Download Homeostasis notes - Lincoln Park High School

(1/15) Bellringer: Homeostasis
1. Define homeostasis.
2. Propose a role for each of the following in maintaining
homeostasis:
a. Receptor
b. Integrator
c. Effector
Copyright © 2010 Pearson Education, Inc.
(1/15) Partner BR:
Fight-or-flight
1. What is the ligand?
2. What type of receptor
does it bind?
3. What is the second
messenger?
4. How does protein kinase
A distribute the signal?
5. Which enzyme breaks
down glycogen?
6. What is the cellular
response?
7. How is this pathway an
example of amplification?
Copyright © 2010 Pearson Education, Inc.
29.1: Multicellular animals require a stable internal
environment
• Homeostasis: all body systems working together to maintain a
stable internal environment
• Regulatory systems consist of:
1. Receptor – receives stimulus & transmits sensory info
to spinal cord & brain (central nervous system)
– chemoreceptors, photoreceptors, thermoreceptors,
& touch/pressure receptors
2. Integrator – processes sensory info & determines
response
– Brain sends out motor commands
3. Effector – carries out response
– Muscles, organs, & glands
Copyright © 2010 Pearson Education, Inc.
Feedback Loop
Copyright © 2010 Pearson Education, Inc.
29.2: Physiological regulation achieves homeostasis of
the internal environment
• Negative feedback: variation triggers response that corrects
situation
– response of effector negates stimulus, restoring
homeostasis
– The nervous & endocrine (hormones) systems operate
thru negative feedback
• Positive Feedback: response of the effector reinforces the
change caused by the stimulus, moving the body away from
homeostasis temporarily until the desired response is carried
out
– Ex: blood clotting process, childbirth
Copyright © 2010 Pearson Education, Inc.
Negative Feedback
Copyright © 2010 Pearson Education, Inc.
Positive Feedback: thrombin
activation starts a positive feedback
loop that leads to more thrombin
formation from prothrombin; the
ultimate response is fibrin formation
to clot the break in the blood vessel
Copyright © 2010 Pearson Education, Inc.
Negative Feedback:
Hormonal control
(CH 30)
• Blood calcium levels are
regulated by 2
hormones: calcitonin &
parathyroid hormone
• Calcitonin is released
by the thyroid when
calcium levels are high,
moving calcium into
bones & increasing
calcium loss at the
kidney
• Parathyroid hormone is
released when levels are
low, adding calcium to
the blood
Copyright © 2010 Pearson Education, Inc.
Negative Feedback:
Hormonal control
• Blood glucose levels are
regulated by 2 pancreas
hormones: insulin &
glucagon
• Insulin is released when
glucose levels are high,
moving glucose out of
the blood and into cells
• Glucagon is released
when levels are low,
adding glucose to the
blood from glycogen
stores in the liver and
muscle
Copyright © 2010 Pearson Education, Inc.
Cell Communication Poster Project Topics
Research topics
Toxin (1)
Poison dart frog, Marine Cone Snails
Plant (2)
Phototropism (auxin), Ripening (ethylene)
Immune
(1)
Drug (1)
B-lymphocytes, T- lymphocytes
Heroin, Ecstasy
Human (1) Vision
Bacteria
(1)
Disease (1)
Clostridium botulinum neurotoxin (botulism)
Diabetes/Insulin (healthy and faulty), Parkinson’s and calcium
channels (healthy and faulty)
Copyright © 2010 Pearson Education, Inc.
(1/19) BR
1. What is a neurotransmitter?
2. Why are reflex reactions so FAST?
Copyright © 2010 Pearson Education, Inc.
CH 34: Neurons & Nervous Systems
• Neurons respond rapidly to stimuli to maintain homeostasis
A. Types & functions
1. Sensory neurons: receive stimuli & transmit info to CNS
2. Interneurons in brain & spinal cord process sensory info
3. Motor neurons: deliver commands from CNS to effector
cells
B. Structure
• Dendrites – antenna-like extensions that receive stimuli
from the environment or another neuron
• Cell body (soma) – contains nucleus & organelles
• Axon – carries outgoing signals called action potentials
• Synaptic terminals – ends of axons where neurons
communicate with effector cells
Copyright © 2010 Pearson Education, Inc.
