Mitosis Flashcards
(25 cards)
Where does mitosis happen in the cell cycle?
Remember this is in M phase
What attach to centromeres?
The centre of the chromosome
Spindle fibres attach here to pull apart sister chromatids
What are homologous chrososomes?
They have the same genes (note this doesnt say alleles) arranged in the same order
These chromosomes are structurally similar
On chromosome come from the mother and one from the father
So what do centromeres join together?
Chromatids
What happens in the different stages of mitosis?
Prophase
- there is condensation of sister chromatids (this just means that they become more condensed (fatter)
- identical copies of the chromatids are made
Metaphase
- this is when there is attachment of mitotic spindles to the centromere’s kinetochore
- this is done by microtubules
Anaphase
- this is when there is the separation of sister chromatids to opposite poles
Telophase
- this is when the nuclear envelope reassembles, at the start of cytokinesis
What does the decatenation checkpoint ensure? And what happens if this checkpoint is bypassed?
This is before the M phase in the cell cycle
This checkpoint is before M phase of the cell cycle. It makes sure chromosomes aren’t tangled.
The checkpoint DELAYS entry into mitosis if the chromosomes arent disentangled.
A bypass of the decatenation checkpoint causes chromosome breakage and nondisjunction during mitosis. This results in aneuploidy (abnormal numbers of chromosomes) and chromosome rearrangements in daughter cells.
Another use of yeast…
What is the advantage of using yeast as model for the cell cycle?
Yeast can grow as haploid (having a single set of chromosomes)
Or as diploid (having a double set of chromosomes)
Yeast also have a rapid division rate of 1 hour
Cell cycle control genes are highly conserved thus the genes that control CDKs in humans are the same as in yeast.
What ways can we use yeast to study mutations in the cell cycle?
Can make yeast temperature sensitive via mutations. And then investigate the effects of said mutations on CDK formation for example
Diploid yeasts can also be used to maintain lethal mutations that are then studied as haploids.
What is the advantage of using xenopus to study the cell cycle?
Their eggs are easy to collect and they are big
They have a rapid division rate
Their large size means they can purify proteins more easily
They can be manipulated by injections of RNAs or chemicals in oocytes.
How can we study the affect of proteins in the cell cycle?
You can deplete the cell cytoplasm of different proteins using antibodies
Or you can remove cytoplasm at different stages of the cell cycle
What is triggered in late G2 of the cell cycle to activate mitosis?
What triggers this? And what does a positive feedback inhibit?
Cdc25 phosphatase in a positive feedback loop mechanism.
This is triggered by S phase cdk complexes
Once this is started a positive feedback loop inhibits Wee1 genes (which stop mitosis) and activate more Cdc25
What is the anaphase promoting complex? And how does it become activate?
Note this says a complex
Thus this is a complex which sees the destruction of proteins
This allows for entry into anaphase
It is a ubiquitin ligase
It becomes active when a Cdc20 sub unit binds to it
What two proteins are targeted by the anaphase promoting complex?
Note one of these protein targets is useful and one isnt.
Also how is the protein complex regulated?
Securin
- which is a protein linkage that holds sister chromatids together
- destruction of the proteins activate a protease that separates sister chromatids leading to anaphase
However the negative protein targets is S phase and M phase cyclins
- if these cyclins are destroyed it means cyclins in S phase and M phase
- this means that the CDK’s targets arent phosphorylated
The complex is regulated by:
- being on in G1 phase
- but being turned off in S phase to allow cyclin accumulation.
- so when its turned back on in M phase there are enough cyclins for it to work.
Note we can get chromosome gene mutations in two ways which cause a PHENOTYPIC change, known as a two hit hypothesis.
What is a loss of heterozygocity mutation? And what is an example
And what is a hemizygosity mutations?
Heterozygosity mutation is when one allele is correct and one allele is incorrect causing a phenotypic change
- An example of this is with the tumour suppressor gene. A phenotypic change here is seen with inactivation of its proteins function EG RB
Hemizygosity mutations:
- is where you have one copy of an allele. If this is a mutant then you get a phenotypic change.
How do heterozygosity mutations occur?
Chromosomes may end up in the wrong daughter cells
This is caused by the failure of chromosomes to split normally
Thus there is a lagging chromosome during anaphase
Thus chromosome is non disjunctional which means there is a failure for chromosomes to split normally
What are the three types of mitotic spindle? And what is there structure?
Interpolar microtubules
- these overlap
Kinetochore microtubules
- these attach to chromosomes at kinetochores (the proteins found at the centromeres)
Astral microtubules
- contact cell cortex to position the spindle
What is a centrosome?
This is a centriole - which is an organelle by the nucleus of the cell which helps to make microtubules
These are surrounded by the pericentriolar matrix
These nucleate microtubules.
What is described as successful mitosis? Why is this considered a trail and error process?
When sister chromatids go to opposite poles
Is is a trail and error process to get 1 kinetochore to one spindle fibre
What is correct attachment of centromere to spindle fibres and what does this cause?
Correct attachment of spindle fibres to the centromere causes tension
This tension is caused when kinetochore spindle fibres try to pull in opposite directions
But the sister chromatids resist which causes tension
What causes incorrect attachment of spindle fibres to the centromere? And how is this overcome
This is when spindle fibres attach to the wrong position on centromeres
This decreases tension, especially when pulling the chromosomes apart
So then an inhibitory signal is sent
This loosens the microtubule attachment site.
What enzyme does the anaphase promoting complex activate? And what negative effect of this complex poses a problem
Remember this is the complex which destroys the protein secruin which holds chromosomes together. This is activated when the Cdc20 protein binds to it.
The promoting complex can activate separase by phosphrylating it which break down the securin
Remember this APC also breaks down CDKs in metaphase
This causes CDK inactivation which means less separase phosphorylation occurs (remember from previous lectures you learnt Cdc20 is a CDK)
This means separase can’t work aswell
What are the three ways is which hetrozygosity can occur?
By non disjunctional chromosomes (when chromsomes dont separate properly which can lead to cells with both allele copies being incorrect)
By mitotic recombination (this is when chromsomes accidentally swap out correct alleles_)
Cause by gene conversion (this is like mitotic recombination but DNA polymerase accidentally swaps out correct alleles for incorrect ones )
How can hemizygosity occur?
This can happen due in instance of non disjunction
Remember this is when chromsomes dont separate properly
This means that 3 chromsome genes may end up in one cell
But in the other cell there may be only one chromosome gene
Which may be faulty
How can loss of heterozygosity be caused by gene conversion?
Remember loss of heterozygosity means in the cell one chromosome has the corret gene allele and one has a mutant
DNA replication via polymerases may in rare instances jump between chromosomes during chromosome DNA replication
This means that the incorrect mutant alleles may be copied
This may cause cells to have a mutant allele and a correct allele
