Biol 140 - Microbiology Flashcards

Front 1

growth

Back 1

increase in the number of cells

Front 2

binary fission

Back 2

cells elongate & divide into 2 new cells

Front 3

partition that separates the cell into daughter cells

Back 3

division septum -> new cytoplasmic membrane and cell wall material

Front 4

generation time

Back 4

time required to for one cell to divide in two

Front 5

balanced growth

Back 5

all cellular constituents increase proportionally

Front 6

Fts proteins

Back 6

present in all prokaryotes: essential for cell division -> filamentous temperature sensitive

Front 7

FtsZ is related to what eukaryotic protein?

Back 7

tubulin

Front 8

divisome

Back 8

cell division apparatus formed by Fts proteins

Front 9

ZipA: function

Back 9

divisome protein, amchor that connects FtsZ ring to cytoplasmic membrane & stabilizes it

Front 10

FtsI: function

Back 10

peptidoglycan synthesis: contained in divisome; penicillin-binding protein (activity blocked by penicillin)

Front 11

cell division: when does DNA replicate?

Back 11

before the FtsZ ring forms between trhe duplicated nucleoids

Front 12

Min proteins & their functions

Back 12

facilitate location of the cell midpoint -> Min C & Min D inhibit cell division by preventing FtsZ ring from forming; D is spiral that oscillates from pole to pole also localizes in C to membrane; Min E oscillates form pole to pole moving C & D aside - C & D dwell longer at poles than elsewhere so lowest concentration is in middle; this is where FtsZ assembles the ring

Front 13

What Fts protein assists in pulling apart the copies of the chromosome?

Back 13

FtsK

Front 14

What happens as the dividing cell constricts?

Back 14

FtsZ depolymerizes, and triggers grwoth of septim; enzymatic activity of FtsZ hydrolyzes GTP for energy required tp polymerize & depolymerize FtsZ ring

Front 15

autolysins (function)

Back 15

enzymes that create small openings in the wall beginning at the FtsZ ring -> hydrolyze beta1-4 glycosidic bonds connecting NAG and NAM in peptidoglycan backbone: new cell wall material added to holes

Front 16

wall band

Back 16

junction between new and old peptidoglycan -> ridge on cell surface of gram-positive bacteria

Front 17

autolysis

Back 17

spontaneous cell lysis : possible result if new cell wall precursors are not propoerly spliced into existing peptidoglycan

Front 18

bactoprenol

Back 18

lipid carrier molecule; hydrophobic alcohol that binds Nag/NAM/pentapeptide precursor to peptidoglycan; makes them sufficiently hydrophobic to pass thru cytoplasmic membrane then interacts with glycolases

Front 19

glycolases

Back 19

insert cell wall precursors into growing point of cell wall, catalyze glycosidic bond formation

Front 20

transpeptidation

Back 20

process of forming peptide cross-links between muraic acid residues in adjacent glycan chains

Front 21

what cross-links form in gram-negative bactera during trnspeptidation?

Back 21

between diaminopimelic acid on one peptide & D-alanine on adjacent peptide

Front 22

what energy drives transpeptidation

Back 22

initially there are 2 D-alanine residues at end of peptidoglycan precursor: one is removed during transpeptidation -> exergonic reaction -> there's not ATP to supply energy outside of the cell

Front 23

where does transpeptidation occur?

Back 23

outside the cytoplasm

Front 24

in gram-positive bacteria, what crosslinks form during transpeptidation

Back 24

links across the glycine interbridge, typically from L-lysine of one peptide to D-alanine of another

Front 25

what reaction is inhibited by penicillin

Back 25

transpeptidation -> without new wall synthesis, continued autolysin activity leads to osmotic bursting

Front 26

2 reasons penicillin has been a successful drug

Back 26

1) humans are eukarya and lack peptidoglycan so is nontoxic even in high doses; 2) virtually all pathogenic bacteria contain peptidoglycan & are potential targets of the drug

Front 27

iin general, bacteria have __ generation times than microbial eukaryotes

Back 27

shorter

Front 28

exponential growth

Back 28

pattern of population increase where the number of cells double during a constant time interval

Front 29

what do you see when you graph cell numbner on arithmetic coordinates as a function of time?

Back 29

curve with continuously increasing slope

Front 30

what do you see when you gr[aph cell number on a logarithmic scale & time is plotted arithmetically (semilog graph)

Back 30

points fall on a straight line -> use to estimat generation time

Front 31

why does exponential growth lead to large cell populations in so short a period of time?

