2.7. Life cycle control mechanisms, tumors Flashcards

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1
Q

What is the difference between cytokinesis in plant and in animal cells?

A

plant - create a new plasma membrane and cell wall between them during cytokinesis. Vesicles containing elements of the membrane/wall will accumulate, fuse, and separate the cell.
animal - a cleavage furrow appears and divides the cell into two daughter cells (PM is more flexible than CW)

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2
Q

What is the purpose of mitosis for multicellular organisms and what for unicellular?

A

multicellular organisms - growth, development, and tissue regeneration
unicellular organisms (eukaryotic) - reproduction

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3
Q

What is mitotic index and how is it calculated? Which tissues have a high MI and which zero?

A

Mitotic index = (number of cells at any stage of mitosis)/(total number of cells)
- comparing it with the “normal” MI for that tissue/age of the organism
- stomach and skin are easily damaged so have a high normal MI
- muscles, kidneys, and brain have zero because they cannot regenerate

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4
Q

What are the checkpoints in the cell cycle? Outline what is checked in each and why.

A

1| S-phase entry
The most important checkpoint (/stimulus for the S phase)
- if the mitosis is complete
- if the growth/protein synthesis in the cell is adequate (otherwise new cells cannot be made)
- if there is any DNA damage
2| Mitosis entry
- if the DNA replication is complete
- if the growth/protein synthesis in the cell is adequate
- if there is any DNA damage
3| Mitosis exit
Between prophase and metaphase
- if all chromosomes are attached to the spindles

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5
Q

Why do concentrations of some proteins increase and decrease in a regular pattern during the cell cycle?

A
  • same genes are differently expressed in different phases of the cycle - fluctuations coincide with the turning points of the cell cycle
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6
Q

What are cyclin proteins?

A
  • a family of proteins that ensure well-timed cell processes and cell division (their concentrations fluctuate at specific moments in a pattern). The trigger for each phase is at the peak concentration of a specific cyclin.
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7
Q

Which types of cyclin proteins are there? Outline their functions.

A

Cyclin D - Helps in progression through G1 and into S
Cyclin E - Helped the DNA prepare for replication (losing connection with histones – preparing for cyclin A)
Cyclin A - Initiates DA replication in the S phase (by attaching helicase)
Cyclin B - Regulates progression through prophase and metaphase – makes sure that all chromosomes are attached to the spindles

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8
Q

What does a cyclin do after reaching its threshold level? How does this impact the life cycle?

A
  • at the threshold level - binds to and activates kinase enzymes (by phosphorylation, ATP is invested, and the enzyme is excited)
  • activated enzyme will energize molecules (proteins) around it and by increasing molecular movement increase the number and rate of reactions responsible for tasks specific to the phase of the cell cycle that has been entered
  • a new phase started/triggered
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9
Q

What is apoptosis?

A

cell suicide or programmed cell death

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10
Q

What is a tumor? What is it caused by?

A

a disease in which there is a defect in the regulation of the cell cycle (cells divide rapidly) – any outgrowth – caused by multiple gene mutations of cyclin genes

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11
Q

What are cyclin genes responsible for? What types are there?

A
  • they control the cell cycle
    1| Proto-oncogenes
    2| Tumor-suppressor genes
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12
Q

What is the role of proto-oncogenes? Give an example.

A
  • code for proteins that promote division in a regulated manner (when there is a need for them)
  • e.g. cyclin gene
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13
Q

What is the mutated form of proto-oncogenes called? What do they do?

A

oncogene - their protein products (cyclins) do not perform their function properly and stimulate the cell cycle in a non-regulated manner

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14
Q

What is the role of tumor-suppressor genes? Give an example.

A
  • their expression is triggered by DNA mutations – they prevent the mutated cell from dividing by coding for proteins that:
    1| inhibit the cell’s growth and division
    2| fix the DNA mutation
    3| cause apoptosis
    – e.g. p53 (activates genes for apoptosis)
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15
Q

What does the mutated TSG do?

A

it cannot prevent the proliferation of the mutated cell so it divides and a tumor is formed

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16
Q

What are mutagens? Give examples.

A
  • factors that increase the incidence of mutations
  • radiation (UV and X-rays), cigarette smoke, and asbestos (inflammation in lungs)
17
Q

Explain the difference in a primary and secondary tumor. What is the difference between a benign and a malignant tumor?

A

primary tumor - initially formed, there are two types: benign and malignant
- benign grows slowly (cells are tightly interconnected), not life-threatening
- malignant grow aggressively, can invade neighboring tissues or spread to form secondary tumors (in distant parts of the body), are life-threatening

18
Q

What is metastasis?

A

the spreading of cells to form secondary tumors

19
Q

What are protein kinases?

A

enzymes that transfer phosphate groups from ATP to proteins (phosphorylation).
E.g. tyrosine kinase transfers phosphate to tyrosine (an amino acid) in specific proteins.
(phosphorylation of proteins in many cases activates them and removal of the phosphate makes them inactive again)

20
Q

What is the example of protein kinase action in chemical signaling?

A

the insulin receptor - a large transmembrane protein with two tails extending into the cytoplasm that are tyrosine kinases.
The binding of insulin causes conformational changes that connect the two tails to form a dimer - each tail phosphorylates the other tail and this activates the insulin receptor - triggering signal transduction - vesicles containing glucose transporters (channel proteins - uptake of glucose by facilitated diff) to move to the PM and fuse with it - glucose can be used as a substrate in CR