The reason why eukaryotic cells are in need of turning on
and off their genes when necessary because of the reason that they may feel
stress because they are under stress as they have the responsibility of acting
immediately when they needed and by that, they need to be turned on or off in means
of adapting to the stress that they experience.
They can accidentally catch dolphins, turtles, even orcas. Greenpeace is actively trying to get them banned.
Answer:
See details below
Explanation:
We know for sure that PK2 activates PK1 in a significantly signaling pathway. This is mainly because PK1 is permanently activated as a independent response which is observed in the status of PK2, by indicating that PK2 is fully activated downstream of PK1.
In the case that based on observation and experience, a setup were modified in a such a way PK1 was mutationally inactive and PK2 carried an activating mutation, we would not find any response observed since PK2 would not be able to activate PK1. The most importantly is that the logic is whether you discuss that PK1 activated PK2, I responded to this question part mainly based on this sequence.
Answer:
1. nerve stimulus
4. calcium channels open
10. acetylcholine vesicles move to endplate
7. exocytosis occurs releasing acetylcholine into synaptic cleft
3. acetylcholine binds to receptor
6. impulse rides along sarcolemma
9. impulse enters the cells via the t-tubule
5. sarcoplasmic reticulum releases calcium
8. calcium binds to troponin moving tropomyosin out of the way
2. myosin attaches to actin causing a twitch
Explanation:
The central nervous system generates an action potential (<u>1</u>) that travels to the muscle fiber activating the calcium channels (<u>4</u>). Calcium triggers vesicles fusion to the presynaptic membrane (<u>10)</u> releasing acetylcholine (Ach) into the synaptic space (<u>7</u>). Once there, Ach binds to its receptors (<u>3</u>) on the postsynaptic membrane of the skeletal muscle fiber, causing ion channels to open. Positively charged sodium ions cross the membrane to get into the muscle fiber (sarcoplasm) and potassium leaves the cell. The difference in charges caused by these ions transport charges positively the muscle fiber membrane (<u>6</u>). It depolarizes. The action potential enters the t-tubules (<u>9</u>) depolarizing the inner portion of the muscle fiber.
Contraction initiates when the action potential depolarizes the inner portion of the muscle fiber. Calcium channels activate in the T tubules membrane, releasing calcium into the sarcolemma (<u>5</u>). At this point, the muscle is at rest, and the tropomyosin is inhibiting the attraction strengths between myosin and actin filaments. <em>Tropomyosin is obstructing binding sites for myosin on the thin filament</em>. When calcium binds to troponin C, troponin T alters the tropomyosin position by moving it and unblocking the binding sites (<u>8)</u>. Myosin heads join to the uncovered actin-binding points forming cross-bridges <u>(2</u>), and while doing so, ATP turns into ADP and inorganic phosphate, which is released. Myofilaments slide impulsed by chemical energy collected in myosin heads, producing a power stroke. The power stroke initiates when the myosin cross-bridge binds to actin (<u>2</u>). 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. Finally, Z-bands are pulled toward each other, shortening the sarcomere and the I-band, producing muscle fiber contraction.
