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Module 6 > Cellular Control > Flashcards

Cellular Control Flashcards

1
Q

What’s a mutation

A

A random change to the genetic material
-> the rate of these are increased by mutagens

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2
Q

Gene mutations occur randomly, during DNA replication…
What are the two types of mutation that can occur

A
  1. Point
  2. Indel
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3
Q

What’s a point mutation

A

When one base pair is substituted for another

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4
Q

Types of point mutations

A

Silent
Missense
Nonsense

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5
Q

What’s a silent mutation

A

There’s a change to the base triplet, but the triplet still codes for the same amino acid and the sequence is not changed
-> can occur as generic code is degenerate: certain codons may code for the same amino acid
Therefore, primary / secondary / tertiary structure not affect

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6
Q

What’s a missense mutation

A

A change to the codon / base triplet, which causes it to become a termination / stop triplet
This results in:
An incomplete polypeptide chain produced, therefore, the protein is shortened & the protein cannot function

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7
Q

What’s an indel mutation

A

The random insertion or deletion of a nucleotide base pair (not in multiples of 3) into the DNA sequence
-> this can cause frameshifts or the addition / loss of an amino acid

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8
Q

What are the 3 types of indel mutations

A

Insertion
Frameshift
Deletion

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9
Q

What is an insertion mutation

A

When the nucleotide is randomly inserted into the DNA sequence. This changes the amino acid that would be coded for

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10
Q

What is a deletion mutation

A

When a nucleotide is randomly deleted from the DNA sequence. This also changes the amino acid that would be coded for

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11
Q

What is a frameshift mutation

A
  • has a knock on effect of disrupting the reading of codon.
    As the genetic code is non overlapping & read as a triplet of bases
    Therefore changes all subsequent triplets in the DNA sequence
    -> it changes the amino acid sequence produced,
    Therefore altering the ability of the protein to function
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12
Q

What happens to abnormal proteins

A

Degraded in the cell

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13
Q

How can mutations be beneficial

A
  • can result in a characteristic, which offers a selective advantage for the organism
  • enhanced function of the protein
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14
Q

How can a mutation be neutral

A

Can result in a characteristic which offers no selective disadvantage for the organism & no selective advantage either

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15
Q

How can a mutation be harmful

A

Can result in a characteristic which offers a selective disadvantage for the organism
Malfunctioning protein made

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16
Q

How is gene expression controlled

A

A regulatory mechanisms which controls it in Eukaryotes = transcription factors

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17
Q

What are transcription factors + their function

A

Proteins / short non-coding pieces of RNA
Function = attach to DNA @ specific locations

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18
Q

How do transcription factors control which genes turned on / off or activated / suppressed or expressed / not expressed

A

They do this by
- binding to the genes promoter regions
- preventing RNA polymerase binding to promoter regions
- inhibit, allow RNA polymerase to attach to DNA

  • suppress / activate transcription of the gene
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19
Q

Euchromatin vs Heterochromatin

A
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20
Q

What’s the regulatory mechanism that controls gene expression in prokaryotes

A

Lac operon

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21
Q

What is operon

A

A group of genes controlled by the same regulatory mechanism + expressed @ the same time

22
Q

What do structural genes do

A

These code for proteins NOT involved in DNA regulation

23
Q

Structural genes in lac operon

A

Lac Z & Lac Y

24
Q

What do Lac Z & Lac Y both metabolise

A

Lactose
Lac Z -> codes for B galactosidase
Lac Y -> lactose permease

25
Q

What do regulatory genes, like Lac I, code for

A

Proteins involved in DNA regulation
E.g. Lac I codes -> repressor proteins

26
Q

What does the repressor protein Lac I codes for do

A

Binds to the operator (the DNA sequence that gets binded to)
Therefore, preventing RNA polymerase from binding to the promoter region, therefore genes are off, preventing the transcription of structural genes Lac Z & Lac Y

27
Q

How does Lac Operon interact when glucose IS present

A
  • regulatory gene (Lac I) expressed, so repressor proteins made & can bind to the operator, blocking the promoter region & preventing RNA polymerase from binding to the promoter region
    -> transcription can’t happen so enzymes for lactose metabolism not made
28
Q

