Unit 4 Notes

Cell Communication
Unit 3 Notes
Intercellular Signaling—Local
• Cell Junctions—signaling substances in cytosol pass
freely between cells
o Gap Junctions in Animals
o Plasmodesmata in Plants
• Cell-Cell Interaction—
interaction between
molecules that portrude
from cell surface (animals)
o Important in embryonic
development and immune responses
Intercellular Signaling—Local
• Local Regulators—cell secretes a local regulator
molecule which acts on specific nearby target cells
o Paracrine Signaling—regulators (i.e. growth factors) are released into
extracellular fluid)
o Synaptic Signaling—neurotransmitters are released into synapse
Intercellular Signaling—Long Distance
• Hormones—molecules used in plants and animals
for long-distance signaling
o Animals = Endocrine Signaling—hormones move through circulatory
o Plants = Plant Growth Regulators—move through vessels or (more
commonly) diffuse through cells or air
Intercellular Signaling—Long Distance
• Nervous System in Animals—uses a combination of
electrical and chemical signals to send a message
Intracellular Signaling
• Three Major Parts—
o Reception
o Transduction
o Response
• Signaling molecule binds to a receptor protein,
causing it to change shape
o Ligand—molecule that specifically binds to another
molecule (messenger molecule)
• Two Major Types of Receptors
o Plasma Membrane Receptors
o Intracellular Receptors
• Plasma Membrane Receptors—transmembrane
proteins transmit information into the cell by
changing shape or aggregating
o G-Protein-Coupled Receptor—works with the help of a G
o Receptor Tyrosine Kinases—attach phosphates to tyrosines
(amino acid)…leading to activation of proteins
o Ligand-Gated Ion Channels—ligand binds to gated
channel protein and opens gate to let in ions, i.e., Na+,
G-Protein-Coupled Receptors
Tyrosine-Kinase Receptors
• Intracellular Receptors—chemical messengers
(small & hydrophobic) enter cell and bind to a
receptor in the cytoplasm or nucleus
o Testosterone—small steroid hormone
• Activates receptor protein in cytoplasm of target cell by
binding to it
• Activated receptor protein (with attached
testosterone) enters nucleus and turns on specific
genes that control male sex characteristics =
transcription factor (proteins that control which genes
are on and off)
• Cascades of molecular interactions relay signal
from receptors to target molecules
• Information is relayed by shape changes of proteins
• Ex: Protein Phosphorylation & Dephosphorylation
o Protein Kinases—enzymes that transfer phosphate groups
from ATP to a protein (usually activating the protein)
o Protein Phosphatases—enzymes that remove phosphate
groups from proteins (usually deactivating protein and so
turn off pathway)
Phosphorylation Cascade
• Second Messengers—non-protein, water-soluble
molecules or ions that can pass signal to proteins
(1st Messengers are the original ligands)
• Involved in pathways started by G-protein-linked
receptors and receptor tyrosine kinases
• Most common second messengers:
o Cyclic AMP (cAMP)
o Ca2+
• Cyclic AMP (cAMP)
o Adenylyl cyclase converts ATP to cAMP
o cAMP activates a protein kinase
• Ca2+--increase in Ca2+ leads to many responses in
plants and animals
o [Ca2+] in blood and extracellular fluid is often 10,000x greater than
in cell
o Ca2+ is actively transported out of the cell and into ER
o Another molecule, inositol trisphosphate (IP3) stimulates release of
• Cell Signaling leads to regulation of transcription of
cytoplasmic pathways
o Response may be the regulation of protein synthesis by
turning specific genes on or off
o Response may be the regulation of a protein’s activity
Nuclear Response
Cytoplasmic Response
Fine-Tuning Responses
• Signal Amplification
o Number of activated products increases at each catalytic
step of a cascade because enzymes are active long
enough to catalyze many reactions
o Consequence = small number of ligands can lead to large
• Specificity of Cell Signaling and Coordination of
o Specific types of cells have specific receptors, relay
proteins, and/or proteins needed for a response to occur
Fine-Tuning Responses
Signal is
unique to
types of cells.
Fine-Tuning Responses
• Scaffolding Proteins & Signaling Complexes
o Scaffolding Proteins—large relay proteins that other relay proteins
attach to simultaneously
o Same proteins can be involved in multiple pathways
• Termination of the Signal
o Proteins must be inactivated
Cell Cycle
Life of a cell from origin through division.
