Signaling pathways unit study guide

(chapters 11, 48, 43, 39, 9)

Chapter 11: Cell communication
Note: Be careful reading – this chapter often covers too much detail about specific pathways … I want you to
understand the broader picture of how signaling works

Vocabulary: receptor protein, signal transduction, ligand, protein kinases vs. protein phosphatases, second
messenger, phosphorylation

Concepts:
--top p. 211 – signaling proteins and pathways are amazingly similar across MANY species –
another strong piece of evidence for common ancestry

--p. 211 (or from video in class) – define quorum sensing and explain how it works in bacteria
– how can bacteria work together to behave like a multicellular organism?
Quorum sensing is used to determine the density of a bacterial population. This happens because the bacteria
secrete a specific molecule that can be determined by the other bacterial molecule. Once the concentration of
that molecule reaches a certain level(meaning that that level of bacteria is there), then the bacteria can work
together to carry out a reaction(when there are enough of them to make an impact).

--note three types of signaling in multicellular organisms (figures 11.4 and 11.5):
a) direct contact (ex: immune cells checking body cells – ch. 43 coming up)
b) local signaling (ex: neurotransmitter release at synapses – ch. 48 coming up)
c) long-distance signaling (ex: hormones released to bloodstream – ch. 45 coming up)

--3 broad steps to any communication pathway (figure 11.6)

a) reception the signal b) transduction the signal c) response to the message

more detailed discussion:

--signals are also called ligands … this chapter assumes that they are always
chemicals, but what other stimuli can be detected?

step a -any molecules in the body that comes in contact with the receptor.
above --a cell might detect the signal above because it has a receptor protein with a specific shape to fit the
signal

--in multicellular organisms, why do only the intended target cells receive the message?
(p. 214 bottom left)

-because the signaling molecule has a very specific shape like a “lock and key” that must must match the target
cell.

--explain the difference between ligands that bind at membrane receptors facing outside
the cell vs. ligands that bind at receptors floating in the cytoplasm (p. 214 / 217)

-in a cell with receptors floating in the cytoplasm ,the ligand is nonpolar or small enough to pass through the
membrane. On the other hand the ligands that have receptors on the outside of the cell are often water soluble.
step b
above
 --what happens when signal binding occurs at the receptor (p. 214 top right)?
-the receptor protein often undergoes a change in shape in the molecule, which then activate the receptor
directly or causes an aggravation in that molecule, or more..

--now that the change has occurred in the question above, the transduction pathway
often continues by activating other proteins – identify multiple ways that the next
protein in the pathway is activated (p. 219, p. 220)

i) phosphorylation cascade: domino effect of phosphates being removes and added to inactive
protein kinases, activating them, the active kinase is used to phosphorlize another ATP, and the
phosphate is added to another protein. This can work with many proteins.

notice the
step b
above ii)protein phosphates: make the kinases available for reuse-dephosphoralization amplification in
fig. 11.16 – one
activated molecule
might activate 10 –
iii)second messengers cAMP- ions inside the cell, which are activated often when100molecules
of the next
outside the cell cannot pass through the membrane step in the chain

iv)Ca2+: similar to the cAMP

--finally, proteins are activated that carry out the intended response (p. 223)

--perhaps a protein just needs to be activated that was inactive previously –

perhaps this could be an synthesis/cytoplasmic protein that helps convert chemicals into
step c other chemicals, or perhaps open a channel protein to let chemicals cross a membrane
above (ex: neurons in ch. 48 below)

--change the rate of new protein production … so transcription factor proteins are activated to go
the nucleus and bind to a specific gene in DNA code and change the rate that it is copied
(figure 11.15 – more detail coming in molecular genetics)

--signals do not last forever – read p. 227 termination section

--perhaps phosphatases proteins exist to bind to proteins activated by phosphorylation and switch them
off by cutting off the phosphate group (p. 220 mid left)

Chapter 48 – Nervous system

Vocabulary: sensory / motor / interneurons, cell body vs. axon vs. dendrite, synapse, myelin sheath, Schwann
cell, neurotransmitter, action potential, polarization vs. depolarization, Na+ / K+ gated channels, Na+ / K+ pump

Concepts:
48.1 – Overview
--a neuron has three regions in its structure (figure 48.5):
1) Cell body 2) axon 3) dendrites

sends signals to next neuron receives signals from previous neuron

--name the three broad types of neurons on p. 1063

1) sensory 2) interneuron 3) motor
 48.2 – Neuron at rest
--think of the resting situation as “loading the gun”, preparing a neuron to fire when triggered