Back 31

iuncrease in cell numbre increases at an ever faster rate -> later stages in growth have very large numbers of cells

Front 32

what's the relationship between the number of cells present in a culture initially and the number present after a period of exponential growth?

Back 32

N=No 2^n where n is number of generations

Front 33

What is the relationship between the generation time g to the number of generations during period of exponential growth?

Back 33

g = t/n

Front 34

How can you fetermine the generation time of an exponentially growing culture graphically?

Back 34

the slope of the semilog plot: the slope=#n/t; g = #/slope

Front 35

specific growth rate

Back 35

abbreviated as k, what you get as slope from semilog plot (#/g)

Front 36

division rate

Back 36

reciprocal of the generation time -> v; v=1/g units h^-1

Front 37

contrast g and v

Back 37

g -> measure of time for population to double, v is measure of number of generations per unit time

Front 38

IF in 8 h an exponentially growing cell population increases from 5x10^6 cells/ml to 5x10^8 cells'm .calculate g ,n, v, k

Back 38

Number of generations: N2 = N1 * 2^n

5 x 10^8 = 5 x 10^6 * 2^n
log(5 x 10^8)= log(5 x 10^6) * nlog(2)
n = log(5 x 10^8)-log(5 x 10^6))/log(2)
= 2.89

Generation time: g = t/n

g = 8/2.89
= 2.77

Division rate: v=1/g

v = 1/2.77
= 0.36

Growth rate: K = Ln2/g

k = ln2/2.77
= 0.25

Front 39

batch culture

Back 39

culture growing in an enclosed vessel like tube or flask - >exponential growth can't continue indefinitely -> will see lag phase, exp phase, stationary phase and death phase

Front 40

lag phase

Back 40

interval between inoculation and beginning of growth

Front 41

why might there be a lage phase even if inoculum is take from an old culture & transferred to the same medium?

Back 41

cell s are depleted of essentials & time is required for biosynthesis

Front 42

why might there be a lag when inoculum has cells that have been treated with heat adiation or toxic chemicals

Back 42

time required for cells to repair damage

Front 44

the mechanism for generalized transduction

Back 44

lytic cycle: virus DNA integrates into genome, so when DNA from virus is transcribed parts of host DNA are replicated – some phages contain host DNA

Front 45

How does specialized transduction work?

Back 45

host cell's DNA from near where phage inserts itself is integrated with transducing particle – host + more DNA

Front 46

transfer of plasmids from cell to cell mediated by

Back 46

products of tra genes – some interact with oriT region to initiate transfer of ssDNA, others form pili

Front 47

R plasmid

Back 47

plasmid that encodes antibiotic resistance

Front 48

conjugation

Back 48

a method of passing genetic material from cell to cell

Front 49

important features of F plasmid

Back 49

Tra – genes in conjugative transfer; Ori-T origin of transfer for conjugation; Is inertion sequences and Ts – tranposons

Front 50

examples of functions plasmids can confer

Back 50

N2 fixation, antibiotic resistance, nitrogen fixation, conjugation

Front 51

regulation of plasmid replication

Back 51

copy number – number of copies allowed in a cell, incompatibility, controlled by enzymes encoded by the plasmid

Front 52

plasmid

Back 52

extrachromosomal genetic element – not essential, often helpful, no extracellular form

Front 53

transductiion

Back 53

Bacteriophage produced by 1 host cell injects DNA from that cell into another – specific or generalized

Front 54

competence-specific single-stranded DNA binding protein

Back 54

binds SSDNA in transformation, then recA takes over

Front 55

transformation mechanism

Back 55

transforming DNA binds to DNA-binding protein on cell surface, nuclease may cut it, enters and binds cs SSDNABP, then recombination

Front 56

Pre-requisites for transformation

Back 56

cell is competent (naturally able to take up DNA from envrinoment or have competence proteins) OR electroporation

Front 57

Frederick Griffith's experiment with pneumococcus

Back 57

lethal S form had polysaccharide cover that mouse immune system couldn't kill. Mice + live R cells + heat killed S cells still lethal

Front 58

How can we tell whether recombination has occurred?

