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1: GENET 270 > Bacterial Chr. Pt 1 > Flashcards

Bacterial Chr. Pt 1 Flashcards

1
Q

NAPs stands for ______

A

Nucleoid associated proteins (NAPs)

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2
Q

NAPs contribute to organization of ________. They do what?

A

-nucleoid & gene regulation
-bend, wrap & bridge DNA

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3
Q

Different DNA binding modes affect ______

A

-gene regulation & nucleoid shape

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4
Q

Loops of DNA are supercoiled –> DNA is bent back on itself due to ________

A

-under- or overwinding

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5
Q

positive supercoiling (def.)

A

-DNA is over-wound
-DNA strands wrapped around each other more than in relaxed DNA

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6
Q

negative supercoiling (def.)

A

-DNA is under-wound
-DNA strands wrapped around each other less than in relaxed DNA

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7
Q

3 proteins affecting supercoiling

A

1) NAPS
2) Enzymes (RNA & DNA polymerases)
3) Topoisomerases

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8
Q

Supercoiling: NAPs constrain supercoils to ______. Changes in NAP binding can lead to _______ & help with ______ during replication, recombination, and transcription initiation

A

-prevent twisting
-unconstrained supercoils
-DNA strand separation

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9
Q

overwound DNA: ____
underwound DNA: ______
regular duplex DNA: ____

A

< 10.4 bp/turn
>10.4 bp/turn
10.4 bp/turn

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10
Q

Topoisomerase relaxes ______ supercoils by introducing ______

A

-negative
-positive

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11
Q

Gyrase introduces ______ supercoils

A

-negative

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12
Q

When transcribing DNA, behind the RNA poly, DNA is ____. In front of RNA poly(downstream), DNA is ______

A

-underwound (negative supercoils)
-overwound (positive supercoils)

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13
Q

As RNA & DNA polymerases seperate the strands for RNA/DNA synthesis, introduce ______

A

positive supercoils downstream

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14
Q

topoisomerases are enzymes that _____ by ____ supercoils. It is found in all organisms

A

modulate supercoiling
-introducing and removing

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15
Q

Two types of topoisomerases

A

Type I: Cut one strand, pass other through break, reseal
Type II: cut both strands, pass two other strands from same/different DNA molecule, reseal

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16
Q

Example of Type I topoisomerases? function?

A

Major topoisomerase I TopA removes negative supercoils

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17
Q

Example of Type II topoisomerases? function?

A

Topo IV - decatenates chromosomes after replication
Gyrase - introduces –ve supercoils

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18
Q

size of bacterial genome? structure? coding info? encodes?

A

-range from 0.5 Mb (500 genes) to 10 Mb (10,000 genes)
-few introns, less repetitive DNA than euk
-densely packed with coding info (1 gene/1kb; 100 fold higher than us)
-encode proteins, rRNAs, tRNA, sRNAs, small peptides

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19
Q

Bacterial genomes exhibit high degree of SYNTENY —–> _______

A

conservation in genetic linkage

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20
Q

Areas of synteny of bacterial genome disrupted by ______

A

insertions of DNA acquired through horizontal gene transfer (DNA comes from other sources not its parents - ex. prophages, insertion sequence elements, genetic islands)

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21
Q

E. coli O157:H7 example of horizontal gene transfer

A

-contains an extra 1 Mb of DNA from horizontal gene transfer, compared to harmless E. coli K-12
-extra DNA encodes toxins and virulence factors that make this E. coli pathogenic

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22
Q

DNA replication (def.) + always occurs in _____ direction; requires ______ to initiate (primers)

A

-Act of polymerizing dNTP’s to make a new chain of DNA
-5’ -> 3’
-3’OH end

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23
Q

DNA replication involves many proteins: polymerases do what? examples + function?

A

-synthesize DNA
-Pol III: large complex, most DNA replication
-Pol I: replaces RNA primers with DNA

24
Q

DNA replication involves many proteins: primases do what? examples + function?

A

-synthesize primers
-DnaG: makes RNA primers for replication

25
Q

DNA replication involves many proteins: nucleases do what? examples + function?

A

-degrade DNA
-endonucleases: initiate breaks in middle of DNA strands
-exonucleases: initiate breaks at ends of DNA strands, 5’ exonucleases (remove from 5’ direction)- Pol I primer removal; 3’ exonucleases (remove from 3’ direction)- editing

26
Q

DNA replication involves many proteins: ligases do what? +function?

A

-link DNA strands
-create phosphodiester bonds between 5’ PO4 and 3’ OH

27
Q

DNA replication involves many proteins: helicases do what? topoisomerases? clamp? clamp loader?

A

-unwinds dsDNA
-adjust supercoiling
-clamp Pol to template DNA
-loads clamp, binds Pol on both strands & helicase

28
Q

DNA Replication (review)

A

1) Pol III replicates DNA on leading strand, primase synthesizes primer in opposite direction on lagging strand
2) Pol III extends RNA primer -> OKAZAKI FRAGMENT
3) Primase synthesizes another primer
4) Pol III extends this primer until it reaches previous
primer
5) Pol I removes RNA primer & replaces it with DNA
6) DNA ligase seals nick

29
Q

Helicase aka _____; forms ring that travels down _____ prying apart strands; * Very energetically expensive -> uses _____; Ring requires _____ protein to load onto ssDNA

A

-DnaB
-one strand of DNA
-lots of ATP
-DnaC

30
Q

SSB does what?

