread to other tissues.

• Promote angiogenesis, the growth of new blood vessels to supply nutrients.

• Frequently avoid apoptosis, even when damaged.

• Show metabolic changes that support rapid and uncontrolled growth.

how cancer develops

• Cells acquire mutations that allow faster division, escape from cell-cycle controls, and avoid apoptosis.

• Cancer does not form all at once. It develops through multiple mutations that accumulate over time.

Steps

1. Loss of a cell-cycle inhibitor

   • A mutation in a tumor-suppressor gene removes a “brake” on the cell cycle.

   • This causes rapid, uncontrolled divisions, forming a benign tumor.

2. Second mutation in a descendant cell

   • A new mutation activates positive cell-cycle regulators (oncogenes).

   • These cells divide even faster, creating a larger population where more mutations can occur.

3. Additional mutations accumulate

   • With each round of division, the chance of a new mutation increases.

   • Eventually a cell gains enough harmful changes to form a malignant tumor that invades surrounding tissue.

4. Progression to advanced cancer

   • More mutations continue to accumulate.

   • Advanced cancers often have major genomic instability, including mutations in genes that normally keep the genome stable.

Regulators in cancer

• Cancer can arise when positive cell-cycle regulators become overactive or negative regulators are inactivated.

• Oncogenes are overactive versions of normal positive regulators.

• Their normal, healthy form is called a proto-oncogene.

How proto-oncogenes become oncogenes

• Amino acid–changing mutations can alter the protein’s shape, locking it in an always-on active state.

• Gene amplification: cells gain extra copies of the proto-oncogene, producing too much of the protein.

• Chromosomal rearrangements: a proto-oncogene is mistakenly attached to a different gene or regulatory region, creating a fusion protein or unregulated expression.

• Overactive proteins can send growth signals even without growth factors.

• These overactive forms are commonly found in cancer cells, driving uncontrolled division.

Cell cycle exit +G0

• Most cells in the human body are in G₀. It is the default state for differentiated cells.

• Differentiated cells usually stay in G₀ permanently (neurons, skeletal muscle, cardiac muscle).

• Some cells can leave G₀ when stimulated (liver cells can re-enter the cycle during regeneration).

• G₀ is entered when the cell fails the G₁ checkpoint or lacks signals to proceed.

• It is not a “death” state; the cell is metabolically active and performing its specialized functions.

Photosynthesis

Photosynthesis uses solar energy to produce sugar from CO2 and H2O, with a byproduct of O2

• Light dependent reactions and the Calvin cycle

Overall equation of photosynthesis

6CO₂   +   6H₂O   -->   C₆H₁₂O₆   +   6O₂

Where does the light dependent reaction occur?

In the thylakoid

Photons

Light as a form of electromagnetic radiation, which travels as a wave but also behaves as particles

• can be absorbed by a particle, adding energy to the particle which moves to an excited state

Pigments

Molecules that absorb wavelengths in a visible spectrum

• Chlorophyll absorbs blue and red light, with the remaining light as mostly green

Absorption spectrum

plot of light energy absorbed against wavelength

Action Spectrum

how effective different wavelengths of light are at driving photosynthesis.

What are the two pigments in plants?

Chlorophyll a and chlorophyll b

Accessory pigments

Accessory wavelengths are light wavelengths that chlorophyll a does not absorb well, but accessory pigments can absorb and pass to chlorophyll a for photosynthesis.

Carbon fixation

CO₂ is converted into an organic molecule.

Photosystems

Large complexes of proteins and pigments that are optimized to harvest light

• plays a key role in light reactions 

• has pigments for light energy, and a pair of chlorophyll at the core of the photosystem (reaction center, a double chlorophyll) that includes the special pairs (P700 and P680)

• Resonance energy transfer: pigments excited by light transfer their energy to neighboring pigments through direct electromagnetic interactions

What happens when chlorophyll absorbs light?

• When chlorophyll absorbs light, it enters an excited state, then rapidly returns to ground state, releasing an excited electron.

  • The excited electron exists at a higher energy than the ground state,

• Chl* gives the excited electron to an acceptor and becomes oxidized to Chl+

  • the acceptor of the electron is reduced

Light dependent reactions

• Converts light energy and water to produce ATP and NADPH

• Happens in the thylakoid

• PSII → PSI → NADPH

Photosystem II

• Absorbs light energy at 680 nm, requires H2O as a source of electrons, and leads to ATP production

• Light absorption: 

  • energy from photon gets transferred inward from pigment to pigment until it reaches the reaction center where P680 is

  • The energy towards P680 boosts an electron to a high energy level, which gets passed to a primary acceptor (pheophytin

  • The electron that gets passed to the primary acceptor is replaced by breaking H2O → byproduct of 1/2O2 and 2H+ ions 

• ATP production: 

  • ATP is produced when high energy electrons move down the ETC, releasing energy that pumps the H+ ions into the thylakoid 

  • This builds a H+ gradient (along with the H+ ion from water splitting)

  • This ion gradient passes ions to ATP synthase, driving ATP production in chemiosmosis

  • more ATP is needed than NADPH

How does P680 split water?