--to prepare, two ions are concentrated (Na+ / K+) on different sides of the membrane so
that they will rush to the other side (high  low concentration) during neural activity

Na+ is very concentrated (circle one) (outside / inside) the neuron at rest

K+ is very concentrated (circle one) (outside / inside) the neuron at rest

--due to the separation of these ions, we would call this setup (polarized / depolarized)

--which protein is active during rest to create this separation discussed above?
Sodium potassium which requires ATP to pump these ions because this is active transport

--the distribution of ions makes the inside of the cell is more (negative / positive) than the
outside (p. 1064) (note: it is an oversimplification to claim that negative DNA and
proteins are causing this resting voltage, but you do not need to read about the K+ leak channels on p.
1065-6)

48.3 – Neuron during an action potential (or impulse)

--also present in the membrane are gated ion channels (closed during rest, but can open to cause
action potential)

--go to figure 48.11 for what I want you to know (step 1 is rest that is discussed above, and the
following discussion assumes that the stimulus is trying to start an action potential)

--steps 2 and 3: inside becomes more positive when gated Na+ channels open
make sure --FYI (not tested): step 2 shows ligand-gated channels open first (triggered by
you can neurotransmitters discussed below), perhaps triggering voltage-gated channels to
draw the open in step 3
“before /
after” ion
pictures on --this ion movement causes the inside to become (circle one): (polarized / depolarized)
the ch. 48
group--step 4: at the peak voltage, the gated channels above close, and voltage-gated K channels
worksheet open next

--all of this ion movement in steps 2 – 4 involve passive transport

-- do all the ions come in? no, remind yourself what the end result of this
transport is from figure 7.10 (though p. 1069 discusses how very few ions move to cause
the voltage change)

--step 5: all gated channels above are now closed, and ion concentrations are reset to resting
conditions by the sodium pottasium Pumps
(this protein was always active but was overwhelmed by the gated channels opening)
note: this is why the brain requires so much ATP energy to function

--look at figure 48.12 – the electrical signal is the ion movement, and travels in one direction as
the Na+ ions diffuse to the next section and trigger voltage-gated channels to open there
(we will try to show this in a group discussion worksheet)
--note the speed of signal travel – see X-axis units in fig 48.11 and mid left p. 1070
-1-2 milliseconds
--what is the purpose of the myelin sheath wrapped around a neuron’s axon (mid left p. 1071)?
-to speed up the action potention and signal-the current only has to travel through in between the nodes
surrounded by myelin-its space efficiency.

--go to p. 1103 and read paragraph right above fig. 50.4 and also look at figure –
neurons encode information about the intensity of the stimulus by changing what?
-frequency or action potentials since action potentials are all or nothing.

48.4 – Neurons passing information to other neurons

--focus on chemical synapse discussion – at the end of the axon, the action potential triggers a
release of chemicals called neurotransmitters that travel to the next neuron’s dendrites across a tiny gap
called a synapse

--be able to describe the steps of information transfer here (figure 48.16 is very helpful)

step 1: action potential travels down axon of first neuron … this electricity leads to the
release of vesicle containing neurotransmitter

step 2: neurotransmitter leaves first neuron through process of depolarization diffuses (K+ or Na+)
across synaptic cleft and binds to ligand-gated channel on second neuron

step 3: if neurotransmitter is excitatory, it stimulates next neuron by promoting +ion (K+ or Na+)
diffusion through opened ligand-gated channel

if neurotransmitter is inhibitory, it inhibits action potential in next neuron by

promoting –ion (K+ or Cl-)diffusion through ligand-gated channel (top p. 1073)

step 4: neurotransmitter falls off, eventually gets recycled back into first neuron so
process can be repeated

--big picture: why convert the electrical signal into a temporary chemical signal? because the
second neuron can add together the neurotransmitter release of a highly active neuron (fig 48.17b) or
two neurons firing together (48.17c) when deciding to fire itself or not

--so synapses are where information is processed – next neuron fires or not (like a 0 or 1
in computer code) –binary code

--briefly flip to p. 1085 and note specialization of regions in brain – different parts process
different information because different regions receive inputs from different sensory neurons

--for example, what does the cerebellum control (p. 1087)? what kind of information
does it receive?
-movements, balance, and motor skills, blood circulation. –it receives sensory information about the positions or
joints and the length of muscles and input them in auditory or visual systems.

