Brainscape's Knowledge GenomeTM

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


See full index

Mol Cell Bio > Dr Gokhale > Flashcards

Dr Gokhale Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are the structures within the mitochondria?

A
  • Double membrane
  • Outer membrane
  • Inner membrane (folded to form cristae)
  • Matrix
  • Inter membrane space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the structure of the outer membrane?

A
  • Porins for large proteins to enter

- Enzymes embedded for mitochondrial lipid synthesis

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

What happens in the inter membrane space?

A
  • Contains enzymes which use ATP to phosphorylate other nucleotides
  • Where H+ is pumped into to create electrochemical gradient for oxidative phosphorylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the structure of the inner membrane?

A
  • Folded into cristae (increases SA)
  • Contains redox proteins of the electron transport chain
  • ATPases
  • Transport proteins to move things in and out of matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the matrix contain?

A
  • Enzymes for the Krebs cycle
  • mDNA
  • Ribosomes
  • tRNAs
  • Metabolites (ions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the features of mDNA?

A
  • Circular
  • Double stranded
  • Inherited from mother
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is mitophagy?

A

Destruction of damaged mitochondria by an autophagosome

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

How are new mitochondria made?

A
  • Must be made from fission of existing mitochondria, grow (biogenesis)
  • Damaged portions are segregated and destroyed
  • Damage can be rescued under stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do proteins get into the endoplasmic reticulum?

A
  • Proteins translocate as they are synthesised (so unfolded)
  • Signal peptide binds to signal recognition particle (SRP)
  • Docks with SRP receptor protein in translocation complex
  • Protein fed through channel as it is made
  • Signal peptide cleaved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which transport complexes are present in the outer membrane?

A
  • TOM complex

- SAM complex

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

What does the TOM complex stand for?

A

Translocator of the Outer Membrane

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

What does the SAM complex stand for?

A

Sorting and Assembly Machinery

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

Which transport complexes are present on the inner membrane?

A
  • TIM 22 and 23 complexes

- OXA complex

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

What does the TIM complex stand for?

A

Translocator of the Inner Membrane

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

What does the OXA complex stand for?

A

Cytochrome Oxidase Activity

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

What is different about TIM 23?

A

Embedded in the inner membrane but bridges across to the outer membrane

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

How do proteins get into the mitochondrial matrix?

A
  • N-terminal signal sequence binds to TOM complex receptors, polypeptide kept unfolded by chaperones
  • Fully synthesised protein translocates through TOM and the TIM23 (inner) to enter the matrix, chaperones again keeping unfolded through TIM23
  • Signal peptide cleaved off by signal peptidases in the matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In what form are proteins transported into the mitochondria?

A

Fully synthesised (kept unfolded by chaperone proteins)

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

What are examples of chaperone proteins

A

Cytosolic and mitochondrial Hsp70

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

How are chaperones removed?

A

Using energy from ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What effect does the electrochemical gradient in the inter membrane space have on the signal sequence?

A

Drives the peptide through the inter membrane space into the matrix since the signal sequence and the inter membrane space are both positively charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do proteins get embedded in the outer membrane (bilayer)?

A
  • Enter inter membrane space via TOM
  • Kept unfolded by chaperones in IMM
  • Folded and inserted into the bilayer by the SAM complex
  • SAM removes chaperones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What proteins are embedded in the outer membrane?

A

Porins (beta-barrel proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do proteins get embedded in the inner membrane? (method 1)

A
  • Through TOM and into TIM 23
  • Signal peptide cleaved off at TIM 23 to reveal the stop transfer sequence (can’t be put through into matrix)
  • TIM 23 inserts the protein into inner membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do proteins get embedded in the inner membrane? (method 2)

A
  • Protein enters matrix completely via TOM and TIM 23
  • Signal peptide cleaved to reveal a second signal which causes insertion into OXA complex
  • OXA inserts protein into inner membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which complex inserts mitochondrially translated proteins into the inner membrane?

A

OXA complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you get soluble proteins to stay in the inter membrane space?

A

Cleave from the stop transfer sequence after insertion into inner membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How are multipass proteins inserted into the inner membrane?

A
  • Loops through TOM

- Chaperones bind to guide the protein towards TIM 22 which inserts the protein in the correct orientation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the features of peroxisomes? (4)

A
  • Single membrane
  • No DNA
  • No ribosomes
  • Found in all eukaryotic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the function of peroxisomes?

A
  • Contain oxidative enzymes catalase and uric oxidase
  • Removes hydrogen atoms to form hydrogen peroxide
  • Peroxidases use peroxide to form water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the role of peroxisomes in the liver?

A

Detoxification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are new peroxisomes made?

A

Fission of existing peroxisomes with peroxisomal precursor vesicles from the endoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do proteins get into peroxisomes?

A
  • Signal sequences
  • Translocators in the membrane called peroxins which use ATP
  • Proteins don’t need to be unfolded
  • Pex5 binds to signal sequence and accompanies proteins through the membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What syndrome is caused by a mutation in Pex5?

A

Zellweger syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the stages of the cell cycle?

