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What are the three stages of cell signaling (signal transduction pathway)?
Answer: Reception, Transduction, Response.
Reception: a ligand binds a specific receptor. Transduction: the signal is relayed and often amplified through a series of molecular changes (e.g., a phosphorylation cascade). Response: the cell's activity changes — gene expression, enzyme activation, cytoskeletal rearrangement, etc.
Define ligand.
Answer: A signaling molecule that binds to a specific receptor and triggers a response in the target cell.
Ligands can be hormones, neurotransmitters, growth factors, or other local regulators; they may be hydrophilic (bind surface receptors) or hydrophobic (cross the membrane to bind intracellular receptors).
What is direct contact (cell-junction) signaling?
Answer: Cells communicate by physical contact — through gap junctions in animal cells or plasmodesmata in plant cells, or by recognizing membrane-bound molecules on an adjacent cell's surface.
Example: immune cells recognizing surface proteins on other cells (cell-cell recognition) without release of a diffusible ligand.
What is paracrine signaling?
Answer: A cell secretes local regulator molecules that diffuse through extracellular fluid to act on nearby target cells.
Example: growth factors that stimulate nearby cells to divide during tissue repair.
What is synaptic signaling?
Answer: A nerve cell releases neurotransmitter molecules into a synapse, which diffuse the short distance to stimulate the target cell.
A specialized, very fast form of paracrine signaling.
What is endocrine (hormonal) signaling?
Answer: Specialized endocrine cells secrete hormones into the bloodstream, which carries them throughout the body to reach distant target cells.
Slower but longer-lasting than paracrine signaling; example: insulin released by the pancreas acting on liver, muscle, and fat cells.
What is autocrine signaling?
Answer: A cell secretes a signaling molecule that binds to receptors on its own surface, affecting itself.
Important in cancer, where tumor cells can stimulate their own uncontrolled growth via autocrine loops.
What are the main categories of cell-surface receptors tested in this unit?
Answer: G-protein-coupled receptors (GPCRs), receptor tyrosine kinases (RTKs), and ligand-gated ion channels.
All are membrane-spanning proteins that bind hydrophilic ligands unable to cross the plasma membrane on their own.
How does a GPCR pathway work?
Answer: Ligand binds the GPCR → receptor activates an associated G protein by catalyzing exchange of GDP for GTP → activated G protein dissociates and activates another protein (e.g., an enzyme), triggering a response → G protein hydrolyzes its GTP to GDP and turns itself off.
The G protein acts as a molecular on/off switch; GPCR pathways are involved in vision, smell, and many hormone responses.
How do receptor tyrosine kinases (RTKs) work?
Answer: Ligand binding causes two RTK monomers to dimerize; their cytoplasmic tyrosine residues then autophosphorylate; the phosphorylated tyrosines serve as docking sites that activate multiple relay proteins, triggering several transduction pathways at once.
Because one activated RTK can trigger multiple pathways simultaneously, RTK malfunction (e.g., overexpression) is strongly linked to cancer.
What is a ligand-gated ion channel receptor?
Answer: A membrane receptor that opens or closes a channel to allow or block the flow of specific ions (e.g., Na+, Ca2+) when a ligand binds, changing ion concentration inside the cell and triggering a response.
Example: neurotransmitter receptors at a synapse that open Na+ channels, depolarizing the postsynaptic neuron.
Where are intracellular receptors located, and what kind of ligands use them?
Answer: In the cytoplasm or nucleus; they are bound by small, hydrophobic ligands that can diffuse across the plasma membrane, such as steroid hormones (e.g., testosterone, estrogen) and nitric oxide.
The ligand-receptor complex often acts directly as a transcription factor, binding DNA and regulating gene expression.
Define second messenger and give examples.
Answer: A small, nonprotein, water-soluble molecule or ion that relays and amplifies a signal within the cell after receptor activation. Examples: cyclic AMP (cAMP), calcium ions (Ca2+), IP3, and DAG.
Second messengers rapidly diffuse through the cytosol, allowing one receptor activation event to affect many target molecules.
How is cAMP produced and what does it do downstream?
