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Flashcards in Meiosis/Mitosis Deck (35)
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1
Q

Why does meiosis end in haploid cells?

A

To keep the same number of chromosomes from generation to generation

2
Q

How does meiosis achieve genetic diversity

A

crossing over - chiasmata

random assortment

3
Q

Define mosaicism, what does degree of mosaicism depend on?

A

Two or more cell lines in an individual - depends on how early in the zygote the mitotic non-disjunction occurs. Earlier = more cells affected

4
Q

What can non-disjunction in mitosis vs meiosis cause? When is the exception?

A

Mosaicism vs Aneuploidy. If non-disjunction occurs in the first zygotic mitotic division it will appear as aneuploidy not mosaicism.

5
Q

When is one time you may see monosomy as viable?

A

If it is the X chromosome - Turners Syndrome

6
Q

Mosaicism is an example of a ________ mutation

A

Somatic

7
Q

Meiosis error is an example of a ________ mutation

A

Germline

8
Q

Name 3 consequences (disease etc) of faulty meiosis

A

Miscarriage
Mental retardation
Infertility

9
Q

Are Kleinfelters and Turners example of mosaicism or aneuploidy? Are they inherited?

A

Can be both. Aneuploidy in meiosis = more symptoms. So can be both germline and somatic mutations. Not inherited. Mostly infertile

10
Q

What does degree of mosaicism depend on?

A

How early the mutation is - earlier = more cells affected

11
Q

What is SRY?

A

Sex determining region on Y chromosome.

12
Q

What are the relevance of PAR regions? What type of gene are they called?

A

PAR1&2 on XY are only regions that should be crossed over during meiosis as only homologous genes. Other genes are sex-linked. They are pseudoautosomal and are the regions that help line up X with Y in meiosis

13
Q

Which is more severe, aneuploidy in sex chromosomes or autosomes?

A

Autosomes as they are more likely to be genes essential for life. Can survive with 1/3 chromosomes (with 2/3 in normal/Kleinfelters one X is usually inactivated anyway)

14
Q

What is anaphase lag, what can anaphase lag cause? When is it useful?

A

It is delayed chromosome movement/faulty spindle attachment leading to aneuploidy or mosaicism. It is useful in trisomy rescue as can make the cell normal

15
Q

What are microtubules made of?

A

Tubulin

16
Q

What are amplified centrosomes? What can this cause? Why?

A

Increased number of centrosomes making the cell multipolar, happens in cancer cells. They do have a mechanism to help prevent it called clustering - helps reduce aneuploidy so cancer cells can live on. Number of centrosomes at each end determines polarity and where chromosomes will go. Inhibit cancer cell clustering as a therapeutic target - wouldn’t affect cells that don’t cluster i.e normal cells.

17
Q

How would a cancer drug that targets tubulin help treat cancer? e.g. Paclitaxel

A

Microtubules prevented from assembling - Prevents metaphase/anaphase leads to mitotic arrest = prevents division of cancer cells, prolonged cell cycle arrest = apoptosis

18
Q

What is the centrosome made up of?

A

Microtubules/Centrioles etc (whole organelle)

19
Q

How can an increase in centrosomes add to cancer heterogeneity?

A

Increase in centrosomes = multipolar cell division = aneuploidy in cancer cells = mutations and genetic variation = tumour heterogeneity

20
Q

What are 4 things that all lead to cancer plasticity (heterogeneity)?

A
  • Aneuploidy
  • Translocations
  • DNA damage
  • Treatment resistance - mutation
21
Q

Name 3 tumour suppressors

A

APC, p5, BRCA1/2

22
Q

Name 3 Oncoproteins

A

RAS, Myc

23
Q

Name two viral proteins that can inactivate p53

A

E6/E7

24
Q

Do cancer cells have active telomerase? What could you use this for? Whats the risk?

A

Yes - could target in treatment to increase cancer cell genetic instability = apoptosis. Risk of increasing tumour heterogeneity.

25
Q

What is XP Xeroderma Pigmentosa disease? What kind of inheritance?

A

Autosomal recessive, reduction or elimination of NER DNA damage repair - damage from UV light cannot be repaired = sunburn, skin cancer, sensitive eyes.

26
Q

What is the effect of UV on DNA? which method of DNA damage repair is used to fix this?

A

Photon of light absorbed by DNA causes a thymine dimer (pyrimidine dimer). These are repaired by NER.

27
Q

What chromosomal mutations could Non-homologous end joining DNA repair lead to (2)?

A

Inversion, translocation, if two or more DBSs are present in the vicinity

28
Q

Cancer cells are mostly aneuploidy true or false

A

True

29
Q

Whats the relevance of separase in mitosis?

A

It is an enzyme that coordinates the loading/unloading of cohesin with the sister chromatids - allows metaphase to occur. Essential for separation of chromosomes

30
Q

What does cohesin do in the cell cycle? Whats its structure? How is it implemented in cancer?

A

Cohesion holds sister chromatids together & stabilises, it gets cleaved in metaphase. Is a ring. If not cleaved, can cause aneuploidy –> cancer

31
Q

What doe ESCO1/2 do in mitosis? What happens if these are mutated?

A

Are acetyl transferases. Acetylates SMC3 protein - closes cohesion ring, allows stable association of two sister chromatids.
Cancer.

32
Q

What is SMC protein? What is the relevance of SMC in mitosis?

A

subunits of cohesin - form ring structure with other proteins. Gets acetylated by ESCO1/2 which closes the ring to stabilise sister chromatids

33
Q

Name 6 important proteins involved in chromatid cohesion and separation during mitosis and what they do?

A

Cohesin - load onto chromosomes -glue chromatids together
Separase - enzyme
SMC proteins
ESCO1/2 - acetyl transferases close cohesin ring, stable association of chromatids
Wapl - regulate loading/unloading of cohesin
SMC2/3 - get acetylated to close cohesin ring
PDS5A/B - control loading and unloading of cohesin

34
Q

How does cohesin interact with DNA?

A

Dynamically

35
Q

When is cohesin loaded/removed?

A

Loaded in telophase

Removed prophase-metaphase