(nothing else needs to be read in chapter 49)

Chapter 43: Immune system – defenses against invaders
Vocabulary: nonspecific (innate) vs. specific (acquired) immunity, phagocytes, apoptosis, antigen, antigen
receptors vs. antibodies, clonal selection, humoral vs. cell-mediated immunity, helper T vs. cytotoxic T
lymphocyte, B lymphocytes, memory lymphocytes, primary vs. secondary immune response, HIV / AIDS

Concepts:
43.1 – Mechanisms of innate immunity (or nonspecific defenses)
--briefly note p. 947 – invertebrate animals seem to only have a nonspecific set of defenses
--go to figure 39.26 (p. 861) – read the captions and explain how plants defend themselves from
pathogens (they do not have white blood cells)
-plants defend themselves because they have a pathogen that tries to invade the body, a signal is sent from that
affected leaf to another leaf due to a hypersensitive response. Then the signal transduction pathway starts in
another leaf, which results in the plant building resistance.
--external nonspecific defenses simply try to prevent invaders from getting into the body to begin
with – name two examples of an external defense and how they deter invaders
skin-first barrier between the blood and the outside environment.
Mucous-the mucous around your body traps unwanted bacteria and sends it out,

--internal nonspecific defenses also protect body cells by either attacking the invader directly,
attracting attention to an invader problem, or warning healthy body cells – discuss the
role of phagocyte white blood cells – p. 950 (do not worry about types of phagocytes)

-to engulf any immediate invader and destroy it.

43.2 – Acquired immunity – creating the tools for a specific response (vertebrates only)
--p. 952 – unlike phagocytes above, lymphocytes white blood cells have specifically
shaped membrane proteins to bind to a particular molecule on the surface of a pathogen

--any molecule on the surface of a pathogen (perhaps a protein or carbohydrate) that acquired
immune cells recognize is called an antigen (don’t worry about epitope)

--so each lymphocyte cell produces membrane receptors with a certain shape to try and fit these
molecules above specifically – notice bottom p. 952 that each lymphocyte cell may
produce ~100,000 of these receptors, but they are all (identical / different) for each cell

--skip pgs. 953-955, start p. 956 with “origin of self-tolerance” and read rest of section
--p. 956 – there should be mechanisms to remove lymphocytes with receptors that bind to
our own body’s proteins (p. 907) … otherwise our own body cells could be
attacked (though see autoimmune disease p. 965)

--problem: many pathogens mutate quickly (especially viruses / bacteria, as we’ll see in spring)
so how can immune system stay current with changing molecule shapes?
-the immune system can stay current with changing molecules because the lymphanote will begin to reproduce
when in comes in contact with the right antigen, then allowing the immune system to reproduce that specific
molecule, allowing it to stay consistent.
--solution: clonal selection – ALL types of lymphocytes do this (p. 956 and figure 43.14)
step 1: generate many lymphocytes, each trying out 1 random receptor protein shape
step 2: (further below): mass produce cells with successful receptors

--how does body know which “successful” lymphocytes to clone? only those lymphocytes clone
 because only they do what? This occurs because the antibody comes in contact with the right receptor on
the lymphocytes and when that happens it activated the lymph note which then begins to reproduce
rapidly(ONLY that specific cell though)

--p. 956 – note that all lymphocyte types make short-term cells (do not worry about term effector
cells) and also long-term memory cells that hold the information for correct
receptor shape for that pathogen

--explain how the secondary immune response is different from the primary immune response
(description bottom right p. 956, also figure 43.15)
-Antibodies are already made for that specific pathogen in secondary immune response due to the memory t-
cells and b-cells, which means less time looking for them when the pathogen has invaded, as well as less time f
the antibodies to be distributed and destroy the pathogen. In primary immune response the T-cells and B-cells
have to be found, then replicated, which therefore does not happen as rapidly.

--why is the secondary immune response different? what are the memory cells doing
when they detect the returning pathogen? (p. 957)

-secondary immune response is different as it is much faster because memory cells are rapidy reproducing
through cloning once they detect the new pathogen. (Does not have to go through antigen presenting cell step
or helper t-cell usually; more efficient).

--using the memory discussion above, explain the purpose of vaccination (p. 963)

-a vaccination is used because your body will have fought off a small amount of the virus, meaning that
your body has now generated the memory t-cells and the memory b-cell. This will allow for your body to
fight off the actually virus much faster and more efficiently when your body encounters the virus in real
life because you will therefore have “immunity” to it.

43.3 – What do B cell and T cells do after cloning to destroy a specific pathogen
--there are three types of lymphocytes – each of them does clonal selection discussed above
Where does it look for
Type of lymphocyte What is its job? (see figs 43.16, 17, 18, 20)
pathogen?
-important because it activates the cytotoxic
(does not engage cells and the b-cells as it releases cytokines,
Helper T cell
pathogen directly) to activate it because it has the same antigen
receptor.
-It looks for the cell-mediated response – define:-often cause
pathogen in the cells apoptosis of the cell, specialized T-cells
Killer/cytotoxic T cell
that have been overtaken destroy the infected host cells.
by it.
-in the blood and lymph humoral response – define: antibodies help
B-cell
nodes neutralize or eliminate toxins and pathogens
in the blood.