Cell Cycle Phases
Mitosis and Interphase
Mitosis (M Phase)
Mitosis—Division of the Nucleus
Cytokinesis—Division of the cytoplasm
Mitosis + Cytokinesis = ~10% of Cell Cycle
Mitosis Phases
Mitosis (M Phase)
• Mitosis allows cell to go
from 4n  2n
• Produces somatic cells
• Does not produce
gametes (1n)
• Interphase—phase in which the cell grows,
metabolizes, and copies DNA
• Interphase = ~90% of Cell Cycle
• Split up into 3 smaller phases
o Gap 1 Phase (G1)—Takes up ~35% of Interphase
• Growth
• Cell is 2n
o Synthesis Phase (S)—Takes up ~35% of Interphase
• DNA Replication occurs
• Cell goes from 2n  4n
o Gap 2 Phase (G2)—Takes up ~ 30% of Interphase
• More Growth—Particularly molecules for division
• Cell is 4n
Phases of Mitosis
Objective 11
Animal Cell
Phases of Mitosis
• Prophase
o Chromatin condenses into chromosomes (made of sister chromatids
attached at centromere)
o Microtubules form
o Centrioles/Centrosomes move to poles
Phases of Mitosis
• Metaphase
o Microtubules attach to the kinetochores of each sister chromatid
o Chromosomes line up along the metaphase plate
Phases of Mitosis
• Anaphase
o Sister Chromatids split and move to poles
Phases of Mitosis
• Telophase
o New nuclei form
o Microtubules degrade
o Cytokinesis occurs
Phases of Mitosis
Plant Cell
Reproduction in
Prokaryotic Cells
DNA, Binary Fission & Budding
Objective 14
Bacterial DNA
• One loop of DNA attached to Cell Membrane
o Still highly folded to fit into cell
o Only one set of genes (not one from “mom” and one from “dad” like in
• May contain 1 or more Plasmids
o Tiny loops of extra DNA that are able to move from 1 bacteria to another
o Allows for recombination = advantage!
Binary Fission
• Asexual Reproduction of most Prokaryotes
• Basic Steps:
o DNA Replication—unzips to copy
o Cell Pinches
• New cells should be clones
o No genetic recombination
o Only variation through mutations
• Rate = divides as fast as
every 20 minutes
• Some prokaryotes reproduce in this manner—
Asexual Reproduction
• Basic Steps
o Cell Develops a bulge or bud
o DNA copies
o Bud Breaks Off
Listeria monocytogenes
Control of Cell Cycle
Checkpoints & Regulatory Proteins/Conditions
Objective 12
Check Points
• Between G1 and S
o Go ahead signal from the environment is needed (i.e. growth factors from
other cells)
o Then…there are checks for enough mass and the condition of the DNA
o If there is no signal…cell goes to G0 (non-dividing state)
• Most cells in G0 never divide (i.e. nerve/muscle) or they only divide if
there is an injury
• Between G2 and M
o Checks for mass and correct DNA replication
o If all okay…cell commits to divide
• Note: Cancer often occurs because cell is quickly
pushed from G1  S without proper checks
• Regulatory Proteins/Enzymes
o Cyclin-Dependent Kinase (Cdk)—enzymes needed to drive the cell cycle
• Cyclin-Dependent Kinase (enzyme that activates or deactivates other
molecules by phosphorylation) only works when activated by cyclin—
a protein that rises and falls in the cell cycle
o Example: Maturation Promoting Factor (MPF)—
• Cyclin increase in concentration in G2 and bind with a specific Cdk to
form MPF
• MPF signals the start of Mitosis
• At end of mitosis, enzymes break down cyclin…so no MPF…and no
more dividing (Cdk concentration remains the same)
• Other internal signals
o Kinetochores must be attached before anaphase can occur—
unattached kinetochores send a signal to stop sister chromatids from
• External Signals
o Growth Factors—proteins released by certain cells that stimulates other
cells to divide
o Density-Dependent Inhibition—Crowded cells stop dividing because there
aren’t enough growth factors and nutrients for it to divide
o Anchorage-Dependence—If cells aren’t attached to the extracellular
matrix, they do not get growth factors—so don’t divide
Cancer and the Cell Cycle
Objective 13—Define cancer and explain how aberrations in
the cell cycle can lead to tumor formation.
• Complex collection of diseases that can arise in
almost any tissue in the body.
• All cancers arise as a result of the loss of cell cycle
Cytotoxic T Cell Attacking a
Cancer Cell
Cancer Cell
• Uncontrolled growth
• Lack of response to stop signals
• Immortality
• Ability to divide infinitely
• Recruits food supplies (angiogenesis)
• Random migration
Cancer Cell
Benign versus Malignant
Benign (not cancer)
Malignant (cancer) cells
tumor cells grow
invade neighboring tissues,
only locally and
enter blood vessels, and
cannot spread by
metastasize to different
invasion or metastasis
Benign (not cancer)sites
tumor cells grow
only locally and cannot spread by invasion
or metastasis
Cancer-Related Genes
• Stability Genes—code for proteins that keep
genetic alterations to a minimum
o If mutated, mutation rates increase
• Oncogenes—code for proteins that promote cell
o If mutated to be overly active = cancer
• Tumor Suppressor Genes—code for proteins that
inhibit cell from progressing from G1S
o If mutated to be underactive = cancer
o Example TP53 codes for p53 protein = transcription factor that normally
inhibits cell growth and stimulates cell death when induced by cellular
Check Points

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