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17 Cards in this Set
- Front
- Back
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Global regulatory mechanisms |
Allow bacteria to respond to complex environmental changes or undergo sweeping changes in their physiology Global gene expression regulated by present AND active sigma factors!!!! |
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Catabolite Repression |
allows bacterium to use most efficient carbon source first (glucose) lac, mal, and arg operons regulated by catabolite repression Specific + global regulatory mechs used in combo |
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Diauxic growth curve |
Double growth or 2 phases caused by the presence of two sugars on a culture growth media, one of which is easier for the target bacterium to metabolize. Grows on glucose 1st then on lactose once glucose runs out |
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Catabolite activator protein (CAP) |
(In absence of glucose) CAP =activator / cAMP= co-activator--> tx. glucose↓ → cAMP↑ |
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Transcription of carbon utilization genes is linked to metabolism thru PTS system |
Glucose present: Enzyme IIA inhibits entry of alt. sugars by binding to their transporters Glucose absent: binds to adenylate cyclase and stimulates production of cAMP |
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Glucose and CAP relationship |
glucose present--> caMP is low; sugar entry inhibited CAP is off of the DNA & LacI is on--> tx repressed glucose absent/ lactose present--> cAMP is high; sugar entry permitted CAP binds to DNA & LacI turned off--> tx is activated |
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How do cells respond to and recover from shock? |
1. cells synthesize chaperones-> assist w/ folding 2. cells synthesize proteases-> dgrade dameged proteins 3. heat shock-induced genes have promoter seq. that bind to σ32 (↑ activity of σ32) |
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Recovery from Heat Shock |
one of the genes turned on by σ32 is dnaK. dnaK creates a homeostatic mech. that returns cell to its normal state |
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dnaK gene |
tx of dnaK gene activated by σ32--> denatured proteins refolded/ dnaK lvls ↑ & there's enough dnaK to rebind σ32 --> σ32 inactivated and/or degraded by FtsH // refolded proteins released |
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SOS response to DNA damage |
1. RecA bind to ssDNA exposed by UV damage or stalled replication forks 2. RecA-ssDNA stimulates LexA auto-cleavage always a steady-state level of LexA in the cell due to (-) feedback loop: ↑lexA= no tx / ↓lexA= tx |
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LexA & umuDC / sulA |
umuDC--> performs trasnlesion DNA sythesis sulA--> inhibits cell division |
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LexA repession --> activation |
- LexA represses some genes by binding to SOS boxes - UV damages--> dsDNA breaks ; ssDNA is exposed - RecA+ssDNA stimulates autocleavage of LexA - LexA-repressed genes are turned on and LexA protein is depleted in cell. |
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How do cells reset after DNA damage is repaired? |
1. sulA degraded by protease--> division restarts 2. UmuDC degraded by ClpCP protease--> mutagenic replication stops ** Cells deactivate/degrade proteins that responded to stress ** |
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Stringent Reponse |
enables bacteria to survive nutrient deprivation -> uncharged tRNA accumulate in cell -> RelA senses uncharged tRNA when it enters A site of translating ribosome ->RelA synthesizes pppGpp from GTP and ATP *ppGpp= alarmone |
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What does ppGpp do? |
induces a slow growing state that helps cell survive AA starvation 1. inhibits chromo replication 2. slows tx by binding to RNAP 3. favors binding of alt σ factors other than main σ70. (this directs tx of stress response genes) |
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2 component signal transduction |
1. histidine kinases in CM--> 2. external signal dimerization cross- phosphorylation--> 3. phosphoryl group transferred to Asp residue on a response regulator---> 4. increase/decreases its activity |
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What do activated response regulators do? |
1. activate/ repress tx 2. output domains can be enzymes turned on/off by phosphoylation of receiver domain (cell motility, virulence, biofilm formation) 3. receiver domain acts alone by binding to a downstream protein only in one state (governs direc. of flagellar rotation in chemotaxis) |