--each type of lymphocyte encounters the antigen in different locations – identify which
 description below matches which lymphocyte type from the table above

1) encounters the pathogen (and antigen on its surface) directly in body fluids – b-cell
use figures 43.16 –
_______________
43.18 to help2)you
encounter
certain phagocytes that present the antigen on their membrane – helper t-cell
_______________
3) encounter an infected body cell that presents the antigen on its membrane –cytotoxic t-cell

--the rest of the chapter from p. 963 on is interesting, but not required, with one exception below:
--HIV virus breaks into what type of cells specifically (p. 967) ? helper T-cells
--explain why HIV infection eventually leads to AIDS (note what the acronym means)
-Acquired Immunodeficiency Syndrome-AIDS-HIV can lead to aids because the virus can infect cells and
multiply, and the helper T-cells cannot go through specific responses because they are compromised due to it
blocking the CD-4 protein. In addition because cell death keeps occurring, there is also a lack of helper t-cells.

Chapter 39 – Plant signaling

Vocabulary: phototropism, photoperiodism, circadian rhythms, germination vs. dormancy, phytochrome,
gravitropism

39.1 – Reviewing signal transduction pathways

--read this section not for the details but for an excellent review of a signal transduction pathway
from chapter 11 … first column page 789 – an early plant’s priority is to grow how?

Thick roots?

--a ligand is received by the plant that tells it to start making chlorophyll
(example of signaling pathway that results in new protein production from chapter 11)
--the phytochrome receptor receives this ligand (p. 838 top left)

39.2 – Plant hormones

--SKIP almost all this section (we will NOT memorize plant hormones) – from p. 841 what is a tropism
generally, and what is phototropism more specifically?

Tropisim: any plant growth that results in a plant growing towards or away from a stimuli
Phototropism: tropisim, but the stimuli is light

--why is phototropism advantageous to plants (do NOT worry about mechanism fig. 39.5) because
where plants may be crowded, it allows them to go toward sunlight, which allows for more photosynthesis.
--another example of the signaling pathways leading to new protein production – germination
after dormancy – what are some different ligands that trigger germination in different
species? Auxin, gibberlins, ethylene (p. 846 … do NOT worry about ABA hormone discussion)

--why is seed dormancy adaptive? why does it help young plants survive?
-seed dormancy is adaptive because it needs certain temperatures, moisture and light or hormones to break. This
helps young plants therefore survive, because if the conditions are not ideal, they will not break dormancy and
die.

39.3 – Keeping track of time as an organism

--this section is too technical … I am only interested that you reading the pages below:
 --MOST organisms are equipped to detect different types of time (not just plants), including:
1) day / night cycles (what time of day is it?)
--the broad term for cellular mechanisms that trigger responses on ~ a 24 hour cycle is
Circadian rhythym (p. 852)
(by the way … can this get messed up? yes … ever had jet lag?)

--what events in a plant might be linked with detecting time of day (p. 851 bottom right)?
how about animals?

-changes in light level and temperature-opening and closing of the stomata and production of photosynthetic
enzymes.

2) seasonal cycles (what time of year is it?) – detecting the season is a concept generally
called photoperiodism (p. 853)

--as the name above implies, organisms tell the season by detecting changes in what?
-implies that an organism detects changes in seasonal photoperiod, or the duration of light in the day.

--what events in a plant’s life might be linked with detecting the season? (some animals
also need to do this – perhaps for initiating hibernation / estivation, for example)
-flowering and ending dormancy

-- skip rest of chapter 39 (except for the plant immune part already covered in ch. 43 above)

Chapter 9: Cell cycle (mitosis)

Vocabulary: chromosome vs. chromatin vs. sister chromatids, centromere, interphase (G1, S, G2, G0 subphases)
vs. mitosis (prophase, metaphase, anaphase, telophase subphases) vs. cytokinesis, spindle fibers, kinetochore,
mitosis vs. binary fission, checkpoint, cyclin, CDK, cancer, metastasis

Concepts:
-- cell division serves 3 basic purposes (fig 9.2) … humans only use it for 2 of these below
1reproduction 2) growth and development 3) tissue renewal
*remind yourself why multicellular organisms grow by increasing the number of cells, not the size of cells (fig. 4.6)
Cell size would decrease the efficiency of the cell
9.1 – Overview of eukaryotic mitosis
-- the goal in cell division is to make sure the two cells have the same DNA at the end
(in particular, each and every chromosome because they carry different genes)