1. Label the cell body, axon,
dendrites, synaptic terminals,
and effector on your neuron
diagram.
2. Draw a line that shows the
direction in which information
travels along a neuron.
Copyright © 2010 Pearson Education, Inc.
Structural Neurons
1. Multipolar neuron:
•
Most common neuron in
brain & spinal cord
•
All motor neurons that
synapse at skeletal muscles
2. Unipolar neurons:
•
Sensory neurons of
peripheral nerves
3. Bipolar neurons:
•
Special sense organs (sight,
smell, hearing)
Copyright © 2010 Pearson Education, Inc.
Reflexes
• Reflex: automatic response to stimulus that bypasses the brain
– Reflex arc: response opposes original stimulus
1. Stimulus activates sensory neuron
2. Integration by interneuron in spinal cord
3. Motor neuron carries command
4. Effector response
Copyright © 2010 Pearson Education, Inc.
Figure 8-28
Copyright © 2010 Pearson Education, Inc.
A Flexor Reflex
Figure 8-30
Copyright © 2010 Pearson Education, Inc.
Stretch Reflex
Figure 8-29
Copyright © 2010 Pearson Education, Inc.
Membrane Potential
• Membrane Potential – charge difference on either side of the
plasma membrane
– Resting Potential of neuron is negative (-70mV) because
of Na+ / K+ pump
• Uses ATP to actively transport 3 Na+ out and 2 K+ in
Copyright © 2010 Pearson Education, Inc.
Figure 34.5 Ion Transporters and Channels (Part 1)
Na+–K+ pump (ATPase)
Outside of cell
Sodium–
potassium pump
3 Na+
2 K+
ATP
ATP
Pi
K+
Inside of cell
Copyright © 2010 Pearson Education, Inc.
ADP
Na+
K+
Pi
Figure 34.5 Ion Transporters and Channels (Part 2)
Na+–K+ channels
Outside of cell
Leak K+
channel
Voltage-gated
K+ channel
Closed
Closed
Open
Inside of cell
Copyright © 2010 Pearson Education, Inc.
Voltage-gated
Na+ channel
Open
3. Analyze the
graph to define
depolarization and
repolarization.
Copyright © 2010 Pearson Education, Inc.
Action Potential
• Action Potential: an electrical impulse sent by a neuron down
its axon
– occurs when a stimulus causes a neuron to depolarize
(become less negative) to threshold (-60mV)
– All-or-none principle: if an action potential begins, it will
occur at the same magnitude every time; there is no
variation in the size/strength of an action potential
– 4 steps:
Copyright © 2010 Pearson Education, Inc.
1. Stimulus causes a depolarization to threshold
Copyright © 2010 Pearson Education, Inc.
2. Voltage-gated channels open, & Na+ rushes into the cell,
causing further depolarization
Copyright © 2010 Pearson Education, Inc.
3. Na+ channels close & K+ voltage-gated channels open
• K+ rushes out, repolarizing the cell
Copyright © 2010 Pearson Education, Inc.
4. Resting membrane potential (-70mV) restored
Copyright © 2010 Pearson Education, Inc.
Figure 34.7 The Course of an Action Potential (Part 2)
Resting
potential
Threshold
Resting membrane
potential restored
Undershoot
Outside of cell
Voltage-gated
K+ channel
Voltage-gated
Na+ channels
K+ channel
Activation gate
Inactivation gate
Inside of cell
Copyright © 2010 Pearson Education, Inc.
Voltage-gated
Na+ channels open
Voltage-gated Na+
channels close &
K+ channels open
Action potentials travel much faster down axons insulated by
myelin (figure b). Draw and label myelin on your neuron.
Figure 8-9
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Myelin is shown in red below, insulating the axon. In
reality, the lipid-rich myelin has a glistening white look.
Copyright © 2010 Pearson Education, Inc.
Myelin-producing
Schwann cells
Site and
direction
of myelin
growth
Nodes of Ranvier
Nucleus of Schwann cell
(specialized glial cell)
Mitochondria
Axon
Copyright © 2010 Pearson Education, Inc.