A
  • G1
  • S
  • G2
  • M
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens during G1?

A
  • Cell increases in size
  • Ribosomes and RNA produced
  • Preparation for DNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens during S phase?

A

DNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What happens during G2?

A
  • DNA checks

- Prepare for division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the restriction point?

A

Point of no return at the end of G1 which is a check for favourable conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When in the cell cycle does the cell respond to growth factor signals?

A

G1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the purpose of the checkpoint in S phase?

A

Check for DNA damage during synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the purpose of the checkpoint in G2?

A

Check for unreplicated DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the purpose of the checkpoint during mitosis?

A

Check for chromosome attachment to the spindle fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is quiescence?

A

G0 phase

Cells can exit into G0 before the restriction point if growth factors are withdrawn (reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the stages of mitosis?

A
  • Prophase
  • Metaphase
  • Anaphase
  • Telophase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What does CDK stand for?

A

Cyclin dependent kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which proteins control transitions between cell cycle phases?

A

Cyclin and CDK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How do kinases activate proteins?

A

Phosphorylate to turn on using ATP

49
Q

How do cyclin and CDK work together in the cell cycle?

A
  • CDK is inactive until cyclin binds
  • Then active so can phosphorylate target proteins
  • Cyclin then destroyed leaving CDK inactive again
  • Multiple cyclins and CDKs associated with different phases of the cycle
50
Q

Which cyclin controls transition into mitosis?

A

Cyclin B

51
Q

Which cyclin controls transition into S phase?

A

Cyclin A

52
Q

Which cyclin increases after the restriction point?

A

Cyclin E

53
Q

What drives the cell cycle?

A

Collapse of cyclin levels

54
Q

How are cyclins and CDKs regulated?

A

CDK inhibitors

55
Q

What is the complex which drives the transition into mitosis?

A

M-CDK (cyclin B with a CDK)

56
Q

What processes does M-CDK trigger?

A
  • Assembly of mitotic spindle
  • Sister chromatids attached to go to opposite poles
  • Chromosome condensation
  • Breakdown of nuclear envelope
  • Rearrangement of the actin cytoskeleton and golgi apparatus
57
Q

How is M-CDK activated?

A
  • CAK attaches an activating phosphate
  • Wee1 attaches an inhibitory phosphate (still inactive)
  • Cdc25 removes the inhibitory phosphate =active
  • Active M-CDK inhibits Wee1 = more active M-CDK
  • Active M-CDK activates Cdc25= more active M-CDK
58
Q

What is CAK?

A

CDK activating kinase

Phosphorylates to activate M-CDK

59
Q

What is Wee1?

A

CDK inhibitory kinase

(Phosphorylates to inhibit M-CDK

60
Q

What is Cdc25?

A

A phosphatase

Removes a phosphate

61
Q

What is believed to activate Cdc25?

A

S-CDK complexes

62
Q

What does APC stand for?

A

Anaphase promoting complex

63
Q

What controls the transition from metaphase to anaphase?

A

APC

Driven by protein destruction

64
Q

What does APC do?

A
  • Ubiquitin ligase
  • Adds ubiquitin to the cyclin in M-CDK which targets it for destruction (S and M cyclins)
  • Leaves the CDKs inactive so can’t phosphorylate their target proteins
  • Also destroys securin which causes the separation of sister chromatids
65
Q

What is securin?

A

Holds sister chromatids together

66
Q

What are the 2 targets of APC?

A
  • S/M cyclins

- Securin

67
Q

What is loss of heterozygosity?

A

Loss of one copy of the wildtype allele (LOH)

68
Q

What is hemizygosity?

A
  • Physical loss of one copy of a chromosome

- Dangerous if you are left with a mutant allele with no wildtype active copy to balance it out

69
Q

What is chromosome non-disjunction?

A

When chromosomes end up in the wrong daughter cell

70
Q

What are astral microtubules?

A

Connects the cell cortex to the mitotic spindle

71
Q

What is a kinetochore?

A

Where spindle fibres attach to separate the sister chromatids
(Centromere holds the sister chromatids together)

72
Q

What are kinetochore microtubules?

A

Attach at the kinetochore of chromosomes

73
Q

What are interpolar microtubules?

A

Overlap in the middle to aid separation

74
Q

How do kinetochore microtubules attach to chromosomes?

A
  • Trial and error
  • When they are correctly attached the correct level of tension is detected
  • If incorrectly attached the tension is lower which triggers inhibitory signals, try again
75
Q

What activates APC?

A

Cdc20

76
Q

What does APC do to securin?

A
  • Ubiquitinates securin which releases and activates the separase which is bound to securin
  • Separase cleaves cohesin proteins which hold sister chromatids together during anaphase
77
Q

How can LOH occur in normal cells?

A
  • Non-disjunction
  • Mitotic recombination
  • Gene conversion
78
Q

What is LOH by non-disjunction?

A
  • One daughter cell ends up with 3 chromosome copies, other ends up with 1
  • Extra chromosome is deleted
  • Ends up with 2 copies of the mutant allele after losing the normal allele
  • Or the cell with 1 could end up hemizygous for the mutant which can cause problems
79
Q

What is LOH by mitotic recombination?