• P680 has a electronegativity for electrons — it is hungry for electrons 

• causes the electron from H2O to get pulled off 

• this happens at the manganese center, which splits water

  • binds 2 H2O molecules at once 

  • extracts 4 electrons, releasing H+ ions and produces a O2 molecule

Photosystem I

Absorbs light energy at 700 nm, passes an excited electron to NADP+ → reducing it to NADPH

• Light absorption: 

  • electron from PSII arrives in PSI, which joins the P700 chlorophyll in the reaction center 

  • when the photon is absorbed, it gets passed inwards to P700 which excites it to a higher energy level 

  • the electron gets transferred to a second primary acceptor 

  • The electron is replaced by the PSII’s transferred electron 

• NADPH Formation: 

  • the excited electron travels down a second ETC 

  • at the end of the ETC, the electron is passed to NADP+ to make NADPH

PSII vs PSI

PSII:

• P680

• Pheophytin as primary acceptor

• electrons from H2O

PSI:

• P700

• Ao7.8 as primary acceptor

• electrons from PSII

Non-cyclic photophosphorylation/Linear photophosphorylation

the normal, one-way flow of electrons through Photosystem II → Photosystem I, producing both ATP and NADPH.

• needs light to be absorbed 2 times, hence the 2 photosystems

• creates ATP and NADPH

Cyclic electron transport/cyclic photophosphorylation

• After the electron leaves PSI, it cyclically flows back to the cytochrome complex in PSI

• uses only photosystem I and produces ATP; an electron is passed from an excited chlorophyll and recycles back to the same chlorophyll.

• WHY?

  • to control the ratio of NADPH when NADP+ is too high

  • when a lot of ATP is needed

  • prevents excess light from damaging the photosystem proteins

Calvin Cycle

• Happens in the stroma, where sugar is synthesized 

• COs’s carbon is fixed and used to build G3P, a 3 carbon molecule 

• For every 3 CO2, 9 ATP are used, and 6 NADPH are used. 6G3P are produced, 1 for sugar, and the rest for regeneration

• Carbon fixation → reduction → regeneration 

Calvin Cycle’s carbon fixation stage

CO2 is fixed by Rubisco to RUBP (a five carbon acceptor molecule)

• makes a six-ccarbon compound that splits into 2 molecules of a three-carbon compound, 3 PGA

• rubisco catalyzes the reaction

Calvin cycle’s reduction phase

• Energy is added when ATP and NADPH convert 3-PGA into G3P.

• 1ATP phosphorylates 3-PGA to produce 1,3-bisphosphoglycerate, adding a phosphate group.

• 2 NADPH donates two electrons to reduce 1,3-bisphosphoglycerate.

• As it gains electrons, it loses a phosphate, forming G3P and releasing 2NADP⁺ and 2Pi.

• For every three CO₂ molecules, the cycle produces one net G3P that is usable.

• Two G3P molecules are needed to synthesize 1 glucose, so:one
  6 CO₂ → 2 G3P → 1 glucose.

Calvin cycle’s regeneration phase

• G3P molecules are used to be recylced to create RuBP

• requires ATP and involves complex networks of reactions

• In order to create 1 G3P, 3 CO2 molecules must enter, providing 3 new atoms of fixed carbon

  • 3CO2 → 6 G3P, one used for glucose and 5 used for regneration

Molecule intake, output, and reactions in Calvin Cycle

3CO2 + 3 RuBP acceptors → 6 G3P (1 for glucose, 5 for recycling) 

9 ATP → 9 ADP (6 in reduction, 3 in regeneration) 

6 NADPH → 6 NADP+ (in redudction) 

2 G3P → 1 sugar molecule (this requires 6 turns of the calvin cycle) 

Ecological importance of photosynthesis

• introduce chemical energy and fixed carbon into the ecosystem by using light to synthesize sugars

C3 plants

• C₃ plants use the Calvin cycle directly to fix CO₂ into a 3-carbon compound (3-PGA).

• On hot, dry days, stomata close to prevent water loss.

• When stomata close:

  • CO₂ levels drop inside the leaf.

  • O₂ levels rise inside the leaf.

• Rubisco begins binding O₂ instead of CO₂, starting photorespiration.

• The incorrect product splits into a 2-carbon compound.

• Peroxisomes and mitochondria convert this 2-carbon compound and release CO₂.

• Photorespiration is a disadvantage because it:

  • Wastes ATP/NADPH

  • Releases CO₂

  • Produces no sugar

• Examples of C₃ plants: rice, wheat, soybeans.