Cell Communication & Cell Cycle: every key term you need (+ practice quiz)
64 flashcard terms for AP Biology Unit 4, written to match the course framework. Study them here, then drill them as interactive flashcards, or test yourself with the 20-question quiz — free, no account needed.
The process by which cells send, receive, and respond to signals, coordinating activity across tissues and the whole organism.
Signal Transduction Pathway
The sequence of molecular steps — reception, transduction, response — that converts an extracellular signal into a cellular action.
Ligand
A signaling molecule (hormone, growth factor, neurotransmitter) that binds specifically to a receptor to trigger a response.
Reception
The first stage of cell signaling: a signal molecule (ligand) binds to a specific receptor protein, whose shape matches the ligand.
Receptor Specificity
A receptor binds only ligands whose shape complements its binding site — another example of structure determining function.
Transduction
The stage where receptor binding triggers a series of relay molecules (often a phosphorylation cascade) that convert and amplify the signal inside the cell.
Response
The final stage of a signaling pathway: a specific cellular change — gene transcription, enzyme activation, cytoskeletal rearrangement, or another action.
Signal Amplification
Each step of a cascade can activate multiple downstream molecules, so one signal molecule can ultimately affect thousands of target molecules.
Local Signaling — Paracrine
A cell secretes signals that diffuse a short distance to affect nearby cells (e.g., growth factors during tissue repair).
Local Signaling — Synaptic
A neuron releases neurotransmitters directly across a synapse to a neighboring cell — fast, short-range communication.
Long-Distance Signaling — Endocrine
Specialized cells secrete hormones into the bloodstream, which carries them throughout the body to distant target cells.
Autocrine Signaling
A cell secretes a signal that also binds receptors on itself, reinforcing its own behavior (common in immune cells and cancer).
Cell-Surface Receptor
A membrane protein that binds a ligand unable to cross the membrane (e.g., peptide hormones), transmitting the signal without the ligand entering the cell.
G-Protein-Coupled Receptor (GPCR)
A common cell-surface receptor that, once activated by a ligand, switches on a G protein inside the cell to relay the signal.
Receptor Tyrosine Kinase (RTK)
A cell-surface receptor that, upon ligand binding, dimerizes and phosphorylates itself, activating multiple signaling pathways at once.
Ion Channel Receptor
A receptor that opens or closes to let specific ions flow across the membrane in response to a ligand, rapidly changing the cell's electrical state.
Intracellular Receptor
A receptor located inside the cell (cytoplasm or nucleus) that binds small, hydrophobic ligands (like steroid hormones) able to cross the membrane directly.
Second Messenger
A small, diffusible molecule (e.g., cAMP, Ca²⁺) generated inside the cell that relays and amplifies a signal from the receptor to downstream targets.
cAMP (Cyclic AMP)
A common second messenger produced from ATP by adenylyl cyclase, often activated via a GPCR pathway, that triggers further steps in a cascade.
Phosphorylation Cascade
A chain of protein kinases that each activate the next by adding a phosphate group, amplifying and relaying a signal (common in transduction).
Protein Kinase
An enzyme that adds a phosphate group to another protein (often activating or inactivating it), central to most transduction pathways.
Protein Phosphatase
An enzyme that removes a phosphate group from a protein, reversing a kinase's action and turning a pathway off.
Signal Termination
Pathways must be shut off (ligand degradation, receptor internalization, phosphatases) to allow the cell to respond to new signals appropriately.
Apoptosis
Programmed cell death — a genetically controlled, orderly process that eliminates damaged, unneeded, or potentially dangerous cells without harming neighbors.
Apoptosis Signaling
Internal or external signals can trigger a caspase cascade that dismantles the cell in an organized way, distinct from uncontrolled cell death.
Why Apoptosis Matters
It sculpts development (e.g., removing webbing between fingers), eliminates infected or cancerous cells, and maintains tissue balance.
Cell Cycle
The ordered sequence of growth and division a cell undergoes: interphase (G1, S, G2) followed by the mitotic phase (mitosis and cytokinesis).
Interphase
The longest part of the cell cycle, when the cell grows and copies its DNA; divided into G1, S, and G2 phases. No visible division occurs.
G1 Phase
'Gap 1' — the cell grows, carries out normal functions, and produces organelles and proteins in preparation for DNA replication.
S Phase
'Synthesis' — the cell replicates its entire DNA content, so each chromosome now consists of two identical sister chromatids.
G2 Phase
'Gap 2' — the cell continues growing and produces proteins needed for mitosis, checking that DNA replication is complete and undamaged.
Mitotic (M) Phase
The phase in which the replicated chromosomes are divided into two nuclei (mitosis) and the cytoplasm splits (cytokinesis), producing two cells.