Answer: An activated G protein stimulates adenylyl cyclase, which converts ATP into cyclic AMP (cAMP); cAMP then activates protein kinase A (PKA), which phosphorylates various target proteins to produce the cellular response.
Example: epinephrine binding a GPCR raises cAMP, activating PKA to trigger glycogen breakdown in liver cells.
How does the Ca2+/IP3/DAG second-messenger pathway work?
Answer: Activated phospholipase C cleaves membrane PIP2 into IP3 and DAG; IP3 diffuses to the ER and opens Ca2+ channels, releasing Ca2+ into the cytosol; Ca2+ (with DAG) activates protein kinase C and other Ca2+-sensitive proteins, producing the cellular response.
This pathway is often triggered downstream of GPCR or RTK activation and allows cross-talk between pathways.
What is a phosphorylation cascade and why does it amplify a signal?
Answer: A sequential series of protein kinases, each activating the next by phosphorylation, that relays and amplifies a signal from the receptor to the final cellular response; because each activated kinase can phosphorylate many downstream molecules, the original signal is greatly amplified.
A single ligand-receptor binding event can ultimately activate thousands of target molecules through this cascade effect.
What is the difference between a protein kinase and a protein phosphatase?
Answer: Protein kinases add a phosphate group to a protein (usually from ATP), activating or deactivating it; protein phosphatases remove phosphate groups, reversing the kinase's effect and turning the pathway off.
The balance of kinase and phosphatase activity allows pathways to be switched on and off as needed.
What is a negative feedback loop? Give a biological example.
Answer: A response that reduces or shuts down the original stimulus, helping maintain homeostasis.
Example: rising blood glucose triggers insulin release, which lowers blood glucose; as glucose falls, insulin secretion decreases.
What is a positive feedback loop? Give a biological example.
Answer: A response that amplifies or reinforces the original stimulus, pushing the system further in the same direction until a specific endpoint is reached.
Example: during childbirth, oxytocin stimulates uterine contractions, which stimulate more oxytocin release, intensifying contractions until the baby is born. Another example: the blood clotting cascade.
What are the phases of the cell cycle, in order?
Answer: Interphase (G1 → S → G2), followed by the Mitotic (M) phase, which includes mitosis and cytokinesis.
G1: cell growth and normal functions; S: DNA replication, each chromosome duplicated into two sister chromatids; G2: further growth and preparation for mitosis.
What is the G0 phase?
Answer: A non-dividing, resting state in which cells have exited the cell cycle, either temporarily or permanently.
Example: most mature neurons and muscle cells remain in G0 permanently and do not divide.
What are the three major cell cycle checkpoints?
Answer: The G1 checkpoint (restriction point), the G2 checkpoint, and the M (spindle assembly) checkpoint.
At each checkpoint, regulatory proteins check whether conditions are right for the cell cycle to continue.
What is checked at the G1 checkpoint, and why is it significant?
Answer: Cell size, nutrient availability, growth factor signals, and DNA integrity are checked; it determines whether the cell proceeds into S phase or enters G0.
Known as the 'restriction point' because once a cell passes it, the cell is committed to completing the cycle and dividing.
What is checked at the G2 checkpoint?
Answer: Whether DNA replication was completed accurately and whether any DNA damage is present, before the cell is allowed to enter mitosis.
If damage is detected, the cycle halts to allow repair or triggers apoptosis if damage is irreparable.
What is checked at the M (spindle assembly) checkpoint?
Answer: That all chromosomes are properly attached to spindle fibers at the metaphase plate before the cell is allowed to proceed into anaphase.
Prevents unequal distribution of chromosomes (aneuploidy) in daughter cells.
What are cyclins and CDKs, and how do they interact?
Answer: Cyclins are regulatory proteins whose concentrations rise and fall cyclically through the cell cycle; CDKs (cyclin-dependent kinases) are enzymes that are only active when bound to a specific cyclin. The cyclin-CDK complex phosphorylates target proteins to drive the cell cycle forward.
Cyclin levels rise through interphase as they are synthesized and fall sharply after mitosis begins, as they are tagged with ubiquitin and degraded by the proteasome.
