Brainscape's Knowledge GenomeTM

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


See full index

1st year: MCO > Lectures 34-43 > Flashcards

Lectures 34-43 Flashcards

1
Q

How much % of the world’s DNA belongs to bacteria?

A

30%

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

What makes up a significant part of the body?

A

Bacteria

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

Why is bacteria a good model organism?

A

Haploid (1 copy of each gene) - easy to study
Asexual reproduction - easier to understand
Short generation times - grow quickly
Grow on plates with defined media
Easy to store
Easy to genetically manipulate

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

Bacterial genome

A

Single circular double stranded DNA chromosome
Less space between genes (inter-gene space)
Rare introns
Functionally related genes grouped - operon
Plasmids - extracellular chromosomal DNA replicate independently

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

Binary fission

A

Bacterial asexual reproduction
Common in prokaryotes

Elongates, contents increased, DNA replicated + segregated —> 2 identical daughter cells
Septum forms in middle, grows from both sides of cell

E.coli does this in 20 min

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

E.coli

A

Can grow on simple inorganic nutrients + carbon source
Need glucose, phosphate, pH control, nitrogen, trace metals
Prototroph - doesn’t require nutritional factors (opposite to auxotroph)

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

Biosynthetic auxotroph

A

Need additional nutrients, usually AA

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

Catabolic auxotroph

A

Lost ability to degrade/catabolise carbon source

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

Conditional lethal mutants

A

Genes essential for survival don’t work under certain conditions
But under some conditions can still make functional proteins even if still mutant

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

Example of conditional lethal mutant

A

Temperature sensitive mutant - only grow at permissive temp e.g mutant protein folds correctly at lower temp due to lower E in system

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

Wild type

A

Normal species

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

Mutant

A

Genome carries mutation with respect to wild type

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

Mutation

A

Inheritable change in gene sequence of nucleic acid

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

Allele

A

Sequence variant of a gene

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

Mutagenesis

A

Process by which mutants are produced

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

Mutagens

A

Chemical and physical agents which cause mutations

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

Shared pathways

A

Some produce metabolites as precursors for more than 1 pathway
Loss of 1 enzyme leads to requirement for more than 1 AA

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

Purines

A

pur

gua, ade

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

Pyrimidines

A

pyr

thy, cyt, ura

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

Vitamins

A 
biotin (bio)
riboflavin (rib)
NAD (nad)
thiamine (thi)
pyridoxine (pdx)
pantothenic acid (pan)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

rpoA

A

Encodes alpha-subunit of RNA pol

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

polA

A

encodes DNA pol I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

polC

A

encodes DNA pol III

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

sugars

A 
arabinose (ara)
mannose (man)
xylose (xyl)
galactose (gal)
melibiose (mel)
lactose (lac)
rhamnose (rha)
maltose (mal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Drugs + bacteriophage resistance

A

azide (azi)
rifampicin (rif)
streptomycin (strA)
phage T1 (tonA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Nonsense suppressors

A

suppressor (sup)

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

super/sub script

A 
Temp sensitive (ts)
Cold-sensitive (cs)
amber mutation (am)
ochre mutation (oc)
amber mutation (um)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

stop codons

A

amber UAG
ochre UAA
opal UGA

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

leuA-

A

mutation

Requires leucine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

leuA+

A

Not wild type but not require leucine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Triangle symbol

A

Deletion

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

R

A

Resistant

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

( )

A

Lysogenised by bacteriophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

/F’

A

Carries F’ plasmid

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

Lamarckian evolution

A

vital force

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Luria-Delbruck experiment (1943)

A

early belief: add toxic agent to bacterial culture and entire culture becomes resistant so agent makes cells resistant (Lamarckian)

hypothesis: if Darwinian-random mutations prior to selective agent, if Lamarckian-mutants after selective agent

L model prediction: no mutations till after T1, same no. mutations every time
D: random mutations at any generation so diff no. in diff plates

method: E.coli plated with T1 phage, start with Tonˢ (T1 sensitive) then some Tonᴿ grow
results: big variation in no. resistant colonies so Darwinian
conclusion: variations because mutate at diff times in diff generations so had diff length of time to grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Newcombe experiment

A

start with Tonˢ on 2 plates
a: spread bacteria around b: leave
spray both with T1

more colonies on plate A because respreading means little pile of resistant bacteria gets spread and each give rise to own resistant colonies
not spreading means pile of resistant gets bit bigger

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

Lederberg x2

A

replica plating
pick out phenotypes that can’t easily select for

master plate with E.coli Tonˢ and made lots replica plates
sprayed with phage
position of Tonᴿ colonies same on each plate so phenotype present before env. change of introducing T1

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

replica plating

A

plate put onto cloth, imprint of what on plate onto cloth, new plate onto cloth so transferred onto new plate, exact copy

