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102 Theme 3 > L4 DNA and Chromosomes > Flashcards

L4 DNA and Chromosomes Flashcards

1
Q

What does the M Phase consist of, in abstract terms?

A

Mitosis (nuclear division)

Cytokinesis (cytoplasmic division)

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2
Q

M Phase - what are all 6 stages called? [6]

A 
Prophase 
Prometaphase 
Metaphase 
Anaphase 
Telophase 
Cytokinesis
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3
Q

What is a telomere?

A

Structure at the end

Get shorter as you age

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4
Q

What is a centromere?

A

Where two chromatids meet

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5
Q

What is a kinetochore?

A

Give rise to spindle microtubules

Pull chromatids apart

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6
Q

Prophase - what happens?

A

Replicated chromosomes condense

Mitotic spindle (outside nucleus) assembles between 2 centrosomes as they move apart

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7
Q

Prometaphase - what happens?

A

Starts breakdown of nuclear envelope abruptly

Chromosomes attach to spindle microtubules via kinetochore and undergo active movement

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8
Q

Metaphase - what happens?

A

Chromosomes aligned at equator of spindle - midway between spindle poles.
Paired kinetochore microtubles attach to opposite poles of spindle

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9
Q

Anaphase - what happens?

A

Sister chromatids synchronously separate and each is pulled slowly towards the spindle pole attached
Kinetochore microtubles get shorter and spindle poles move apart –> segregation

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10
Q

Telophase - what happens?

A

Sets of chromosomes arrive at spindle poles. Nuclear envelope forms - 2 nuclei
Division of cytoplasm begins with assembly of contractile ring

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11
Q

Cytokinesis - what happens?

A

Cytoplasm divided by contractile ring of actin and myosin filaments, pinches in cell to create 2 cells

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12
Q

Cell cycle checkpoints - what are they?

A

Controlled by cyclins and protein kinases (Cdks) – phosphorylation of cdk/cyclin complexes

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13
Q

Chemotherapy drugs target which stages of cell replication?

A

S and M phases – kill rapidly replicating cells

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14
Q

p53 - what is its significance?

A

~50% cancers have mutations in p53

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15
Q

DNA replication - why is it important?

A

Must replicate 6 billion bp
Accuracy and speed required (~100nt/s)
Complementary bp
Polar strands (opp direction)

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16
Q

Nucleotide added to which end?

A

3’ end

17
Q

DNA synthesised direction/energy?

A

5’ to 3’

Breakdown of triphosphate bond = energy

18
Q

Leading/lagging strand - what do they mean?

A

Leading strand – continuous synthesis
Lagging strand – discontinuous synthesis
(Okazaki fragments)

19
Q

Origins of replication

A

~10,000 origins of replication: speeds up process to ~1h

20
Q

DNA replication enzymes [6]

A
  1. DNA Helicase: Unwinds double helix
    1. DNA Polymerase: adds nucleotides to 3’ end of leading strand
    2. Exposed lagging strand protected by single-strand DNA binding proteins
    3. DNA Primase: adds small RNA primer to lagging strand
    4. DNA Polymerase: adds nucleotides to 3’ end of lagging strand
      DNA Ligase: joins together small gaps
21
Q

Werner syndrome - what is it?

A

1/200,000 in USA
DNA Helicase mutation - premature aging disorder
Errors in DNA replication and repair

Increased risk of cataracts, atheroscleoris, osteoporosis and cancer

22
Q

DNA polymerase is responsible for…

A

Monitor bp between new/old strands & catalyse nucleotide addition reaction
Proofreading
Clips off mismatch

23
Q

Primers are responsible for…

A

Created by primase
10 nucleotide long
RNA primer needed for leading and new primer for lagging at intervals
DNA polymerase elongates fragment until next primer (deoxyribonucelotide)

24
Q

What does nuclease do?

A

Degrade RNA primer & repair polymerase replaces it with DNA

25
Q

What does DNA helicase do?

A

uses energy from ATP hydrolysis to properl itself forward
Pries double helix apart
DNA topoisomerase relieve tension and produce nicks in DNA backbone

26
Q

DNA topoisomerase - function?

A

relieve tension and produce nicks in DNA backbone

27
Q

Sliding clamp - function?

A

keep DNA polymerase firmly attached to template - form a grip around new double helix & allows polymerase enzyme to move

28
Q

Preventing mutations - how?

A

Proof-reading capacity of DNA polymerase during DNA replication

Excision repair systems act throughout cell life repairing DNA damage

Polymerase can detect distortion in shape due to wrong base pair (rungs no longer same length)

29
Q

DNA damage - how?

A

Large number of genes devoted to DNA repair

Internal sources: Products of normal cell function

External sources: Mutagenic chemicals (benzene, cigarette smoke)
UV
Ionising radiation

30
Q

Characterising mutation - how?

A

Effect on heritability (somatic or germ line)

Scale of mutation (chromosome or SNP)

Effect on normal function (loss or gain of function)

31
Q

Monogenic genetic disease - overview

A

Substitution: Sickle-cell anaemia
Deletion: Cystic fibrosis
Insertion: Huntington’s disease

32
Q

CF

A

Deletion

• Abnormal lung mucus leading to infection
• 9,000 cases in the UK 
• Impaired chloride transport (loss of function)
• 70% of patients share 3bp deletion in CFTR gene on chr 7 (cystic fibrosis transmembrane conductance regulator)
33
Q

Sickle cell disease

A

Substitution

Single nucleotide substitution in HBB gene (beta chain of haemoglobin)
• Misshapen blood cells do not survive as long (can cause anaemia) and clog up capillaries
~12,500 SCD in the UK

34
Q

Huntington’s disease

A

• Neurodegenerative disease (starts to appear age 30-50)
uncontrollable muscular movements
loss of memory and depression
difficulties with speech and swallowing
• Damage of the nerve cells in areas of the brain
• ~7,000 cases in the UK
Caused by increase in number of CAG trinucleotide repeats (encoding glutamine) in the Huntingtin (HTT) gene

35
Q

Polyglutamine

A

residues stick together creating a toxic product (gain of function) which causes neuron cell death through multiple mechanisms

36
Q

Xeroderma pigmentosum

A 
• Most mutations in DNA repair lethal
	• XP: mutation in UV repair
		Unable to remove thymine dimers
		Autosomal recessive disorder
	• Acute sun sensitivity
	• Hypo- and hyper-pigmentation
	• Multiple cancers at young age
	• Mental retardation
Progressive degeneration

102 Theme 3 (12 decks)

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