What is MPF (maturation-promoting factor)?
Answer: The complex of cyclin B and Cdk1 that triggers the cell's transition from G2 into mitosis.
MPF phosphorylates proteins such as nuclear lamins, causing nuclear envelope breakdown, and promotes chromosome condensation.
List the stages of mitosis in order.
Answer: Prophase, Prometaphase, Metaphase, Anaphase, Telophase (mnemonic: PPMAT).
Mitosis is followed by cytokinesis, which divides the cytoplasm into two daughter cells.
What happens during prophase?
Answer: Chromatin condenses into visible chromosomes (each consisting of two sister chromatids); the mitotic spindle begins to form from the centrosomes; the nucleolus disappears.
The nuclear envelope is still intact at this stage.
What happens during prometaphase?
Answer: The nuclear envelope fragments, and spindle microtubules attach to the kinetochores at each chromosome's centromere.
Some microtubules attach to chromosomes while others interact with microtubules from the opposite pole.
What happens during metaphase?
Answer: All chromosomes line up at the metaphase plate (the cell's equator), each attached to spindle fibers from opposite poles.
This alignment is checked by the M (spindle assembly) checkpoint before anaphase can begin.
What happens during anaphase?
Answer: Sister chromatids separate at the centromere and are pulled by shortening spindle fibers toward opposite poles of the cell.
Once separated, each chromatid is considered its own chromosome.
What happens during telophase?
Answer: Chromosomes arrive at opposite poles and decondense back into chromatin; nuclear envelopes re-form around each set of chromosomes, producing two nuclei within one cell.
Telophase typically overlaps with the start of cytokinesis.
What is cytokinesis?
Answer: The division of the cytoplasm that produces two separate daughter cells; it typically begins during telophase.
Cytokinesis completes the cell division process started by mitosis.
How does cytokinesis differ between animal and plant cells?
Answer: Animal cells form a cleavage furrow — a contractile ring of actin filaments that pinches the cell into two; plant cells build a cell plate from Golgi-derived vesicles that fuses to form a new cell wall separating the daughter cells.
Plant cells cannot form a cleavage furrow because of their rigid cell wall.
What is apoptosis?
Answer: Programmed cell death — a genetically controlled process in which a cell destroys itself in an orderly fashion.
Important in normal development (e.g., removing webbing between fingers) and in eliminating damaged, infected, or potentially cancerous cells.
What are the hallmark cellular changes during apoptosis?
Answer: Cell shrinkage, chromatin condensation, membrane blebbing, DNA fragmentation, and formation of apoptotic bodies that are engulfed by phagocytes.
Unlike necrosis, apoptosis does not spill cellular contents and therefore does not cause inflammation.
What is cancer at the cellular level, and which gene categories are most often implicated?
Answer: Cancer results from uncontrolled cell division caused by mutations in genes that regulate the cell cycle — especially proto-oncogenes and tumor suppressor genes.
Multiple mutations typically must accumulate in a single cell line for cancer to develop.
Distinguish a proto-oncogene from an oncogene.
Answer: A proto-oncogene is a normal gene that promotes cell division; when mutated or overexpressed, it becomes an oncogene, which causes excessive, uncontrolled cell division.
Think of proto-oncogenes as a 'gas pedal' that gets stuck down once mutated into an oncogene.
What is a tumor suppressor gene, and what is a key example?
Answer: A gene that normally inhibits cell division or promotes DNA repair/apoptosis; loss of its function removes this 'brake' on the cell cycle, contributing to cancer. Example: p53, the 'guardian of the genome.'
p53 halts the cell cycle to allow DNA repair, or triggers apoptosis if the damage is irreparable; it is mutated in the majority of human cancers.
What is the difference between a benign and a malignant tumor?
Answer: A benign tumor remains localized and does not invade surrounding tissue; a malignant tumor invades nearby tissues and can metastasize (spread) to other parts of the body via the blood or lymphatic system.
Cancer cells in malignant tumors often lose contact inhibition and anchorage dependence, allowing them to grow and spread uncontrollably.
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