A

Bits of chromosomes swapped during G2 or M phase so could end up homozygous for mutant alleles

80
Q

What is LOH by gene conversion?

A
  • DNA polymerase jumps to the template strand of the wrong homologous chromosome during translation so the product ends up as a combination of both
  • Causes a problem if it happened to copy a mutation so now both chromosomes carry the mutant allele
81
Q

What is a bivalent?

A

A pair of homologous chromosomes

82
Q

What is a chiasma?

A

Point of contact between 2 chromosomes during crossing over in meiosis

83
Q

How are homologous chromosomes paired up during meiosis 1?

A
  • Synaptonemal complex:
  • Cohesin connects chromatin to the axial core
  • Transverse filaments hold the axial cores together
84
Q

What is the difference between meiosis 1 and 2?

A

In meiosis 1, homologous chromosomes are separated. In meiosis 2, sister chromatids are separated =haploid

85
Q

What is aneuploidy?

A

Wrong number of chromosomes

86
Q

What is the p arm of a chromosome?

A

Shorter arm

87
Q

What is the q arm of a chromosome?

A

Longer arm

88
Q

What is monosomy?

A

Only 1 copy of a chromosome present

89
Q

What is trisomy?

A

3 copies of a chromosome

90
Q

What is polyploidy?

A

A whole extra set of chromosomes (i.e. 3n, 4n etc)

91
Q

When during meiosis is non-disjunction most severe?

A

Meiosis 1

92
Q

What is haploinsuffiency?

A

When you lose one copy of an allele and having only one copy of the allele is not sufficient to produce the amount of the protein product required (dose matters)

93
Q

What is monoallelic expression?

A

When a phenotype is the result of the expression of one allele and the other is silent. Can lead to problems if an allele is lost

94
Q

What are the 2 main routes of cell death?

A
  • Apoptosis

- Necrosis

95
Q

What is necrosis?

A

Uncontrolled cell death from physical damage e.g. infection, hypoxia, ischaemia, bacterial toxins etc.

96
Q

What is apoptosis?

A

Controlled cell death

97
Q

What is hypoxia?

A

Low oxygen concentration

98
Q

What is ischaemia?

A

Loss of blood supply

99
Q

When does apoptosis occur? (7)

A
  • Tissue size maintenance
  • Removal of developmental cells (growth factors)
  • Removal of immune cells
  • Hormonal (menstrual cycle)
  • Anoikis (inappropriate interactions)
  • DNA damage
  • Virally infected cells
100
Q

What are the characteristics of necrosis?

A
  • Membrane integrity compromised
  • Organelle and cell swelling
  • Increased intracellular calcium
  • Autolysis
  • Cell lysis (bursting)
  • Causes an inflammatory response
101
Q

What is autolysis?

A

Enzymatic digestion of cells by the action of its own enzymes

102
Q

What are the characteristics of apoptosis?

A
  • Shrinkage
  • Nuclear breakdown
  • DNA fragmentation
  • Apoptotic bodies
  • Phagocytosis
  • No inflammatory response
  • Energy required
103
Q

What are apoptotic bodies?

A

Vesicles containing dying bits of the cell

104
Q

What is autophagy?

A

Controlled degradation/recycling of damaged cell components

105
Q

Which genes control apoptosis?

A

Ced genes

106
Q

What mediates apoptosis?

A

Caspases

107
Q

Which amino acid is in the active site of caspases?

A

Cysteine

108
Q

Which amino acid is in the cleavage site of caspase target proteins?

A

Aspartic acid

109
Q

How do caspases work?

A
  • Apoptotic signal activates adaptor proteins
  • Adaptor proteins activate inactive monomers of initiator caspases
  • Active initiator caspases activate executioner caspases which cleave target proteins leading to apoptosis
110
Q

Which number caspases are initiator caspases?

A

8 and 9

111
Q

Which number caspases are executioner caspases?

A

3, 6, 7

3 is the main one

112
Q

What do caspases target?

A
  • Nuclear lamins (breakdown nuclear lamina)
  • PARP (DNA repair enzyme)
  • Actin cytoskeleton
113
Q

What does PARP stand for?

A

Poly ADP-ribose poylmerase

DNA repair enzyme

114
Q

What are the two pathways which initiate apoptosis?

A
  • Extrinsic

- Intrinsic

115
Q

What is the extrinsic pathway of initiating apoptosis?

A
  • Killer lymphocyte with a Fas ligand binds to Fas death receptor on target cell
  • Triggers assembly of the initiator caspase complex via the DISC
  • Activates initiator caspase 8
116
Q

What is the DISC in apoptosis?

A

Death-inducing signalling complex

117
Q

What is the intrinsic pathway of initiating apoptosis?

A
  • Triggered by developmental/ stress signals
  • Causes release of cytochrome C from mitochondrial inter membrane space
  • Triggers assembly of apoptosome which recruits and activates initiator caspase 9
118
Q

What are Bcl2 proteins?

A

Apoptosis regulators kept in balance in the mitochondria (pro and anti)

Mol Cell Bio (7 decks)

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