In: Biology
12) The toxin produced by the bacterium Clostridium
botulinum is a potent neurotoxin. When
used in high doses, the toxin causes death through paralysis. When
used in high doses,
the toxin causes death through paralysis. However at low doses the
toxin can be used for
cosmetic purposes or to treat overactive muscles. Botulinum toxin
(BTX) prevents
neurons from being able to activate muscle contractions. BTX
accomplishes this through
proteolytic activity (by degrading specific proteins). (6
points)
- One explanation is that BTX prevents the budding of
neurotransmitter containing
vesicles from the Golgi apparatus. If this explanation is correct,
what class of proteins
would BTX most likely target for degradation? Briefly
explain.
- Another explanation is that BTX prevents the fusion of
neurotransmitter containing
vesicles with the plasma membrane. If this explanation is correct,
what class of proteins
would BTX most likely target for degradation. Briefly
explain.
- In the presence of BTX, the membrane protein is found in
intracellular vesicles,
however none is seen on the plasma membrane. Which explanation, a
or b, does this
data support?
Statement B is true another explanation is that BTX prevents the
fusion of neurotransmitter containing
vesicles with the plasma membrane.because as you can see two
process one showing normal neurotransmitter release and one in
presence of Botulinum toxin
So Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals (and humans) as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells, such as neurons, muscle cells and gland cells. Neurotransmitters are stored in readily releasable pools of vesicles confined within the presynaptic terminal. During neurosecretion/exocytosis, SNAREs play a crucial role in vesicle docking, priming, fusion, and synchronization of neurotransmitter release into the synaptic cleft. So we can understand that SNARE proteins important for fusion but in image below we can see that BTX damages or degrades the SNARE proteins both present on the vesicle and membeane. hence can not fuse with membrane for release of neurotransmitter. thats why statement B is right.