Cell cycle Regulation\ Flashcards
Cell fusion experiment procedure
Cancer cells were fused from different stages of the cell cycle to determine if the nucleus’ would influence each other
Cell fusion experiment results
The concluded that the cytoplasmic molecules caused G1– S and G2–M
Experiment determining how cell fusion worked
Hartwell used baking yeast and grew yeast mutants at a normal temperature and then heated them up. He identified where the mutants got stuck. Compared their DNA with DNA from healthy cells
Cell phase experiment results
Some problems were DNA replication, mostly they were cell cycle regulation problems
Paul Nurse’s experiment
Similar to Hartwell but he used fission cells instead of budding cells. He discovered CDC2
CDC2 discovery
Encodes a protein needed for G2–M phase. Protein Kinase (inactive or active proteins). All cells have this gene suggesting that it occurred early in the evolutionary pathway
Cyclins
Proteins that control the cell cycle
3 checkpoints in the cell cycle
Prevent critical phases form starting to early, or with improper cells. G1/s, G2/M, mitotic spindle checkpoint
G1/S checkpoints
Decides if a cell will start duplicating its DNA.
G1/S stops if…
DNA is damaged from radiation or chemicals. If extracellular signals (hormones, growth factors) are not present
G2/M checkpoint
Decides if a cell will enter mitosis
G2/M stops if
DNA was not properly replicated or is damaged
Mitotic spindle checkpoint
Checks if spindles are properly attached and that chromosomes are properly lined up on the metaphase plate. Essential for producing identical cells
Cell regulation involves
Cyclins and cyclin dependent kinases
Cdks
Protein kinase (phosphorylates and regulates target protein activity, cyclin dependent, and the concentration remains constant which cyclin concentration changes
Cyclin dependent
Is only active when cyclin is present and bonded to it
Each Cdks
Is active at a different time and regulates cell activities
Cyclin cdks complex regulation
Integrated into each checkpoint
G1/S Cyclin cdks complex regulation
G1/s cyclin binds to cdk2 at the end of G1 causing the cell to commit to DNA replication
G2/M Cyclin cdks complex regulation
S cyclin binds to the cdks2 in the S phase, DNA replication is initiated and the cell progresses through S phase
Mitotic spindleCyclin cdks complex regulation
My cyclin binds to cdks1 in G2 causing G2 to become mitosis.
M phase promoting factor
MPF, know as the M cyclin-cdk1 complex. Activates APC at the end of metaphase (if the spindles are properly attached)
Anaphase promoting complex
Degreades anaphase inhibitor allowing anaphase to occur
In late anaphase it degrades M cyclin which deactivates cdk1
Deactivation of Cdk1 leads to
chromosomes to elongate, nuclear envelope to form, and the cytoplasm to divide
External signal molecules
Control the cell cycle and are peptide hormones, growth or death factors
How do external signal molecules work
They bind to receptor sites, triggering reactions in the cell. Often add phosphate groups to cyclin-cdk complexes.
External signal molecules can
Speed up, slow down, stop or bring a cell back from G0
Contact inhibition
Occurs when cells recognize contact with other cells or molecules in ECM. Shunts cells into G0 for fully mature organs
Contact inhibition division inhibition
Is a cell is touching the cells on all sides it is good. If it is no, a cell will divide to make a cell
Asymmetric cell division
When daughter cells are decidedly different. Happens in growth, development, and STEM cells
STEM cells
Makes 1 cell for growth and maintenance and 1 as a stem to replenish the stem cell pool. The same cell has 2 different fates
Why do STEM cells do what they do
Because they can specify where the organelles go in cell division. Only some proteins end up in the progenitor cell, allowing it to have a special function
Niche
Local area where the cell is dividing
Improper external niche leads to
Brain and other forms of cancer.
Cellular senescence
An anti tumor mechanism. A cells loss of proliferative ability over time (stops dividing)
Hayflick factors
Reasons why cells stop dividing. DNA damage or they run out of telomeres
DNA damage
DNA sequencing, chromosome structure, genes for fixing DNA are destroyed
Shortening telomeres
No DNA can repair, so some is lost every time a cell divides.
Telomeres
Repetitive DNA sequences added to teh end of chromosomes by the enzyme telomerase
What is telomeres are renewed or removed
Renewed-By drugs, a person has a higher chance of getting cancer
Removed-A person can become more resistant to cancer
Cancer
Produces a tumor by uncontrollable growing and dividing.
Metastasis
Altering of cancer cells to contact inhibition causing them to move from the original tumor and spread throughout the body
Tumors impair…
Steal blood flow, compress or break through tissue
Oncogenes
The process that tumors often occur because of gene mutations to cyclin cdk system
Apoptosis
Programed cell death, can be internal or external
Caspases
The enzyme that causes the cell to stop dividing and die. Encoded by cell death abnormal gene (CED-3)
If a cell is predestined to die
Internal EGL 1 protein is made and binds to CED-9 protein causing the release of CED-4 and active azotosome. CED-3 is activated and the cell dies
Causes of death
Nuclear DNA deration and disrupted mitochondrial function
Dead cells are consumed by neighboring cells
Why do cells die
To fulfill their purpose, reduce uncontrolled division, avoid mutant cells
