I would say C. Why I say this is because fur is used to keep an animal warm. If the animal no longer needs to be kept warm, then it no longer needs the thick fur.
Answer:
The correct statement is - option B.
Explanation:
Unmyelinated axons are the axon that lacks the covering of scwann cells that form the myelin sheath which helps in the transfer or transmit the signals faster and more effectively in neurons. It acts as the insulating layer.
In absence of the myelin sheath, the action potential found everywhere along the length of the axon which leads to slow propagation than in myelinated axons.
Thus, the correct answer is - option B.
Answer:
When a muscle cell contracts, the myosin heads each produce a single power stroke.
Explanation:
In rest, attraction strengths between myosin and actin filaments are inhibited by the tropomyosin. When the muscle fiber membrane depolarizes, the action potential caused by this depolarization enters the t-tubules depolarizing the inner portion of the muscle fiber. This activates calcium channels in the T tubules membrane and releases calcium into the sarcolemma. At this point, <em>tropomyosin is obstructing binding sites for myosin on the thin filament</em>. When calcium binds to the troponin C, the troponin T alters the tropomyosin by moving it and then unblocks the binding sites. Myosin heads bind to the uncovered actin-binding sites forming cross-bridges, and while doing it ATP is transformed into ADP and inorganic phosphate which is liberated. Myofilaments slide impulsed by chemical energy collected in myosin heads, <u>producing a power stroke</u>. The power stroke initiates when the myosin cross-bridge binds to actin. As they slide, ADP molecules are released. A new ATP links to myosin heads and breaks the bindings to the actin filament. Then ATP splits into ADP and phosphate, and the energy produced is accumulated in the myosin heads, which starts a new binding cycle to actin. Z-bands are then pulled toward each other, thus shortening the sarcomere and the I-band, and producing muscle fiber contraction.
The point at which the toxin would interrupt normal cell signalling in the pathway is the signal amplification.
This is because of the G-protein uncoupling and inhibition of signal amplification by pertusis toxin. Pertusis toxin released by the bacteria Bordetella pertusis and prevents signal that is amplifying from the protein. The G-protein coordinates the interaction between membrane bound receptor proteins and the effector proteins involved in the intracellular signalling. The toxin promotes the uncoupling of this heterotrimetric protein and also inhibits the amplification thus preventing the interaction of the receptor proteins and the second messengers.