Myelin is formed
by 2 types of glia
(support cells of
the nervous
system)
(1/20) BR: Rabies
The rabies virus infects the CNS through a mechanism called
retrograde flow. A bite from a rabid animal initially injects the virus
into peripheral tissues at the surface of the skin. With this in
mind, answer the following.
1.What type of neuron does the virus initially infect?
Copyright © 2010 Pearson Education, Inc.
Synapses
• Synapse – site where a neuron communicates w/
another cell
– Presynaptic neurons transmit action potentials to
postsynaptic neurons or effector cells (e.g., muscle
cells) by releasing neurotransmitters
• Neurotransmitters must bind to a specific receptor
on the postsynaptic cell to have an effect
– Can have an excitatory or inhibitory effect on
the postsynaptic cell depending on receptor
(e.g., epinephrine during fight-or-flight
response)
– effect also depends on balance of excitation/inhibition by
different neurotransmitters
Copyright © 2010 Pearson Education, Inc.
Synapses
• At a cholinergic synapse the neurotransmitter is
acetylcholine
1. Ca++ trigger the presynaptic neuron to release
acetylcholine (Ach) into the synaptic cleft
2. ACh binds to ligand-gated Na+ channels on the
postsynaptic membrane, causing depolarization as
Na+ enters the cell
3. Acetylcholinesterase breaks down ACh in the
synaptic cleft into acetate & choline which are
recycled back into the presynaptic cell
Copyright © 2010 Pearson Education, Inc.
Figure 8-11
Copyright © 2010 Pearson Education, Inc.
Figure 8-11
Copyright © 2010 Pearson Education, Inc.
Figure 8-11
Copyright © 2010 Pearson Education, Inc.
Figure 8-11
Copyright © 2010 Pearson Education, Inc.
Neuromuscular
Junction (synapse of a
neuron with a muscle cell)
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Thick filament
(made of myosin)
Thin filaments
(made of actin)
Thick filament
(made of myosin)
Copyright © 2010 Pearson Education, Inc.
At rest, the active sites
on actin molecules
are blocked by
tropomyosin, which is
held in place by
troponin.
An arriving action
potential triggers the
release of Ca2+ (a 2nd
messenger!) from the
smooth ER…
Ca2+ exposes active sites on actin molecules by
binding to troponin
Copyright © 2010 Pearson Education, Inc.
Myosin heads from thick filaments bind to actin
active sites forming cross-bridges
Myosin
head
Myosin
head
Copyright © 2010 Pearson Education, Inc.
Myosin heads all pivot towards the center of the muscle
fiber, pulling thin filaments inward & causing contraction
Figure 7-5
Copyright © 2010 Pearson Education, Inc.
ATP causes myosin heads to detach
Figure 7-5
Copyright © 2010 Pearson Education, Inc.
ATP is hydrolyzed, and myosin is
reactivated to bind to actin
Figure 7-5
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Exit
Tetrodotoxin is a neurotoxin in puffer fish that blocks
voltage-gated sodium channels in a neuron’s plasma
membrane from opening. What effect would this have on the
neuron’s function?
Action Potential animation
Copyright © 2010 Pearson Education, Inc.
(1/21) Bellringer: Action Potential review
1. Mark on the graph in
your notes when Na+
are entering the cell and
when K+ are leaving
the cell. Then describe
what is happening in
each of the 4 steps of
an action potential
detailed in the graph.
Copyright © 2010 Pearson Education, Inc.
(1/21) Bellringer
2. Nonspecific defenses (i.e, innate
immunity) protect the body by
responding to all possible pathogens the
same way (does not involve producing
antibodies to combat specific
pathogens). What are some of our
nonspecific defenses that protect us
from infection?
Copyright © 2010 Pearson Education, Inc.
