Topic 8 A Flashcards

(32 cards)

1
Q

What are the 6 types of mutations?

A

Substitution, deletion, addition, duplication, inversion and translocation

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

What are hereditary mutations?

A

When a gamete contains a mutation for a genetic disorder

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

What is a frameshift mutation?

A

When the numbe rof bases cahnge causing a shift in the base triplet that follows so triplet code is read differently

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

What are mutagenic agents?

A

Something that increases the rate of mutations

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

How do tumour suppressor genes control cell division?

A

Slow cell division by producing proteins that stop cell division or cause apoptosis

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

What happens if a mutation occurs in tumour suppressor geness?

A

They will be inactivated, protein it codes for isn’t produced and cells uncontrollably divide causing a tumour

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

How do proto-oncogenes control cell division?

A

Produce proteins that stimulates cell division

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

What happens if a mutation occurs inproto-oncogenes?

A

Gene can become over reactive, stimulates cell to divide uncontrollably resulted in a tumour. Mutated gene is called oncogene

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

What are malignant tumours?

A

Cancerous, grow rapidly and invade and destroy surrounding tissue. Cells can break off and spraed to other parts of the body

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

What are benign tumours?

A

Non cancerous, grow slower and covered in fibrous tissues that stop cells invading other tissues. Can cause blockages and put pressure on organs, some can become malignant

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

How are tumour cells different from normal cells?

A

Larger and darker, irregular shape, dont produce all proteins needed top function, different antigens, dont respond to growth regulating processes and divide more frequently

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

How does methylation cause tumour growth?

A

Adding methyl groups is important to regulate gene expression, control if a gene is transcribed and translated

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

What happens when tumour suppressor genes are hypermethylated?

A

Methylation happens too much, genes not transcribed, proteins they produce to slow cell division isnt made so cells uncontrollably divide

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

What happens when tumour suppressor genes are hypomethylated?

A

Methylation happens too little, cause them to act as onco-genes, production of proteins that encourage cell division is increased so cell divides uncontrollably

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

How can oestrogen cause breast cancer?

A

Increased exposure over a long period of time can increase risk, stimulate certain breast cells to divide uncontrollably, if cells become cancerous replication could be further assisted by oestrogen, can introduce mutations directly into DNA

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

What does totipotent mean?

A

Can specialise into any type of cell

17
Q

What does pluripotent mean?

A

Can specialise into any cell but placenta cells

18
Q

What does multipotent mean?

A

Can differentiate into a few cells

19
Q

What does unipotent mean?

A

Can differentiate into one cell

20
Q

Where do adult stem cells come from?

21
Q

Where do embryonic stem cells come from?

22
Q

Where do induced pluripotent stem cells come from?

A

Created in lab

23
Q

What do transcription factors do?

A

Control rate of transcription

24
Q

How do transcription factors work?

A

Move from cytoplasm to nucleus and bind to specific DNA sites called promoters (found near start of target gene, the one they control the expression of)

25
What are activators?
Stimulate or increase rate of transcription
26
What do repressors do?
Inhibit or decrease rate of transcription
27
How does oestrogen affect transcription?
Bind to transcription factors called oestrogen receptor forming and oestrogen-oestrogen receptor complex, moves from cytoplasm to nucleus and binds to specific DNA sites near start of target gene. Can act as an activator of transcription
28
How does RNA interference affect gene expression?
mRNA leaves cytoplasm, double stranded siRNA associates with several proteins and unwinds, one strand is selected the other broken down, single strand binds to target mRNA as its complementary proteins associated with siRNA cut mRNA into fragments so it can no longer be translated, fragments are then broken down
29
How does miRNA work in mammals?
Less specific, long folded strand which is processed into a double strand, then two single strands, one strand associates with proteins and binds to target mRNA, the miRNA protein complex physically blocks the translation of target mRNA, it is then either stored or broken down
30
How does epigenetic work?
Attach and remove chemical groups from DNA or histone proteins, can be inherited
31
How does methylation work as an epigenetic control?
Methyl group attached to DNA coding for a gene, attaches where cytosine and guanine bases are next to eachother, Increased methylation changes DNA structure so transcriptional machinery cant interact with genes so gene is not expressed
32
How does acetylation of histones work as epigenetic control?
When histones are acetylated, chromatin is less condensed so transcriptional machinery can access DNA so genes can be transcribed. When acetyl groups are removed, chromatin becomes more condensed and the genes in DNA can't be transcribed as the transcriptional machinery cannot access it. Histone deacetylase enzymes are responsible for removing histone groups