Back 58

-if recipient is mutant that can't make an AA you know it shouldn't grow unless got new DNA - use selectable markers

Front 59

3 ways donor DNA gets into cell

Back 59

transformation, transduction, conjugation

Front 60

homologous recombination mechanism

Back 60

strands similar so base-pairs can form – endonuclease cuts strand frmo donor DNA, ssBPs bind hanging strand and RecA forms cross-strand exchange, nucleases cut link & ligase sews it up

Front 61

What is the Ames test for?

Back 61

to see if chemical causes mutation

Front 62

how does the Ames test work

Back 62

take an auxotroph e.g. Histidine of Salmonella or trp of E coli – put in plate lacking nutrient – if it grows it mutated

Front 63

What's the SOS response

Back 63

when there's DNA damage – SOS can fix but is error prone

Front 64

umuD and uvrA code for

Back 64

SOS response – enzymes that repair DNA – umuD is error-prone and uvrA is accurate

Front 65

LexA function

Back 65

represses transcription of umuD/uvrA genes – inactivated by recA for SOS response

Front 66

2 categories of DNA-repair systems

Back 66

error free, error prone – error prone involves guesses! Only for a lot of damage

Front 67

2 kinds of radiation

Back 67

ionizing forms free radicals, non-ionizing causes pyridine dimers

Front 68

UV light can cause what

Back 68

formation of pyrimidine dimers between adjacent bases – disrupt replication

Front 69

in what ways can chemicals eff with DNA

Back 69

change base-pairing properties, crosslink different DNA strands so replication fails, insert between 2 base pairs and mess up polymerase

Front 70

base analogs

Back 70

similar to bases that bind to wrong partner – causes substitutions e.g. 5-bromouracil and 2-aminopurine

Front 71

5-bromouracil

Back 71

can base pair with G causing AT to GC substitution

Front 72

2-aminopurine

Back 72

can base pair with C causing AT to GC substitutions

Front 73

suppressor mutation

Back 73

restores wild-type phenotype – may not be in same place as original mutation

Front 74

revertant

Back 74

strain that has regained wild-type phenotype from mutant : same-site or second-site (suppressor) mutation

Front 75

frameshift mutations

Back 75

insertions, deletions cause reading frame shift – correct one can be restored by another insertion or deletion mutation

Front 76

missense mutation

Back 76

new codon encodes a different amino acid than the original codon

Front 77

nonsense mutation

Back 77

new codon is stop codon

Front 78

silent mutation

Back 78

new codon encodes same amino acid as original

Front 79

penicillin selection

Back 79

penicillin only kills growing cells in a culture so all normal cells will die and mutants will remain

Front 80

replica plating

Back 80

Auxotroph screening technique – make imprint of plate with all colonies growing, then transfer the velveteen imprint to 1 plate with incomplete medium & 1 with comple & compare

Front 81

screening

Back 81

identification of organisms by phenotype or genotype without inhibiting or enhancing the growth of any particular type – used when looking for unselectable phenotypes

Front 82

selectable phenotype

Back 82

results from mutation that won't allow growth in particular conditions that don't allow wildtype growth

Front 83

mutation

Back 83

change or lesion in gene that disrupts function to make another allele

Front 84

auxotroph

Back 84

mutant unable to make a particular nutrient

Front 85

2 key findings in microbial genetics

Back 85

DNA holds genetic code, not proteins & transduction (sexual corssing)

Front 86

Tar transducer of E. coli: aspartate

Back 86

MCP that senses aspartate, malate (attractants); Co, Nickel (repellants)

Front 87

repellents increase what

Back 87

autophosphorylation of Che A causing more tumbles

Front 88

What allows MCPs to adapt?

Back 88

CheR methylates MCPs – when fully methylated there's no activity: CheB-P demethylates MCP faster but CheR is always kicking – when completely insensitive eventually CheA is phosphorylated and causes a tumble

Front 89

MCPs interact with what cytoplasmic protein?

Back 89

CheW

Front 90

HeA-P transfers a phosphoryl group to

Back 90

either CheY (direction of rotation) for tumble OR CheB which goes to demethylate MCPs

Front 91

MCP

Back 91

Methyl-accepting chemotaxis proteins

Front 92

what kind of regulatory system is involved in quorum sensing

Back 92

2-component regulatory system

Front 93

2-component regulatory system

Back 93

sensor kinase + response regulator – transmembrane protein sensor-P b/c of a signal, transfers P to response regulator that either binds or stops binding to activator binding site to allow transcription, phosphatase resets system