Prophase
Chromosomes condense and become visible; the mitotic spindle begins to form; the nuclear envelope starts breaking down.
Metaphase
Chromosomes, each with two sister chromatids, line up along the cell's equator (metaphase plate), attached to spindle fibers from opposite poles.
Anaphase
Sister chromatids separate and are pulled by spindle fibers to opposite poles of the cell — ensuring each daughter cell gets one full copy.
Telophase
Chromosomes arrive at the poles and decondense; two new nuclear envelopes re-form, marking the end of nuclear division.
Cytokinesis
Division of the cytoplasm, completing the split into two daughter cells. In animals, a cleavage furrow pinches the cell in two; in plants, a cell plate forms.
Sister Chromatids
Two identical copies of a chromosome, produced by DNA replication in S phase, joined at the centromere until anaphase separates them.
Centromere
The region where sister chromatids are held together and where spindle fibers attach via the kinetochore.
Mitotic Spindle
A structure of microtubules, organized from centrosomes, that moves and separates chromosomes during mitosis.
Cell Cycle Checkpoints
Internal surveillance points (G1, G2, and M checkpoints) that verify conditions are correct before the cycle proceeds — a key regulatory safeguard.
G1 Checkpoint (Restriction Point)
Checks cell size, nutrients, and DNA integrity before committing to DNA replication; the main decision point for whether to divide.
G2 Checkpoint
Verifies that DNA replication is complete and undamaged before the cell enters mitosis.
M (Spindle) Checkpoint
Ensures all chromosomes are properly attached to spindle fibers before anaphase begins, preventing unequal chromosome distribution.
Cyclins and Cdks
Cyclin-dependent kinases (Cdks) are enzymes activated by binding cyclin proteins; their rising and falling levels drive the cell through checkpoints.
Cyclin-Cdk Complex
Cyclin concentrations rise and fall through the cycle, and only when bound to the right cyclin does a Cdk become active and trigger the next phase.
Growth Factors
External signaling proteins that bind receptors (often RTKs) to stimulate cells to pass the G1 checkpoint and divide.
Density-Dependent Inhibition
Normal cells stop dividing once they contact neighboring cells and physical space is limited — a contact-based control on growth.
Anchorage Dependence
Normal cells require attachment to a surface (extracellular matrix) to divide; unattached cells typically stop the cycle.
Loss of Cell Cycle Control
Cancer cells ignore density-dependent inhibition and anchorage dependence, dividing uncontrollably and forming tumors.
Proto-Oncogene
A normal gene that promotes cell division (e.g., encoding growth factors or receptors); mutation can turn it into a cancer-causing oncogene.
Oncogene
A mutated or overexpressed proto-oncogene that drives excessive, unregulated cell division — a gain-of-function cancer mutation.
Tumor Suppressor Gene
A gene (like p53) that normally restrains cell division or triggers apoptosis of damaged cells; its loss-of-function allows uncontrolled growth.
p53
A key tumor suppressor protein that detects DNA damage and halts the cell cycle for repair or triggers apoptosis if damage is irreparable — 'guardian of the genome.'
Two-Hit Hypothesis
Cancer typically requires mutations in both copies (alleles) of a tumor suppressor gene, since one working copy is often enough to maintain control.
Metastasis
The spread of cancer cells from their original site to other parts of the body via blood or lymph, forming secondary tumors.
Benign vs. Malignant Tumors
Benign tumors grow but stay localized; malignant tumors invade surrounding tissue and can metastasize — the defining feature of cancer.
Carcinogens
Agents (chemicals, radiation, viruses) that increase the likelihood of mutations leading to cancer by damaging DNA or disrupting cell cycle control.
Cell Cycle Regulation and Cancer
Cancer is fundamentally a disease of cell cycle dysregulation — loss of checkpoint control, unchecked cyclin-Cdk activity, and evasion of apoptosis.
Quorum Sensing (Bacterial Signaling)
Bacteria release and detect signaling molecules to sense population density and coordinate collective behaviors like biofilm formation.
Yeast Mating Signaling
Yeast cells release mating-type-specific peptides that bind GPCRs on potential partners — an evolutionarily conserved example of signal transduction.
Evolutionary Conservation of Signaling
Core signaling components (GPCRs, kinases, second messengers) are shared across yeast, plants, and animals, indicating deep evolutionary origin.
Feedback in Cell Signaling
Cells often use negative feedback (shutting off a pathway once the response occurs) to keep signaling responses appropriately timed and sized.
Structure-Function Theme in Signaling
Every step — receptor shape, kinase active sites, ligand structure — again illustrates that molecular structure enables specific function.