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

point mutation

A

change to 1 base pair

substitution, deletion, insertion

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

indel mutation

A

insertion and deletion

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

transition mutation

A

1 purine to another purine or pyrimidine to another pyrimidine

43
Q

trasnversions

A

purine to pyrimidine or other way round

44
Q

consequences of point mutation

A

in promoter: can affect transcription

in coding region: silent/missense/nonsense

45
Q

silent mutations

A

code for same AA

usually 3rd pair substitution

46
Q

missense mutations

A

amino acid substitution

usually 1st or 2nd pair changes

47
Q

nonsense mutations

A

leads to stop codon

48
Q

inverions

A

change orientation, flips around

49
Q

tandem repeats

A

genome duplicated and inserted

can lead to overproduction of proteins

50
Q

transposons

A

nucleotide sequences that can move themselves around

have encoded mechanisms that allow to cut out and insert elsewhere

51
Q

reversion

A

usually point mutation

results in restoration of original sequence

52
Q

tautomer

A

isomers that exist together in equilibrium

base can switch to tautomer so pair with different base (enol-rare to keto-normal) - isomerisation switch

53
Q

suppressor mutation

A

2 mutations but restores phenotype
intragenic: 2nd suppresses 1st
frameshift suppression: most sequence okay
intergenic: 2nd mutation in diff gene e.g. nonsense
nonsense suppression: mutation to tRNA, inserts AA instead of stop codon so can get back to original sequence except for 1 AA

54
Q

supF

A

suppresses amber mutations

insert glycine at stop codon site

55
Q

example of mutagens

A 
nitrous acid
reactive oxygen species
alkylating agents
intercalating agents
UV light
56
Q

mutation rates

A

frequency per generation

can’t record silent mutations

57
Q

deamination of bases

A

removal of amine group (NH2 replaced by =O)
caused by nitrous acid
cytosine converts to uracil, guanine to xanthine (not problem), adenine to hypoxanthine (pairs with C so problem)

58
Q

reactive oxygen species

A

natural side product of aerobic R
from chemical reactions caused by UV light/ionising radiation
cause changes to DNA (oxidation and addition to double bonds)
so can change base pairings

59
Q

alkylating agents

A

chemicals that react with DNA adding alkyl groups (CH3CH2-)
e.g. EMS often used in chemotherapy - changes base pairings
affect coiling because extra bulky group
affect how proteins bind to DNA

60
Q

intercalating agents

A

flat multiple ring structures so squeeze into DNA
binds between base pairs so leads to frameshift
stretch and distort helix

61
Q

UV light causes 2 pyrimidines to form dimers

A

kink in DNA so point mutation or polymerase falls off

62
Q

segregation of mismatched base pairs

A

deamination of 1 strand so 1 daughter cell wild type and 1 mutatn so culture is a mixture of diff genotypes

63
Q

phenotype lag

A

phenotype not seen for several generations e.g. resistance to T1 because protein that phage binds to decreases over generations till none so then resistant

64
Q

select mutants

A

easy for drug/phage resistance on plates

can’t see replication errors because all dead so need conditional lethal mutants

65
Q

cross feeding

A

blocked metabolic pathways, provide each other with metabolites so depend on each other to grow
look like prototrophs but aren’t

66
Q

ames test

A

identify mutagenic chemicals
plate w/ or w/o chemical
difference in no. bacteria if mutagenic

BUT metabolite may be mutagenic instead of chemical itself

67
Q

operon

A

in prokaryotes
group of genes under control of same promoter
regulated together
different places where translation can start so more than 1 protein

68
Q

housekeeping genes

A

required to be active all the time (constitutively expressed)
not all genes are like this because switch off when not needed to save energy

69
Q

Lac operon

A

not constitutively transcribed

breaks down lactose

70
Q

diauxic growth

A

2 growth phases
1st: glucose used up
lag phase: E.coli can’t grown so turn lac genes on
2nd: lactose used

71
Q

LacY
LacZ
LacA

A

β-galactosidase permease - lets lactose enter cell
β-galactosidase - cleaves glycosidic bond, to glucose and galactose
galactoside acetyl-transferase - transfer acetyl group to galactosides and glucosides

72
Q

default when glucose used

when use lactose

A

LacI protein binds to operator so blocks promoter so RNA pol. can’t bind to operon off

allolactose (comes from LacZ- small amount always present) is inducer, disables repressor protein LacI by binding to it so RNa Pol. binds promoter and makes mRNA of lac genes

73
Q

other processes involved in glucose and the lac operon

A

glucose inhibits adenylatee cyclase enzyme which makes cAMP, so CAP in certain conformation
no glucose means CAP changes conformation so binds to promoter and helpds RNA Pol. bind so transcription is enhanced

74
Q

competence

A

ability of bacerial cell to take up extracellular DNA from env.

75
Q

artificial transformation

A

electroporation: DNA into bacterial cell with electric pulse by creating pores in membrane

76
Q

natural transformation

A

1 cell releases, other cell takes up

77
Q

horizontal gene transfer

A

transformation
transduction
conjugation
transposition

78
Q

when are cells naturally competent?