A

Coat unwound DNA to prevent reannealing

31
Q

Replication of DNA on both strands must be _____

A

coordinated

32
Q

How is DNA replication (speed of polymerization & unwinding) coordinated on two template strands?

A

-DNA Pol on leading & lagging strand interact with sliding clamp DnaN
-DNA Pol on leading & lagging strand connected by t protein, which also binds DnaB helicase
-Helicase interacts with primase
-DNA template on lagging strand is looped around

33
Q

Trombone Model for coordination of leading & lagging strand DNA replication

A

A) Pol III synthesizes DNA on lagging strand from primer
B) Lagging strand DNA loops out as both Pol on leading & lagging strands progress
C) When lagging strand Pol runs into Okazaki
fragment at site 1, it dissociates. Leaves DnaN sliding clamp behind. Hops ahead to next priming site, associates with new clamp. Leading & lagging strand Pol remain associated throughout.
D) Pol III synthesizes DNA on lagging strand from
next primer

34
Q

lagging strand template is ___. Leading strand template?

A
  • 5’ to 3’
    -3’ to 5’
35
Q

Damaged DNA on the lagging strand stalls DNA poly. How does the cell overcome this?

A
  • Pol III released at lesion, leaving DnaN clamp behind
  • Pol III restarts synthesis at new primer
  • DNA gap repaired by another mechanism
36
Q

We intially thought that DnaG primase does not do this activity. What is it?

A

synthesize primers on leading strand (Now know that primase can make primer at sites of stalled Pol III on
leading strand)

37
Q

Damaged DNA on the leading strand stalls DNA poly. How does the cell fix this?

A

-DnaG primase makes primer at stalled sites on leading sites
-Pol III released at lesion & continues synthesis from new primer
- 3 t proteins in clamp loader assembly complex may bind 3 Pol III, so that one is in reserve to re-continue DNA synthesis on other side of lesion

38
Q

Why does the cell use translesion polymerases to deal with damaged DNA?

A

-Pol III cannot synthesize over lesions because it has a small catalytic pocket where it checks base-pairing accuracy before adding DNA (highly accurate)

39
Q

What are translesion polymerases? How does the cell use translesion polymerases to deal with damaged DNA?

A

-Other polymerases in the cell (Pol II, IV, V) that can synthesize DNA over lesions but their accuracy and speed varies
- the cell has a polymerase switching mechanism induced by DNA damage that switches DNA poly III for a translesion polymerase that synthesize DNA over lesions

40
Q

what is the biggest problem for replicating polymerases? (physical blocks). why?

A

-transcription
-DNA pol & RNA pol can run into each other preventing DNA replication

41
Q

There are two types of physical blocks to DNA replication. What are they?

A

1) Head-on conflicts between DNA and RNA pol
2) Co-directional conflicts between DNA and RNA pol

42
Q

DNA Pol & RNA Pol head on conflicts are more detrimental. Why? (3 reasons)

A

-moving primase & helicase on lagging strand are displaced
-increased positive supercoiling between the complexes

43
Q

How has the genome evolved to avoid head on conflicts between DNA pol and RNA pol?

A

most genes are oriented in same direction replication fork travels on leading strand

44
Q

co-directional conflicts happen between DNA pol and RNA pol. Why?

A

replication fork moves 10-20 times faster than transcription machinery; detrimental when multiple RNA pol involved ie. at rrn operons (ribosomal rna operon)

45
Q

what is the speed of RNA pol? DNA pol III?

A

-30-90 NTS/SEC
-1000 NTS/SEC with editing

46
Q

How to deal with physical blocks to DNA replication

A

1) Genome organization: highly transcribed rRNA & tRNA genes co- oriented with replication (on leading strand) + other genes = prevents headon collisions
2) RNAP Terminators (Proteins) (Mfd, NusA, etc.)
3) RNAP Modulators
4) Extra Helicases (not DnaB)
5) Pol II removal of RNAP & restart replication

47
Q

codirectional collision vs head on

A

bump into each other (back to back) vs bump into each other head on

48
Q

RNA polymerase makes 3 types of rna?

A

mRNA, rRNA, tRNA

49
Q

What are the two RNAP terminators protein?

A

Mfd protein (mutation frequency decline)
NusA protein

50
Q

What do RNAP Terminators do when RNAP encounter DNA damage?

A

-NusA binds to stalled pol, Mfd causes dissociation of RNAP from stalled transcription complexes then recruits UvrAB repair proteins

51
Q

What are 4 RNAP Modulators?

A

-ppGpp, & DksA, GreA, GreB proteins

52
Q

How do RNAP Modulators work?

A

-their conc increases in response to many stresses to dislodge RNAP complexes stalled at DNA lesions and dislodge RNAP to prevent collisions with DNAP without DNA lesions

53
Q

How do DksA, GreA, and GreB dislodge RNAP?

A

they insert their coiled-coil domain into secondary channel of RNAP

54
Q

What extra Helicases (not DnaB) exists?

A

-Rep, UvrD, DinG

55
Q

What do Rep, UvrD, DinG do to deal with blocks to DNA replication?

A

-they Prevent head-on collisions by helping replication fork get through genomic regions where: DNA binding proteins are found, ReCa coated ssDNA is found

56
Q

How does DNA Pol III remove RNAP & restart of replication? when does this occur?

A

-DNA pol kicks RNAP ff leading strand and replication is restarted using RNA transcript as primer
-occurs in co-directional conflicts`

1: GENET 270 (15 decks)

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