Upgrade to remove ads
AP Biology Chapter 12 Part 2
Terms in this set (9)
Why does a multicellular organism need to control and coordinate cell division? What might be the consequences of uncontrolled cell division in a multicellular organism?
Cells divide for 3 reasons: reproduction, growth, repair and renewal.
Reproduction --reproduce asexually--one-celled organism use mitosis as a way of reproduction
Growth--cell division helps growth by taking you from a fertilized egg to a multi-celled organism
Repair and renewal -- replaces cells that die from normal wear and tear or from injury
Coordination of cell division in multicellular organisms is critical for normal growth, development and maintenance. Cells have an upper and lower size limit. If it was too small it would not contain all organelles. It can't be too big because of the ratio of the cell surface area to volume. An increase in size can result in a surface area too small for the adequate exchange of materials. Some cells must be large for a purpose To maintain a suitable size, growth and division must be coordinated, if a cell doubles in size the daughter cells will be too big or too small, this will happen with each generation and the cell will die. Coordination of cell growth and division is important for cells to stay the same size from generation to generation. Coordinating the timing of cell division, and rates of cell division so that all cells are not on the same cycle. This is important because if all cells were on the same cycle then you wouldn't have cells available for functions at all times. The frequency of cell division varies by cell type. (example embryos have a less than 20 minute cell cycle, skin cells every 12-24 hours, liver cells once every 1-2 years, mature nerve and muscle cells not at all)
Control of cell division is important because too much cell division can cause mutation and overgrowth of cells resulting in cancerous growths. A multicellular organism uses:
Internal Controls to coordinate and control this division.
A multicellular organism must have MPF, which is Cdk and Cyclin put together. This turns on other proteins for mitosis.
External Controls to coordinate and control this division:
Growth factors -- coordination between cells, protein signals released by body cells that stimulate other cells to divide-- Positional Inhibition--Animal Cells must be anchored (attached to a substrate)to divide -- Also they cannot be too crowded ("Density Dependant Inhibition")- Crowded cells stop dividing. Each cell binds a bit of growth factor so that there is not enough activator left to trigger division in any one cell.
Cancer is essentially a failure of cell division control. It is unrestrained and uncontrolled cell growth.
Growth factors can create cancer -- proto-oncogenes normally activate cell division. When these genes become mutated and are permanently switched to an on position, they can cause cancer by continuous and uncontrolled division of cells. Tumor suppressor genes which normally inhibit cell division can be switched to an off position and tumors will grow uncontrollably causing cancer.
All cancers have to shut down p53 activity. Gene p53 plays a key role in the G1/S restriction point. p53 halts cell division if it detects damaged DNA -- it can stimulate repair enzymes to fix DNA, force cell into the G0 resting stage, keep cell in G1 arrest, cause apoptosis of damaged cell.
Development of Cancer occurs after a cell experiences 6 key mutations. 1- unlimited growth (turn on growth promoter genes) 2 - ignored checkpoints (turn off tumor suppressor genes -p53) 3-escape apoptosis (turn off suicide genes) 4- unlimited division (turn on chromosome maintenance genes) 5-promotion of blood vessel growth (turn on blood vessel growth genes) 6 - overcome anchor and density dependence (turn off touch-sensor gene)
What does it mean when we say that there are several "checkpoints" that occur during the cell cycle?
The cell cycle control system directs the sequential events of the cell cycle. This control system is regulated by internal and external controls, and there are specific checkpoints where the cycle stops until the go-ahead is given. The checkpoints include a G1 checkpoint, a G2 checkpoint, and a spindle checkpoint. There are many other checkpoints, but these are the most important ones. The checkpoints work by triggering signaling pathways that activate or inactivate a set of core proteins that move the cell cycle forward.
What are the "questions" that a cell must "answer" during each of the following checkpoints: a. G1/S checkpoint
a. The G1 checkpoint is the primary point at which a cell must choose whether to divide or not. Once the cell passes this checkpoint, it becomes committed to division. The G1 checkpoint checks for cell size, nutrients, growth factors, and DNA damage. Some questions it would "answer" are about these factors. For example, "Is the cell large enough to divide?" "Is the cell receiving positive cues (such as growth factors) from neighbors?" and other questions like this. If a cell does not receive the go-ahead cues, it may leave the cell cycle and enter a resting state called the G0 phase.
What are the "questions" that a cell must "answer" during each of the following checkpoints: b. G2 checkpoint
n the G2 checkpoint, evidence of DNA damage and DNA replication completeness is checked. The purpose of this checkpoint is to ensure that the daughter cells have complete, undamaged DNA. So the questions asked would be, "Is any of the DNA damaged?" and "Was the DNA completely copied during S phase?" If damage is detected, the cell will pause at the checkpoint to allow for repairs or completion of DNA replication. If the damage cannot be fixed, the cell may undergo apoptosis, programmed cell death.