TYPE OF CELL
FUNCTION
Basophils (I, A)
Release histamine; may promote
development of T cells
Eosinophils (A)
Kill antibody-coated parasites
Neutrophils (I)
Stimulate inflammation; engulf and
digest microorganisms
Mast cells (I)
Release histamine when damaged
Monocytes (I, A)
Develop into macrophages and
dendritic cells
Macrophages (I, A)
Engulf and digest microorganisms;
activate T cells
Dendritic cells (A)
Present antigens to T cells
B lymphocytes (A)
Differentiate to form antibodyproducing cells and memory cells
T lymphocytes (A)
Kill virus-infected cells; regulate
activities of other white blood cells
Natural killer cells (I) Attack and lyse virus-infected or
cancerous body cells
Copyright © 2010 Pearson Education, Inc.
• White Blood Cells
(leukocytes) defend the
body against pathogens
& abnormal cells
Phagocytes
Lymphocytes
LYMPHOPOIESIS:
lymphocytes formation
• T cells are Thymusdependent
• B cells complete their
development in the Bone
marrow
Copyright © 2010 Pearson Education, Inc.
Lymphoid
Anatomy
• Organs integral
to defense are
the lymph
nodes, thymus,
and spleen
Copyright © 2010 Pearson Education, Inc.
31.1 Animals use Innate and Adaptive Mechanisms to Defend
Themselves against Pathogens
• Innate immunity: nonspecific defenses do not distinguish 1
threat from another; they’re indiscriminate!
1. Physical Barriers – skin, mucus, lysozyme, stomach
acid
2. Phagocytes engulf pathogens thru endocytosis
(phagocytosis)
• Ex: Macrophages (also monocytes, neutrophils,
eosinophils)
3. Natural Killer (NK) cells (a type of lymphocyte) attack
cancer & virus-infected cells by detecting surface
proteins called antigens
Copyright © 2010 Pearson Education, Inc.
Phagocytosis
• Do not distinguish 1 threat from another; indiscriminate!
1. Physical Barriers – skin, mucus, stomach acid
2. Phagocytes
• Macrophages & other phagocytes (neutrophils,
eosinophils, microglia)
• Diapedesis – squeeze b/w endothelial cells
Phagocyte
• Chemotaxis
3. Immunological Surveillance
• NK cells attack foreign, abnormal (e.g., cancer), &
virus-infected cells by detecting surface proteins called
antigens (AG)
Yeast cell
Copyright © 2010 Pearson Education, Inc.
Nonspecific Defenses
4. Complement proteins – assist phagocytes, activate
inflammation, cause lysis of pathogens
5. Interferons – cytokines released by virus-infected cells
that trigger antiviral defenses in neighboring cells
(are these autocrine, paracrine, juxtacrine, or endocrine
signals?)
Copyright © 2010 Pearson Education, Inc.
(1/21) Bellringer
3. Infection or injury leads to INFLAMMATION. Explain
some of the familiar signs of inflammation (e.g., at a
wound on the surface of your skin).
Copyright © 2010 Pearson Education, Inc.
Nonspecific Defenses
6. Inflammation
– Mast cells release histamine & prostaglandins
– Capillary permeability increases, causing swelling
– Blood vessels dilate, increasing blood flow to the area
– temperature increases, increases enzyme reaction
rate (speeding recovery)
• May lead to fever
Copyright © 2010 Pearson Education, Inc.
The
Inflammatory
Response
Copyright © 2010 Pearson Education, Inc.
The Inflammatory Response
Copyright © 2010 Pearson Education, Inc.
Innate Immunity is
nonspecific
Copyright © 2010 Pearson Education, Inc.
(1/22) BR
1. Name 3 types of leukocytes (white blood cells) that
provide nonspecific defense (innate immunity) for the
human body, then explain the function of each.
Yeast cell
Copyright © 2010 Pearson Education, Inc.
Axon
Motor neuron
Presynaptic cell
(motor neuron)
Muscle fiber
Axon
terminal
Below is a diagram of a synapse
between a neuron and a muscle cell.
2.What is the ligand released from
the neuron?
3.What happens when the ligand
binds to a receptor on the
postsynaptic cell?
Acetylcholine
molecules in
vesicle
Na+
Action
potential
Ca2+
Synaptic cleft
Acetylcholine
receptor
Na+
Postsynaptic cell
(muscle cell)
Copyright © 2010 Pearson Education, Inc.
