Essential Cell Biology 5th edition

Answers A:41
cells that evolved. New cell membranes are made by
expansion of existing membranes, and the ER is never
made de novo. There will always be an existing piece of ER
with translocation channels to integrate new translocation
channels. Inheritance is therefore not limited to the
propagation of the genome; a cell’s organelles must also
be passed from generation to generation. In fact, the ER
translocation channels can be traced back to structurally
related translocation channels in the prokaryotic plasma
membrane.
ANSWER 15–22
A. Extracellular space
B. Cytosol
C. Plasma membrane
D. Clathrin coat
E. Membrane of deeply invaginated, clathrin-coated pit
F. Captured cargo particles
G. Lumen of deeply invaginated, clathrin-coated pit
ANSWER 15–23 A single, incomplete round of nuclear
import would occur. Because nuclear transport is fueled by
GTP hydrolysis, under conditions of insufficient energy, GTP
would be used up and no Ran-GTP would be available to
unload the cargo protein from its nuclear import receptor
upon arrival in the nucleus (see Figure 15–10). Unable to
release its cargo, the nuclear import receptor would be
stuck at the nuclear pore and not return to the cytosol.
Because the nuclear cargo protein is not released, it would
not be functional, and no further import could occur.
Chapter 16
ANSWER 16–1 Most paracrine signaling molecules are very
short-lived after they are released from a signaling cell: they
are either degraded by extracellular enzymes or are rapidly
taken up by neighboring target cells. In addition, some
become attached to the extracellular matrix and are thus
prevented from diffusing too far.
ANSWER 16–2 The protein could be an enzyme that
produces a large number of small intracellular signaling
molecules such as cyclic AMP or cyclic GMP. Or, it could
be an enzyme that modifies a large number of intracellular
target proteins—for example, by phosphorylation.
ANSWER 16–3 The mutant G protein would be almost
continuously activated, because GDP would dissociate
spontaneously, allowing GTP to bind even in the absence
of an activated GPCR. The consequences for the cell would
therefore be similar to those caused by cholera toxin, which
modifies the α subunit of G s so that it cannot hydrolyze
GTP to shut itself off. In contrast to the cholera toxin case,
however, the mutant G protein would not stay permanently
activated: it would switch itself off normally, but then
it would instantly become activated again as the GDP
dissociated and GTP re-bound.
ANSWER 16–4 Rapid breakdown keeps the intracellular
cyclic AMP concentrations low. The lower the cAMP levels
are, the larger and faster the increase achieved upon
activation of adenylyl cyclase, which makes new cyclic AMP.
If you have $100 in the bank and you deposit another $100,
you have doubled your wealth; if you have only $10 to start
with and you deposit $100, you have increased your wealth
tenfold, a much larger proportional increase resulting from
the same deposit.
ANSWER 16–5 Recall that the plasma membrane
constitutes a rather small area compared with the total
membrane surfaces in a cell (discussed in Chapter 15). The
endoplasmic reticulum is especially abundant and spans the
entire volume of the cell as a vast network of membrane
tubes and sheets. The Ca 2+ stored in the endoplasmic
reticulum can therefore be released throughout the cytosol.
This is important because the rapid clearing of Ca 2+ ions
from the cytosol by Ca 2+ pumps prevents Ca 2+ from
diffusing any significant distance in the cytosol.
ANSWER 16–6 Each reaction involved in the amplification
scheme must be turned off to reset the signaling pathway
to a resting level. Each of these off switches is equally
important.
ANSWER 16–7 Because each antibody has two antigenbinding
sites, it can cross-link the receptors and cause them
to cluster on the cell surface. This clustering is likely to
activate RTKs, which are usually activated by dimerization.
For RTKs, clustering allows the individual kinase domains
of the receptors to phosphorylate adjacent receptors in
the cluster. The activation of GPCRs is more complicated,
because the ligand has to induce a particular conformational
change; only very special antibodies mimic receptor ligands
sufficiently well to induce the conformational change that
activates a GPCR.
ANSWER 16–8
A. True. Acetylcholine, for example, slows the beating of
heart muscle cells by binding to a GPCR, and stimulates
the contraction of skeletal muscle cells by binding to a
different acetylcholine receptor, which is an ion-channelcoupled
receptor.
B. False. Acetylcholine is short-lived and exerts its effects
locally. Indeed, the consequences of prolonging its
lifetime can be disastrous. Compounds that inhibit the
enzyme acetylcholinesterase, which normally breaks
down acetylcholine at a nerve–muscle synapse, are
extremely toxic: for example, the nerve gas sarin, used
in chemical warfare, is an acetylcholinesterase inhibitor.
C. True. Nucleotide-free βγ complexes can activate ion
channels, and GTP-bound α subunits can activate
enzymes. The GDP-bound form of trimeric G proteins is
the inactive state.
D. True. The inositol phospholipid that is cleaved to
produce IP 3 contains three phosphate groups, one of
which links the sugar to the diacylglycerol lipid. IP 3 is
generated by a simple hydrolysis reaction (see Figure
16−23).
E. False. Calmodulin senses but does not regulate
intracellular Ca 2+ levels.
F. True. See Figure 16−35.
G. True. See Figure 16−29.
ANSWER 16–9
1. You would expect a high background level of Ras
activity, because Ras cannot be turned off efficiently.
2. Because many Ras molecules are already GTP-bound,
Ras activity in response to an extracellular signal would
be greater than normal, but this activity would be liable
to saturate when all Ras molecules are converted to the
GTP-bound form.