What are the "questions" that a cell must "answer" during each of the following checkpoints: c. spindle checkpoint
The spindle checkpoint, or the M checkpoint, looks for chromosome attachment to the spindle at the metaphase plate. It examines if the chromatids are correctly attached to the spindle microtubules since the separation of the sister chromatids is an irreversible step. The cell scans the metaphase plate for "straggler" chromosomes that are in the wrong place. It will pause mitosis until this chromosome is captured by a spindle.
Diagram the relationship between cdK and cyclin.
Cdk and cyclin are two regulatory proteins involved in cell cycle control. The proteins combine into a MPF, maturation-promoting factor, that triggers a cell's passage past the G2 checkpoint into the M phase. These proteins are specific to each checkpoint and allow progression after the cycle has been halted. Cdks need cyclins in order to function. When cyclin is present, Cdks can phosphorylate the substrate or protein. Therefore, cyclins mediate Cdk binding and the activation of a substrate.
Illustrate and explain a mitosis-promoting factor.
A mitosis-promoting factor, or maturation-promoting factor, takes place at the G2 checkpoint. The MPF is also a heterodimer made up of cDk and cyclin B. This factor is the complex of proteins that make sure the M phase successfully begins. MPF phosphorylates the histone protein H1 and the nuclear envelope protein lamin. The phosphorylation degrades the nuclear envelope and condenses the chromatin to prepare for the M phase of the cycle. Once the heterodimer is functional, it drives the cell into metaphase. This causes cyclin B to degrade, thus inactivating the MPF. The cyclin B is synthesized once again in the S phase and forms a functional MPF, starting the cycle all over again.
Give an example of an external signal that regulates cell division and explain how it works.
An external signal is density-dependent inhibition, and it works by stopping crowded cells from dividing. The large number of cells in an area force competition for nutrients, growth factors, and space.
Growth Factors are a broad group of proteins that stimulate cell division. They bind to receptors that activate specific genes to trigger cell growth. Cells grow and divide in response to a combination of growth factors. Growth factors affect many different types of cells.
Platelets are sticky fragments of bone marrow cells. They form clots to stop bleeding and store a type of growth factor that helps repair wounds. Other growth factors are target specific.
Erythropoientin stimulates the production of red blood cells. Red blood cells carry oxygen. If you moved from the coast to the mountains, your blood oxygen levels would be lower because the air pressure is lower at higher altitudes. So your body would produce more erythropoietin to increase the number of red blood cells and increase the amount of oxygen in your blood. Growth hormones results in bone growth and affect your protein and fat metabolism.
Compare and contrast the functions of proto-oncogenes and tumor-suppressor genes. Give an example of each and explain why mutations in these genes can lead to cancer.
Proto-oncogenes produce protein products that enhance cell-division or inhibit normal cell death. While, tumor suppressor genes make proteins that prevent cell division or cause cell death. Proto-oncogenes and tumor suppressor work together to regulate cell growth. The proto-oncogenes accelerate growth, while the tumor-suppressor genes slow cell growth. Mutations that produce oncogenes, the mutated form of proto-oncogenes, rapidly accelerate cell growth, while mutations that affect tumor suppressors prevent the normal inhibition of growth. Either of these cause uncontrolled cell growth.
An example of a mutated proto-oncogene is when RAS becomes mutated. RAS is another oncogene that normally functions as an "on-off" switch in the signal cascade. Mutations in RAS cause the signaling pathway to remain "on," leading to uncontrolled cell growth. About thirty percent of tumors, including many important systems, have a mutation in RAS. Most oncogenes are dominant mutations and single copies of this gene can be sufficient for the expression of this growth.
Mutations in tumor suppressor genes result in cells that no longer show normal inhibition of cell growth and division. Theses mutations result in a loss of function, so they are usually recessive. The trait can not be expressed unless both copies of the gene are mutated. An example of this mutated tumor suppressor gene is hereditary retinoblastoma, RB. RB is a serious retina cancer occurring in early childhood. When one parent carries the mutation, there is a fifty percent probability that the offspring will receive this mutation. Most likely the offspring that receives it will then produce a copy of mutated RB in the second gene. The individual then develops retinoblastoma.
This set is often in folders with...
AP Biology Chapter 12 Part 1
AP Biology 13
AP Bio Chapter 4
mitosis. information 5
You might also like...
AP Bio Chapter 12 Mitosis
H Biology 1 - Chapter 8
Other sets by this creator
Biochem Test 3
Biochem Test 2
Com Science Midterm
Other Quizlet sets
Business Chapter 4
Bible Test Old Testament