Adaptive Immunity
• Cellular immunity: T cells respond to antigens bound to
membrane receptors called MHC proteins
– Class I MHC display antigens on cancer or virus-infected
cells (say, “Hey! I’m foreign! Kill me!”)
– Class II MHC display antigens on antigen-presenting
cells like phagocytes (after phagocytosis) & B cells (say,
“Hey! There’s an intruder! Kill them all!”)
Copyright © 2010 Pearson Education, Inc.
Cell with
surface
antigen
Free
antigens
Phagocytosis
Antigenpresenting
cell
Antigen
presentation
on Class II
MHC
Helper
T cell
(TH)
Copyright © 2010 Pearson Education, Inc.
RECOGNITION
PHASE
Cytokine
release activates
other cells
Macrophages are antigenpresenting cells
When MHC proteins
display antigens to
activate helper T cells, is
it an example of
autocrine, paracrine,
endocrine, or juxtacrine
signaling?
Copyright © 2010 Pearson Education, Inc.
Cellular Immunity
a. Helper T Cells (TH) – activated by antigen-presenting
cells
• Stimulate B cells and cytotoxic T cells to divide
• Divide into:
– more TH cells
– Memory T cells (TM): kept on reserve (for
decades) in case of 2nd exposure
b. Cytotoxic T cells (TC) destroy cells with specific
antigen
c. Regulatory T cells (Treg) – suppress immune response
& mediate tolerance to self antigens
Copyright © 2010 Pearson Education, Inc.
Antigenpresenting
cell
Bind
RECOGNITION
PHASE
Helper
T cell
(TH)
Cytokines activate B cells &
cytotoxic T cells (TC)
TC cell
B cell
Cell with
surface
antigen
B cells
differentiate
into plasma
cells
TC cell
Antibodies
Cytokines
HUMORAL IMMUNITY
Copyright © 2010 Pearson Education, Inc.
CELULAR IMMUNITY
ACTIVATION
PHASE
EFFECTOR
PHASE
Humoral (antibody-mediated) Immunity
• Humoral (antibody) immunity: B cells produce
antibodies in response to antigens & pathogens in fluids
– Activated by TH cytokine secretion to divide &
differentiate into:
a. Plasma cells – secrete antibodies (i.e.,
immunoglobulins), proteins w/ specific antigenbinding sites
b. Memory B cells – become plasma cells upon 2nd
exposure to antigen
Copyright © 2010 Pearson Education, Inc.
Adaptive Immunity
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Figure 31.7 Immunoglobulin (antibody) structure
Antigenic
Antigendeterminants
binding site
Variable region
of heavy chain
Constant region
of heavy chain
Light
chain
Heavy chain
Disulfide bonds
Copyright © 2010 Pearson Education, Inc.
Antigen
Variable
region of
light chain
Constant
region of
light chain
Humoral Immunity
– Antibody(immunoglobulin) classes:
1. IgM – 1st antibodies to be released by B cells
2. IgG – 80% of antibodies – fight bacteria & viruses;
can cross placenta
3. IgA – in mucus, tears, saliva, breast milk
4. IgE – stimulates inflammation by binding to mast
cells
5. IgD – bind antigens to surface of B cells  involved
in B cell activation
Copyright © 2010 Pearson Education, Inc.
Figure 31.8 Heavy-Chain Genes
Genes encoding variable region
V1, V2…V~100
(variable)
genes
DNA 1 2 3 4…100
D1, D2…D~30
(diversity)
genes
1
Genes encoding constant region
J1, J2…J6
(joining)
genes
2…30
1…6
µ δ
γ3
γ1
γ2β γ2α ε
Cδ
J2
D3
V21
Copyright © 2010 Pearson Education, Inc.
Constant region
of protein
Variable region
of protein
α
Heavy-Chain Gene Recombination and RNA Splicing during B cell development
DNA rearrangement
Variable region
Constant region
V
D J segments
Embryonic
DNA
μ
VDJ joining
B cell DNA
V
Transcription and
RNA splicing
μ
D J
Transcription
Primary RNA transcript
μ
Splicing
mRNA
Translation
Each B cell’s genome
codes for a unique
immunoglobulin
Copyright © 2010 Pearson Education, Inc.
