Cell Division and Disease - Coggle Diagram
Cell Division and Disease
The process of splitting a cell to create two new daughter cells from one parent cell. The daughter cells have the same number of chromosomes as the parent cell. Prophase is when the chromosomes condense, the spindle fibers form, the nuclear membrane and the nucleolus disappears. Metaphase is when the chromosomes line up in the middle (equator) of the cell. In Anaphase the sister chromatids separate. Telophase is when the nuclear membrane reforms and the chromosomes unwind so that in cytokinesis, the rest of the cell divides.
The G0 phase is the phase in which the cell doesn’t grow or divide, it is before the end of the G1 stage which makes the cell grow and preps for chromosomal replication. The S (synthesis) stage is where DNA replication occurs. G2 is the stage of the cell cycle in which the DNA is duplicated and the cell makes microtubules and other proteins that they need for cell division. Mitosis is the stage of nuclear and cytoplasmic division.
The G1 checkpoint is when the DNA and cell resources get checked by the p53. P53 activates DNA repair and holds the cell in the phase it's in, if the DNA is beyond repair then the p53 triggers apoptosis (programmed cell death). The G2 checkpoint checks both the DNA and protein needed for cell division. In the Mitosis checkpoint, MPF checks whether spindles and chromosomes are connected properly, while also checking that mitosis was completed successfully.
CDK is cyclin-dependent kinase and its levels are always the same, whereas Cyclin levels rise and fall based on which phase of the cycle the cells are in. Both CDK and Cyclin work together to push the cell into the next face. The CDK-Cycline complex is made at the beginning of a phase and broken down by the end of each phase. This gives a signal for the cell to move on if it's passed the checkpoints. If the cell hasn’t passed the checkpoint then the cell is killed or if there is a mutation, then the cell is uncontrollable.
Proto-Oncogenes are genes that control the rate of speed of how fast a cell moves through the cell cycle. When the proto-oncogenes are mutated, they act like accelerators that can’t be stopped, which makes the cell rush through the cell cycle that can develop cancer. As long as there is one mutation out of the pair in the Proto-Oncogenes, that will cause the cell cycle to go faster, which is labeled with the term “dominant”.
Tumor suppressor genes
These genes work to slow down the cell cycle and act as brakes. However, when they are mutated they act like brakes that don’t work. Hence, they can’t stop as nothing happens when you try to activate them. Two mutations out of the pair in this gene can cause the cells to go through the cell cycle faster, which is labeled with the term “recessive”. Mutations in this gene can cause cancer to develop.
DNA is replicated so that new cells can be made and organisms can grow. This process occurs in the S (synthesis phase). The first step is the helicase unwinding the DNA by breaking apart the hydrogen bonds between bases, after that the strands of DNA separate to where DNA polymerase adds the complementary bases to the growing strand with the original strand
Insertion & Substition
A mutation in the DNA replication process or the G2 stage where one base is substituted (put in the place) of another base. A mutation in the DNA replication process or the G2 stage where one or more bases are added to the gene strands.
A mutation in the DNA replication process or the G2 stage in which one or more bases are missing from a gene. This can cause a start or stop codon to not be there, which in turn can make the protein be too long or not form at all.
Effects of Mutations
If there is a loss of a start codon then no protein is made or if the start codon is in a different place then it could make the protein too long. If there is no stop codon then the protein could be infinitely long or way longer than it should be. If the stop codon is too soon then the protein will be too short and broken down. If any base pair is changed then it will code for a different amino acid, which can make a major change in a protein(like a sickle cell) or none at all.