A

when about to enter stationary phase - when stop growing

79
Q

quorum sensing

A

ability to regulate genes based on population density (know how dense culture is)
very dense=take up DNA

80
Q

B.subtilis mechanism for competence

A

cells secrete ComX so conc. increases with cell density

bind to ComP which changes gene regulation so becomes competent

81
Q

RecA

A

DNA repair protein

involved in homologous recombination to integrate new DNA

82
Q

how does bacteria distinguish between DNA of diff species?

A

recognise specific sequences (by sequences in DNA of surface proteins)

83
Q

transduction

2 types

A

genetic exchange in bacteria, mediated by bacteriophages

generalised transduction: transfer any DNA, occasional incorrect packaging so package host DNA instead of viral so when infect new cell, insert host DNA

specialised transduction: transfer specific genes (next to phage DNA) by lysogenic phages
phage DNA cuts self out of host by loop, sometimes loop picks up host genes so carry to next host

84
Q

Lambda phage

A

double stranded linear DNA
tail important for interacting with E.coli
can be lytic or lysogenic

85
Q

lytic cycle of λ phage

A

inserts linear DNA into E.coli and DNA circularises in cell

new virions assembled which lyse the cell and release them

86
Q

lysogenic cycle of λ phage

A

inserts DNA which integrates into E.coli genome

transmitted to daughter cells and lives until trigger for lytic cycle

87
Q

lysogen

A

strain of beacteria carrying a lysogenic phage

prevents other phages infecting it

88
Q

prophage

A

phage in lysogenic state

89
Q

Lederberg and Tatum

A

2 cultures opposite in what can grow on, no colonies on minimal media but wild type growth if mixed together
so shows conjugation - mix DNA

90
Q

Davies

A

2 strains in glass tube with filter that allows media through but not cells
no growth if on minimal media but growth if remove filter because require cell-to-cell contact to transfer DNA

91
Q

plasmids

A

piece of double stranded DNA
most are circular but some linear
incompatible: related plasmids sharing common replication mechanisms can’t coexist
episomes: plasmids that can integrate into host genome

92
Q

role of plasmids

A

carry non essential but highly useful genes (controlling replication and copy no.)
some are conjugative - encode tra genes needed for transfer

93
Q

virulence factors

A

toxins that increase pathogenicity

94
Q

bacteriocins

A

proteins killing/inhibiting closely related species

95
Q

conjugation

A

one bacterium transfers genetic material to another through direct contact

96
Q

process of conjugation

A

bacteria sends out F pilus (fertility factor) - mating pair connection - unidirectional transfer of DNA
cells pull closer when pilus makes contact, pore made and plasmid transferred
both cells retain plasmid

97
Q

rolling circle replication in conjugation

A

DNA nicked at DSO (double stranded origin)

proteins unravel 2 strands so 1 strand goes into new cell and 3’ end recognised by DNA Pol. which synthesises 2nd strand

98
Q

Hfr strain

A

high frequency recombination
F plasmid (episome) integrated into genome by recombination
plasmid nicked in chromosome, unravel and transfer single strand, made into double strand
can’t circularise because not all chromosome transferred so most is degraded but sometimes recombination occurs
new strand has only some genes so not whole F plasmid
F plasmid can excise from genome so become plasmid again, incorrectly takes some host DNA = F’ plasmid

99
Q

recombination

A

break and rejoin DNA into new combination

2 types: homologous and non-homologous

100
Q

homologous recombination

A

switch similar DNA
requires holiday junctions

ALIGNMENT: helices align
BREAKAGE: 1 strand nicked by E.coli enzyme RecBCD at specific sequences
INVASION: free 3’ end pulled off, stabilised by SSB protein and catalysed by RecA, strand invades other double helix because homologous so displacement
CROSS STRAND EXCHANGE: 2nd nick so 2 strands exchange
BRANCH MIGRATION: switch strands, requires RuvAB helicase, cross over=holiday junction - needs to be resolved so rotated to make cross so no crossover
ISOMERISATION: crossing and uncrossing of strands, can result in 2 outcomes, by RuvC nuclease and RuvAB

101
Q

RecA

A

essential for DNA repair
bind to ssDNA
stabilise and help displacement
2 binding sites: hold 2 DNA together and catalyses branch migration

102
Q

RecBCD

A

nuclease - catalyses single stranded nick

helicase - unwind DNA

103
Q

non-homologous recombination

A 
insertion sequences (transposons): hop from 1 position in DNA to another (transposition)
catalysed by transpotase (encoded by insertion sequence), no other genes in them, have tandem repeats at ends needed for insertion, no new phenotype, can disrupt genes, high degree of reversion

transposons: bigger version of insertion sequences, carries additional genes like resistance, can carry tra genes (make pili) so conjugate
tandem repeats bound by transpotase, cuts out transposon from sequence and repair original sequence, carry transposon to new target sequence

replicative transposition: original copy retained and new copy insets elsewhere
conservative transposition: cuts out inserts elsewhere

1st year: MCO (6 decks)

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