V
C segments
D J
μ
Light
chain
Heavy chain
δ
Cytokines
• Cytokines – local (paracrine) chemical signals
– Interleukins – most diverse & important cytokines
• ↑ T cell sensitivity & antibody production, enhance
nonspecific defenses (inflammation, chemotaxis,
phagocytosis, complement, etc.)
– Interferons
– Tumor necrosis factors – kill tumor cells & slow
tumor growth
– Phagocytic regulators – causes monocytes to
transform into macrophages
– Colony-stimulating factors – stimulate blood cell
production
Copyright © 2010 Pearson Education, Inc.
Exit
In adaptive immunity, antibodies are produced by B cells in
response to antigen exposure. Explain the graph below, then
propose an explanation for it.
Copyright © 2010 Pearson Education, Inc.
(1/25) BR: Adaptive Immunity
If your group did not turn in the Control of Blood Glucose
POGIL on Friday, get them out and review the last few
questions as a group!
1. What is an MHC receptor?
2. What is the role of an antigen-presenting cell?
3. Why are B & T cells referred to as being specific?
4. HIV depletes the body’s supply of helper T cells. Why
does this lead to AIDS (acquired immune deficiency
syndrome)?
Copyright © 2010 Pearson Education, Inc.
BR
5. What type of molecule is shown below?
6. On your note sheet, label the antigen, antigen-binding site,
variable regions, and constant regions on the diagram.
Copyright © 2010 Pearson Education, Inc.
Immunoglobulin (antibody) structure
Antigenbinding site
Variable region
of heavy chain
Constant region
of heavy chain
Antigen
Variable
region of
light chain
Constant
region of
light chain
Copyright © 2010 Pearson Education, Inc.
31.3 The Adaptive Immune Response is Specific
• Adaptive Immunity has 4 key features:
1. Specificity
2. Diversity
3. Tolerance (distinguishing self from nonself)
4. Memory
• Primary response – takes 1-2 weeks for peak
antibody levels
• Secondary response – much stronger, faster
response after subsequent encounters with a pathogen
Copyright © 2010 Pearson Education, Inc.
Immunological Memory
• Primary response – takes 1-2 weeks for peak AB levels
• Secondary response – Memory cells immediately
proliferate upon binding to the antigen, preventing illness
Copyright © 2010 Pearson Education, Inc.
Immune Disorders
• Immunological disorders
– Autoimmune Disorders: immune response targets
normal body cells (autoantibodies are made)
• Ex.: multiple sclerosis, rheumatoid arthritis, Type I
diabetes mellitus, Lupus, celiac disease
– Immunodeficiency: immune system does not develop
normally or is impaired
• AIDS (Acquired immunodeficiency syndrome) –
result of HIV (Human Immunodeficiency Virus) killing
TH
Copyright © 2010 Pearson Education, Inc.
Immune Disorders
– Allergies – inappropriate or excessive inflammatory
response to antigens
• Mast cells release histamine in response to allergens
– Anaphylaxis: mast cells throughout body affected
– shock may result from drop in blood pressure
Copyright © 2010 Pearson Education, Inc.
(1/25) BR: Adaptive Immunity
7. What is a vaccine? How do vaccines work?
Copyright © 2010 Pearson Education, Inc.
31.3 The Adaptive Immune Response is Specific
• Adaptive Immunity (Specific defenses)
A. Active immunity–results from the production of antibodies
• Natural: in response to natural exposure to antigens
• Induced: in response to vaccines, which are dead or
weakened pathogens that stimulate an immune
response
B. Passive immunity –transfer of antibodies from
mother to offspring across placenta or in breast milk
Copyright © 2010 Pearson Education, Inc.
Immunological Memory
Copyright © 2010 Pearson Education, Inc.
HIV slowly depletes the body of TH, and AIDS begins when
levels drop below a certain point. Opportunistic diseases are
usually the cause of death in AIDS patients.
Copyright © 2010 Pearson Education, Inc.