-- to make sure that this is done correctly, each chromosome that is initially unpacked in
thin chromatin form gets packed up into condensed form that can be
split more easily

-- when we first see a condensed chromosome in a microscope, it looks like an X – this is

figure 9.4
 two sister chromatids combined together at the metaphase plate region
(this is because the DNA has already been copied before packing)

9.2 – Specifics of cell cycle (eukaryotic cells ONLY)

-- broadly, the cell cycle consists of three broad phases (outer “ring” of pie chart fig. 9.6)
1) interphase 2) M-phase 3) G-0 phase
-- which of these phases is by far the longest (pie chart)? interphase

-- interphase has 3 subphases – discuss each and what is going on in that subphase?

G1-cell grows
S-continues to grow and cop chromosomes
G2-grows more to prepare for cell division

-- mitosis has 4 subphases prophase, metaphase, anaphase, telophase

-- prophase of mitosis

a) packing up the DNA code – before in interphase, each chromosome was in

chromatin form, but now it is packing up into the “X” shape which is sister chromatid
form

-- identical copies are tied together due to interactions between their central regions
of DNA called centrosomes

b) if the DNA is to be split up and moved to separate parts of the cell, then the
Nuclear envelope surrounding and protecting the DNA must be temporarily taken apart
(and then rebuilt at the end once the DNA is split)

c) the spindle fiber microtubules are constructed to pull the DNA apart … they will
attach to a specific protein within the centromere region called kinetochore

(see green circle at bottom figure 9.9)

-- metaphase of mitosis
-- draw me a quick picture of what the DNA looks like lined up in mitosis (note
the difference between this and the lineup of meiosis I once we get to unit 5)
 -- anaphase of mitosis
-- chromosomes are lined up so that the sister chromatids
are split apart in mitotic cell division

-- _kinetochore microtubules within the kinetochore complex spend ATP to walk DNA apart
along spindle fibers that attached earlier
(note that they are walked apart from the center, NOT pulled from the poles)

-- telophase of mitosis
-- now that the DNA has been separated equally, the nuclear envelope/nucleoli
begins to re-form to surround and protect the DNA once more

-- after interphase and mitosis, cytokinesis occurs - what happens here?

-two daughter cells begin to show, there is cleavage furrow in animal cells, and the cytoplasm splits.

-- now that we have discussed the cell cycle in detail, give me the big picture summary – what is
the goal of mitosis generally?
-to duplicate cells, but retain the same material

-- bacteria copying cell division is given a different name – binary fission

because it is much simpler (figure 9.12) - the key difference is that bacteria only have 1 chromosome to
copy and split up (see caption of figure)

9.3 – Regulation of cell cycle

-- some cells in the human body do not divide at all – for example, nerve and muscle cells (p. 192)

-- these cells seem to be locked in interphase, never leaving so we say they stay in G0
subphase within interphase (fig. 9.16a top left)

-- not in book, but why is important to carefully control when cells divide? what are some
expenses of mitosis that we described above in the previous section?

-it is important to control cells when they divide because cells with mutations are often cancer cells and if not
detected, will start to duplicate and form a tumor quickly.

-- explain the general concept of a checkpoint in the cell cycle

-checkpoints in a cycle are either internal or external between the different phases, there Is G2, G1 and M
checkpoints if it does not receive a “GO” it will probably enter G0 phase at the end of G1. They are controlled
by cyclins(G2), external conditions with the proper growth factors, density, or anchors.

-- what controls moving past checkpoints? signaling pathways that often activate
Growth factor proteins (bottom left p. 193) that move the cell past the checkpoint

-- the production or activation of these proteins might be connected to outside environmental

signals … briefly read about the concepts of density-dependent inhibition and anchorage dependence
and summarize what is going on
 -density dependent growth factor is that cells will not grow when they are crowded, beyond a single
layer because they require space. Anchorage dependence is that cells must be connected to another cell of their
type or the inside of a flask, ect. to be duplicated, they cannot be just duplicated anywhere in the body.

-- out of control cell division is the general definition of cancer

-- there are natural protections against this problem - what often happens to cells that divide out of
control or have other mistakes in replication or checkpoints?
-the natural protections are the checkpoints. they will duplicate and form a tumor which is a bunch of cells that
are mutated and out of control.

-- why does chemotherapy often have debilitating side effects (nausea, fatigue)? (p. 196)
Because it kills healthy cells too, meaning that normal body cells are being lost, therefore less function and the
bad side effects.