Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > DNA and Chromosomes - MCB L4 > Flashcards

DNA and Chromosomes - MCB L4 Flashcards

1
Q

Give the 4 phases of cell cycle, in order

A

G1, S, G2, M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens during the G phases?

A

The cell grows e.g. ATP accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which phases comprise interphase?

A

G1, S, G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Centrosomes

A

Things at each pole of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Centriole

A

Organelle inside centrosome that releases spindle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Centromere

A

Between sister chromatids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give the stages of M phase in order

A

Prophase, Prometaphase, Metaphase, Anaphase, Telophase, Cytokinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Telomeres

A

Repeating, non-coding sequences at ends of chromosomes to protect chromosome by protecting coding sequences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Kinetochore

A

Intimately associated with centromere. Spindle fibres join to kinetochore.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Prophase

A

Nucleolus disappears. Chromosomes condense. Mitotic spindles form from centrosomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prometaphase

A

Nuclear membrane disintegrates. Centrosomes move to opposite poles. Kinetochores form and spindle attaches to kinetochores.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Metaphase

A

Chromosomes align at equator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anaphase

A

Sister chromatids separate, centromeres split in two. Now called chromosomes. Pulled towards opposite poles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Telophase

A

Chromosomes arrive at poles. Spindle breaks down. Nuclear envelope reforms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cytokinesis

A

Cytoplasm divides resulting in two genetically near-identical cells. All other components e.g. Golgi are randomly assigned between cells as they can make whatever they lack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What molecules regulate cell cycle? How do they regulate it?

A

Protein kinases and cyclins; they regulate the cell cycle through a series of phosphorylation and dephosphorylation reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If something is sensed to be wrong in the cell cycle, what occurs?

A

Cell cycle stops or cell dies (apoptosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What may occur if the control mechanisms in cell cycle fail?

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which phases do chemotherapy drugs target? What side effect does this have?

A

S and M phases. This means that rapidly replicating cells such as hair cells are killed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If not enough ATP in a cell to divide, what happens?

A

The cell cycle is paused: the control mechanisms signal to ‘wait’

21
Q

What happens in S phase?

A

DNA replication

22
Q

What happens in M phase?

A

Nuclear division and cell division

23
Q

The breaking of the triphosphate bond in nucleotides is useful for what reason?

A

Provides energy for formation of covalent phosphodiester bond between nucleotide and next nucleotide

24
Q

What is the benefit of having multiple replication forks?

A

Allows for genome to be copied far quicker

25
Q

What are the names of the two parts of the replication fork?

A

Leading strand, lagging strand

26
Q

Leading strand. What kind of synthesis?

A

3’ end moving towards fork. Continuous synthesis

27
Q

Lagging strand. What kind of synthesis? Why does it have gaps? What are the fragments called?

A

3’ end moving away from fork. Discontinuous synthesis. DNA polymerase works in 5’ to 3’ direction. So once it has polymerised one part of strand, a new bit has appeared nearer to fork. So polymerase rejoins nearer to fork, leaving gaps and making double stranded Okazaki fragments. Gaps filled by DNA ligase.

28
Q

DNA primase

A

Adds an RNA primer, a foothold for polymerase to bind to. Primer is on both strands.

29
Q

Nuclease

A

Removes primer after polymerase has synthesised DNA. Also removes damaged DNA/ wrong nucleotides.

30
Q

DNA ligase

A

Comes in after nuclease. Tidies up, connects fragments

31
Q

Is DNA primase more active on one strand than the other? Why?

A

More active on lagging strand as it has to keep adding more primers.

32
Q

Werner Syndrome

A

Arises from mutation in DNA helicase. Errors in DNA replication and DNA repair. Cells replicate slower so start to show diseases found in elderly.

33
Q

Name two methods of preventing accumulation of mutations

A

Proof-reading capacity of DNA polymerase. Excision repair systems.

34
Q

Proof reading capacity of DNA polymerase

A

During DNA replication, DNA polymerase is proof-reading the strands. If wrong nucelotide inserted, the position of the free 3’ end of the nucleotide is changed so next nucleotide cannot bind so DNA polymerase stalls, preventing mutation. Wrong nucleotide removed by nuclease.

35
Q

Excision repair systems

A

Throughout cell life, they repair any damage to DNA

36
Q

What internal sources can damage DNA?

A

Products of normal cell function. Cell produces oxygen free radicals and hydrogen peroxide

37
Q

What external sources can damage DNA?

A

Mutagenic chemicals (benzene, cigarette smoke), UV, ionising radiation

38
Q

Synonymous SNP

A

No change in amino acid sequence due to SNP, so function of protein unchanged so not associated with disease state.

39
Q

Non-synonymous SNP

A

Change to amino acid sequence due to SNP so function of protein changed so associated with disease state.

40
Q

Somatic mutation

A

Bad for the individual, affects a particular cell type.

41
Q

Germ line mutation

A

Affect every cell in offspring

42
Q

What are monogenic genetic diseases?

A

Diseases arising due to a single gene disorder

43
Q

Name 3 examples of monogenic genetic diseases, stating what type of mutation is responsible for each and whether the disease is associated with loss or gain of function

A

Substitution: Sickle-cell anaemia. Loss of function. Deletion: Cystic fibrosis. Loss of function. Insertion: Huntington’s disease. Gain of function

44
Q

Sickle Cell Disease

A

Due to single nucleotide substitution in HBB gene (beta-globin chain of haemoglobin). Haemoglobin molecules become sticky, leading to sickle shaped RBCs. Die quickly, so causes anaemia, and clogs up capillaries

45
Q

Cystic Fibrosis

A

3 base pair deletion in CTFR gene which causes protein to not be transported properly so not expressed on outside of cells. The protein is a transmembrane protein involved in chloride transport. So messes up chloride transport particularly in lungs so abnormal mucus leading to infection. Impaired chloride transport so loss of function

46
Q

Huntington’s disease

A

Insertion. Neurogenerative disease. Due to increase in number of CAG repeats in HTT gene. HTT gene is expressed in nerve cells. CAG encodes glutamine and polyglutamine and polyglutamine is sticky so polyglutamines stick together to make a toxic product which kills nerve cells

47
Q

What determines the severity of Huntington’s disease and how early you will get it?

A

The number of CAG repeats; the more polyglutamine the more toxic the gene.

48
Q

How is Huntington’s disease a gain-of-function mutation?

A

Because of the production of a toxic molecule.

Medicine (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions