Concept explainers
A few hours after the death of an animal, the corpse will stiffen as a result of continued contraction of muscle tissue (this state is called roof mortis). This phenomenon is the result of the loss of ATP production in muscle tissue.
a. Consult Figure 7.482 and describe, in terms six-step model of muscle contraction, how a lack of ATP in sarcomeres would result in rigor mortis.
b. The Ca2+ transporter in sarcomeres that keeps the [Ca2+] ~ 10-7 M requires ATP to drive transport of Ca2+ ions across the membrane of the sarcoplasmic reticulum. How would a loss of this Ca2+ transport function result in the initiation of rigor mortis?
c. Rigor mortis s maximal at ̀´ 12 hrs after death by 72 hrs is no longer observed. Propose an explanation for the disappearance of rigor mortis after 12 hrs.
Want to see the full answer?
Check out a sample textbook solutionChapter 7 Solutions
Biochemistry: Concepts and Connections
- Under certain stable concentration conditions, actin monomers in their ATP form will polymerize to form filaments that disperse again into free actin monomers over time. Explainarrow_forwardNitric oxide (NO) is a gaseous molecule with lipid solubility similar to that of O2 and CO2. Endothelial cells lining arteries use NO to signal surrounding smooth muscle cells to relax, thereby increasing blood flow. What mechanism or mechanisms would transport NO from where it is produced in the cytoplasm of an endothelial cell into the cytoplasm of a smooth muscle cell, where it acts?arrow_forwardThe contraction of cardiac muscle cells results from the increase in Ca?+ levels in the cytosol. For these cells to relax, an antiport removes Ca?+ from the cytosol for every Nat that is taken in. Digitalis is a drug that is used to make the heart contract more strongly. This drug partially inhibits the Na*-K* ATPase in the cardiac cells. Applying the concepts from membrane transport, answer the following: a. Propose an explanation for the drug's effect. b. What will likely happen if too much of the drug is taken in? Why do you say so?arrow_forward
- You are a brilliant (but evil) biochemist who is developing a toxin that can be used to paralyze skeletal muscle. Using your knowledge of the sequence of cellular/molecular events that cause a muscle contraction, identify two parts of the process that could be disrupted to cause paralysis, and explain the specific effect of each disruption on contraction. please helparrow_forwardDescribe a negative feedback mechanism for controlling a rising cytosolic Ca2+ concentration in cells that require rapid changes in Ca2+ concentration for normal functioning. How would a drug that inhibits calmodulin activity affect cytosolic Ca2+ concentration regulation by this mechanism? What would be the effect on the function of, for example, a skeletal muscle cell?arrow_forwarda skeletal muscle cell has depleted its stores of ATP how will the altered transport properties of the NKA transporter affect cytosolic calcium concentrations (increase, decrease, no change) relative to normal? Why?arrow_forward
- One of the effects of low oxygen levels in cardiac cells is arise in cytoplasmic calcium levels as a result of the depressedactivity of the plasma membrane’s Ca2+-ATPase. What aresome of the consequences of this phenomenon?arrow_forwardTypically, there is an ion gradient between the cytoplasm and the interior of synaptic vesicles. The ion gradient has a functional role. Which of the following statements best describes the ion gradient across the synaptic vesicle membrane and its role? a.) There is a proton gradient across the synaptic vesicle membrane, and it provides the driving force for the transport of neurotransmitter into the vesicle. b.) There is a sodium gradient across the synaptic vesicle membrane, and it provides the driving force for the transport of neurotransmitter into the vesicle. c.) There is a proton gradient across the synaptic vesicle membrane, and it provides the driving force for the transport of neurotransmitter out of the vesicle. d.) There is a sodium gradient across the synaptic vesicle membrane, and it provides the driving force for the transport of neurotransmitter out of the vesicle.arrow_forwardThe sarcoplasmic reticulum Ca2+-ATPase, pumps 2 mol Ca2+ out of sarcomeres per mol ATP hydrolyzed. Part A: Given the following steady-state concentrations and a membrane potential of 64 mV (inside negative), calculate ΔG for the following active transport process at 37 ∘C and pH=7.4: 2Ca2+(in)+ATP+H2O→2Ca2+(out)+ADP+Pi+H+ ATP=2.8mM,ADP=206μM,Pi=5.4mM,Ca2+(in)=34μM,Ca2+(out)=2.2mM The answer to part A was -7.4 kJ/mol I need help with Part B: Part B: The activity of the Ca2+-ATPase is regulated reversibly under normal conditions to maintain homeostatic concentrations of Ca2+ inside the sarcomere. However, in a rare genetic disorder, irreversible activation of the Ca2+-ATPase can occur. Assuming 37 ∘C, pH=7.4, and the steady-state concentrations for ATP, ADP Pi, and Ca2+(out) given in part (a) calculate the minimum [Ca2+] inside a sarcomere that has irreversibly activated Ca2+-ATPase (i.e., the Ca2+-ATPase activity is always “on”).arrow_forward
- In a rare inherited disorder, called Wilson’s disease, excessive amounts of copper accumulate in liver and brain tissue. A prominent symptom of the disease is the deposition of copper in greenishbrown layers surrounding the cornea, called Kayser–Fleischer rings. A defective ATP-dependent protein that transports copper across cell membranes causes Wilson’s disease. Apparently, the copper transport protein is required to incorporate copper into ceruloplasmin and to excrete excess copper. In addition to a diet low in copper, Wilson’s disease is treated with zinc sulfate and the chelating agent penicillamine (p. 148). Describe how these treatments work. [Hint: Metallothionein has a greater affinity for copper than for zinc.]arrow_forwardThe sarcoplasmic reticulum Ca2+-ATPase, pumps 2 mol Ca2+ out of sarcomeres per mol ATP hydrolyzed. Given the following steady-state concentrations and a membrane potential of 67 mV (inside negative), calculate ΔG for the following active transport process at 37 ∘C and pH=7.4:2Ca2+(in)+ATP+H2O→2Ca2+(out)+ADP+Pi+H+arrow_forwardVery briefly, explain how increased cytoplasmic IP3 levels can then increase cytoplasmic calcium (Ca2+) levels.arrow_forward
- Human Physiology: From Cells to Systems (MindTap ...BiologyISBN:9781285866932Author:Lauralee SherwoodPublisher:Cengage Learning