The course of an HIV infection
Copyright © 2010 Pearson Education, Inc.
Anti-HIV antibody
production takes
months to build, and
levels remain high
for years. When
levels drop due to
TH depletion, AIDS
sets in.
Copyright © 2010 Pearson Education, Inc.
Exit
1. HIV infects TH (helper T cells) by binding to the CD4 receptor on
the surface of the cells. A coreceptor called CCR5 works with CD4
receptors and is necessary for HIV to enter the TH. Some people
have TH with a CCR5 receptor that is smaller and does not make it
to the surface of the cells due to a genetic mutation. What effect do
you think this mutation has on people?
2. HIV tests measure the amount of
anti-HIV antibodies in the blood
(the purple line). If you test
negative for HIV, why should you
get another test 6-12 months later
to be sure?
Copyright © 2010 Pearson Education, Inc.
(1/26) BR: Review for Test
1. What is occurring at #1 in the diagram below? Name the 2 molecules.
2. What activates or opens the transport protein channel that allows the
secondary messengers to enter the cell? What type of diffusion is this?
Copyright © 2010 Pearson Education, Inc.
(1/26) BR
3. Give support for the claim that the cells located in the tip of the
plant shoot detect the light by comparing the results from treatment
group I with the results from group II and group III.
4. In groups IV and V, the tips of the plants are removed and placed
back onto the shoot on either a permeable (IV) or impermeable (V)
barrier. Using the results from treatment groups IV and V, describe
TWO additional characteristics of the phototropism response.
Copyright © 2010 Pearson Education, Inc.
(1/26) BR
5. Predict the most likely consequence for a nursing infant who is
exposed to an intestinal bacterial pathogen (e.g., Salmonella) to which
the mother was exposed three months earlier. Explain your reasoning.
Copyright © 2010 Pearson Education, Inc.
(1/26) BR
6. Draw a diagram similar to the one below for ONE of the
NEGATIVE feedback mechanisms in #12-13 of your Feedback
Mechanisms POGIL.
Copyright © 2010 Pearson Education, Inc.
(1/26) BR
Relay molecules and secondary messengers have essentially the same jobs
in signal transduction pathways. However, relay molecules are almost
always proteins that require activation. They are large and do not diffuse
through the cell quickly. Secondary messengers on the other hand are
small, water soluble molecules that can diffuse quickly. They may or may
not need activation before they are able to move the signal on to the next
step in the process. Cyclic AMP (cAMP) and calcium ions (Ca2+) are
common secondary messengers in human systems.
7. Within an organism it is critical that signals between cells are very
specific. For example, if ligand A is meant to activate immune system
cells to reproduce in response to an infection, it should not also cause
other cells to grow as if they had received a growth hormone. When a
ligand is released, what prevents all of the cells in the body from
being affected?
Copyright © 2010 Pearson Education, Inc.
(1/26) BR: Refer to the handout for #8-9.
8. Which of the following is a valid interpretation of the experimental
results that explains how individuals with type 2 diabetes differ from
individuals without diabetes?
a. The relatively low levels of glucose uptake in individuals with type
2 diabetes indicate that mobilization of GLUT4 to the cell surface
is reduced in muscle cells of those individuals.
b. The relatively low levels of glucose uptake in individuals with type
2 diabetes indicate that no functional GLUT4 protein is produced
in the muscle cells of those individuals.
c. The absence of activated insulin receptors in individuals with type 2
diabetes indicates that no insulin is secreted by the pancreatic cells
of those individuals.
d. The absence of activated IRS-1 in individuals with type 2 diabetes
indicates that no functional insulin receptor protein is produced in
the muscle cells of those individuals.
Copyright © 2010 Pearson Education, Inc.
(1/26) BR
9. Based on the experimental results, which of the following describes
the most likely defect in muscle cells of patients with type 2 diabetes?
a. Insulin receptor proteins do not reach the cell surface.
b. Insulin does not activate its receptor.
c. IRS-1 activation is reduced at high insulin concentrations.
d. GLUT4 blocks glucose from entering cells.
Copyright © 2010 Pearson Education, Inc.