GNAL TRANSDUCTION, THE JOB OF R 
48 
lie unique char- 
acteristics of a 
cell depend, in 
large measure, on 
what kinds of 
receptor proteins it has. Like 
a lock that accepts only an 
appropriately shaped key, each 
different receptor will function 
only when the correctly 
shaped blood-borne molecule 
(called a ligand) attaches to it. 
Many hormones exert their 
effects through receptor proteins 
that transfer the signal and 
generate “second messengers” 
within the cell. One of the best 
understood of these second 
messenger systems employs 
proteins called G proteins. 
In the G protein system, when 
a “first messenger” (such as a 
hormone) reaches the cell surface, 
it hinds to a receptor that then 
sends a signal to a G protein 
located on the interior side of 
the cell membrane. Depending 
on its type, the activated G 
protein then either stimulates 
or inhibits the activity of any of 
a number of enzymes, including 
one called adenylate cyclase. 
Stimulating this enzyme causes 
cyclic AMP, a common second 
messenger, to be produced. 
Cyclic AMP then sets off a 
chain reaction that eventually 
results in changes in the shapes 
of certain proteins in the cell, 
which, in turn, lead to still 
other cellular responses. When 
levels of the first messenger 
drop, the G protein “switches 
off’ and the response terminates. 
The cell appears to employ 
this complex signaling system 
because it increases both the 
efficiency and speed of message 
transmission. A single incoming 
messenger molecule triggers a 
cascade of reactions that even- 
tually results in a large 
amplification of the original 
message. Furthermore, the time 
elapsed between the arrival of 
a signal at a G protein and a 
cellular response is often only 
a few fractions of a second. For 
CEPTOR PROTEINS 
example, light-sensitive eye cells 
respond to as little as one 
photon of light in just a few 
milliseconds through a G 
protein-mediated system. In 
contrast, other cells take as 
long as 30 seconds to respond 
to signals from the environment. 
Certain diseases impair the 
functioning of the second mes- 
senger system and cause 
profound cellular malfunction. 
A toxin produced by the 
organism that causes cholera, 
for example, “locks” the G 
proteins of intestinal cells into 
the “on” position so that they 
are constantly stimulating the 
production of cyclic AMP. 
This causes vast amounts of 
fluid to cross the fining of the 
gut, causing the often-fatal 
diarrhea associated with 
cholera. 
I low a signal brought to 
the cell by a single message 
molecule is amplified 
through the second 
messenger sys tern 
