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MCBG > DNA Replication Errors & Errors In Mitosis > Flashcards

DNA Replication Errors & Errors In Mitosis Flashcards

1
Q

What is aneuploidy? Give an example of aneuploidy and the disease it results in.

A

Error in cell division that results in the daughter cells having the wrong number of chromosomes.

Trisomy of chromosome 21 - Down’s syndrome

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2
Q

Why does aneuploidy of sex chromosomes have less adverse effects than with autosomal aneuploidy?

A

There is variation in the number of X and Y chromosomes between males and females anyway

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3
Q

What can the effect of trisomy in the sex chromosomes result in?

A

Infertility

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4
Q

What can cause aneuploidy?

A

Anaphase lag

Non disjunction

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5
Q

What is nondisjunction? What cells does it result in? Can it happen in mitosis or meiosis?

A

Where both copies of a chromosome go into 1 daughter cell

Results in cells with one copy too many and 1 copy too few

Both mitosis and meiosis

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6
Q

Which chromosomes are used in chromosome analysis?

A

Metaphase chromosomes from an actively dividing cell

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7
Q

A karyotype can be displayed in which two ways?

A

A visual spread of chromosomes grouped by size/shape

Written notation

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8
Q

What would the karyotype for a normal male be?

A

46,XY

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9
Q

What would the karyotype for a Down’s syndrome female be?

A

47,XX,+21

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10
Q

If non disjunction happens in the first post-zygotic division which sort of karyotype will be produced?

A

Non-mosaic karyotype

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11
Q

Monosomy is only viable for life in which case?

A

A female with one X chromosome

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12
Q

If non disjunction occurs after the first post zygotic division which sort of karyotype will be produced?

A

A mosaic karyotype will be produced

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13
Q

What is mosaicism?

A

The presence of two or more cell lines in an individual

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14
Q

If non disjunction happens in meiosis 1, what will be the effect on the four daughter cells?

A

50% trisomy
50% monosomy

(All affected)

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15
Q

If non disjunction happens in meiosis 2 what will be the effect?

A

50% normal
25% trisomy
25% monosomy

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16
Q

What is more important in contributing to genetic diversity; random assortment or crossing over?

A

Both equally important

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17
Q

What is the difference between anaphase lag and nondisjunction?

A

Anaphase lag results in 1 normal cell and 1 monosomic cell

Nondisjunction produces a trisomic and monosomic cell

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18
Q

What is a Robertsonian translocation?

A

Happens between two acrocentric chromosomes, results in the breaking of each chromosome at the centromere and the two longer arms forming a new chromosome and the two shorter arms forming a chromosome (which is usually lost)

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19
Q

DNA damage can be separated into which 2 categories?

A

Endogenous

Exogenous

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20
Q

Give 4 examples of exogenous causes of DNA damage.

A

Ionising radiation
Alkylating agents
UV light
Anti-cancer agents

21
Q

Give two examples of endogenous causes of DNA damage?

A

Dna replication errors

Free radicals

22
Q

What checkpoints exist to repair DNA damage? What happens at these checkpoints to allow time for repair?

A

G1 checkpoint
G2 checkpoint
Checkpoint in mitosis

Temporary cell cycle arrest

23
Q

If dna damage is too high or persists what two mechanisms are used to prevent the DNA damage resulting in cancer?

A

Apoptosis

Senescence = permanent cell cycle arrest

24
Q

By which 2 methods can DNA DSBs be repaired?

A

Homologous-directed repair

Non homologous end joining

25
Q

What does non-homologous end joining involve?

A

KU70/KU80 protect ends
Proteins recruited
Ligation of two broken ends back together

26
Q

What are two types of homology directed repair?

A

Single strand annealing

Synthesis dependent strand annealing (SDSA)

27
Q

What happens in the single strand annealing method of repairing DNA DSBs?

A

Break repaired - leads to deletions

28
Q

What happens in the SDSA method of repairing DNA DSBs?

A

Uses identical DNA molecule to rebuild/repair itself

Uses DNA polymerase

29
Q

What is meant by intra-tumour heterogeneity? What does it result in?

A

Different sub-clones within the same tumour

Tumour evolution and drug resistance

30
Q

What is often seen when using chemotherapy drugs on a heterogenous tumour? What are the disadvantages of using chemotherapy on a tumour with regards to tumour evolution?

A

Initial shrinking of the tumour and then further expansion of resistant sub clones of the tumour (comes back worse and is now resistant)

The chemotherapy itself can cause mutations, some of which could give advantageous resistance mutations –>further evolution

31
Q

How does cisplatin work as a cancer drug?

A

Causes dna damage in cancer cells by forming cross-links

32
Q

What is the main consequence of the shortening of telomeres?

A

Cell death/ageing

33
Q

How is the progressive shortening of chromosomes and telomeres prevented?

A

Telomerase aids in the replication of the ends of chromosomes and prevents chromosome degradation

34
Q

What is a problem that can arise from the ‘non homologous end joining’ repair of DSBs?

A

More than 1 DSB close together may result in the wrong ends being joined together

35
Q

What is chromosomal translocation? What can it result in?

A

Rearrangement of parts between non homologous chromosomes

Gene fusion

36
Q

What is chromosome inversion? How does it occur?

A

Where a segment of a chromosome is reversed end to end

A single chromosome undergoes breakage and arrangement within itself

37
Q

At which point of the cell cycle do non dividing cells enter G0?

A

At a point in G1 called the restriction point.

38
Q

Which organelle is important in ensuring the accuracy of chromosome segregation?

A

The mitotic spindle

39
Q

What is the structure of the mitotic spindle?

A

Part of the cell cytoskeleton - made of microtubules

40
Q

What is the function of a centrosome? How many of them are in each cell? Where do they travel in mitosis?

A

Organises the microtubules in the cell cycle

2 in each cell

To opposite poles of the cell

41
Q

The mitotic spindle is a proven target for successful treatment of…

A

Cancer

42
Q

What is the chromosome status of most cancer cells?

A

Most cancer cells are aneuploid and show chromosome instability

43
Q

Most cancer cells are aneuploidy and have increased copies of certain chromosomes, this results in increased expression of…

A

Oncogenes

44
Q

What is the result of an increased number of centrosomes? In which cells are amplified chromosomes normally found?

A

Multipolar spindles are formed that promote chromosome instability

Cancer cells

45
Q

If cancer cells often show amplified centrosomes, how are only two cells still produced in cell division? How can these mechanisms be exploited in cancer treatment?

A

Cancer cells have mechanisms to cluster these amplified chromosomes to produce two cells with aneuploidy

Inhibiting centrosome clustering in cancer cells —> in cell death and a possible cancer treatment with less side effects as it is specific to cancer cells

46
Q

In which stage of mitosis is there a cell cycle checkpoint? How is this checkpoint ‘passed’?

A

Metaphase

Checkpoint passed if all chromosomes are attached to the mitotic spindle

47
Q

What is cohesin?

A

The molecular glue that holds sister chromatids together, made from 4 proteins and makes a ring structure with dna

48
Q

What is the loading and offloading of cohesin regulated by?

A

Cohesin control proteins

MCBG (15 decks)

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