How does lac operon act when glucose is absent + lactose is present

A
  • lactose binds to the repressor protein
    -> causing the conformational change in the repressor protein shape
    -> so the repressor protein cannot bind to the operator

Therefore:
Promoter region unblocked & RNA polymerase can bind to it
So transcription occurs for structural genes, & enzymes for lactose metabolism are made (e,g, lactose permease, b-galactosidase)

29
Q

When glucose is present what is lactose released from

A

The repressor protein

30
Q

What are introns

A

Regions of DNA sequence which don’t code for proteins

31
Q

What are exons

A

Regions of the DNA sequence that do code for proteins

32
Q

When is primary mRNA formed

A

When all of the genes DNA (exons & introns) are transcribed

33
Q

How is primary mRNA edited

A

RNA splicing

34
Q

What’s the process of RNA splicing

A

Introns removed
Remaining mRNA exons fused together
Form continuous, mature mRNA molecules (ready for translation in the ribosome)

This is important as it ensures only exons of the mRNA are translated to form proteins, therefore, the resulting protein properly has correct function

35
Q

What happens post transcription after the mRNA is edited, and becomes mature…

A

Edited further
-> changes into different versions of mRNA
To make proteins with different functions

36
Q

What are post translational level mechanisms typically regulated by

A

Activation of proteins by cyclic AMP (cAMP)

other ways include
- protein folding
- addicting non-protein groups
- modifying amino acids to make disulphide bonds

37
Q

What are post translational level mechanisms typically regulated by

A

Activation of proteins by cyclic AMP (cAMP)

other ways include
- protein folding
- addicting non-protein groups
- modifying amino acids to make disulphide bonds

38
Q

How is camp formed

A

Derived from ATP
Formed by action of enzyme adenyl cyclase

39
Q

Role of cAMP in lac operon

A
  • if binds to CRP
    -> complex bind to RNA polymerase
  • increases activity of RNA polymerase
  • increases efficiency of transcription of structural genes
40
Q

Role of cAMP in protein kinases

A

Activates PKA (protein kinase A)
- PKA can then go on to activate other proteins & enzymes

41
Q

Role of cAMP in protein kinases

A

Activates PKA (protein kinase A)
- PKA can then go on to activate other proteins & enzymes

42
Q

What are Homeobox genes

A

Regulatory genes which control body development (the position of body parts)
- they regulate mitosis & apoptosis in response to internal & external stimuli
- they’re highly conserved in plants, animals & fungi

43
Q

Examples of body plans Homeobox genes control

A
  • segmentation of organisms into distinct body parts
  • development of body parts & organs
  • control polarity of the organism (which side is the head versus tail)
44
Q

What are hox genes

A

Homeobox genes found in animals, which control body development & determine embryonic body regions along the anterior posterior walls

45
Q

What is a hox cluster

A

A group of hox genes

46
Q

What is the order of hox genes in each cluster is related to

A

The time & order of the regions in the body that they affect

E.g. 4 limbed vertebrates = 4 clusters

47
Q

A mutation of Homeobox genes =

A

A different body arrangement

48
Q

In Homeobox genes, there are (…) base genes, and (…) amino acids

A

180
60

49
Q

What’s the importance of apoptosis & mitosis in cellular control

A

Too much apoptosis / not enough mitosis -> cell loss + degradation may occur
Too much mitosis / not enough apoptosis -> formation of tumours

50
Q

Sequence of apoptosis (programmed cell death)

A
  1. Enzymes break down cell cytoplasm
  2. Cytoplasm becomes dense
  3. Organelles become tightly packed
  4. Small protrusions called ‘blebs’ form cell surface membrane
  5. Chromatic condenses
  6. Nuclear envelope breaks
  7. DNA breaks into fragments
  8. Cell breaks into vesicles
  9. Vesicles ingested by phagocytes
51
Q

Sequence of apoptosis (programmed cell death)

A
  1. Enzymes break down cell cytoplasm
  2. Cytoplasm becomes dense
  3. Organelles become tightly packed
  4. Small protrusions called ‘blebs’ form cell surface membrane
  5. Chromatic condenses
  6. Nuclear envelope breaks
  7. DNA breaks into fragments
  8. Cell breaks into vesicles
  9. Vesicles ingested by phagocytes

Module 6 (7 decks)

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