Mid Term 1 Review Questions (Part 4) Flashcards
what is an operon, what do it do?
a unit of linked genes under the control of one promoter
what do you call the kind of message that an operon sends?
polycistronic messages
what kind of messaging do prokaryotes use?
polycistronic
what kind of messaging do eukaryotes use?
monocistronic
what is quorum sensing?
bacterial cells sensing the density of nearby cells
what is a 2 component system?
aka, what are the two parts, and what is the function?
- sensor and responder
- sense environment and respond to it
pretty please give an example of two component regulatory systems. who are the players, and what happens?
efflux pump operon expression.
- sensor baeS and responder baeR
- baeR is phosphorylated
what is the difference between phase variation and antigenic variation, and how are they used to evade the immune system?
- PHASE: on/off
- ANTIGENIC: change
- EVADE: take off the hat vs. change to a green hat
which type of variation involves switching genes on and off
phase
which type of variation involves changing the genes
antigenic
how is HGT different from mutation?
Generation: HGT occurs within the same generation, whereas mutation is passed from parent to offspring.
Change: mutation yields 1/2 mutated and 1/2 not mutated, HGT yields 100% recipient
Time: HGT brings about more change faster than mutations
what changes can HGT bring about?
disease-causing traits
in which methods of HGT does the donor survive?
conjugation
in which methods of HGT does the donor not survive?
transformation and transduction
what happens to donated DNA if no origin of replication?
has to be integrated into recipient DNA
what is competence?
the ability to uptake naked DNA
how do scientists study transformation if a cell is not inherently competent?
by changing the surface charge of the recipient cell (from negative) to something else in the lab
what charge does DNA have?
negative
what charge does the surface of a cell have?
negative
why does the charge of DNA and surface of a cell present a problem?
means that not all cells are inherently competent
are any methods of HGT resistant to DNase?
yes, transformation
why is transformation sensitive to DNase?
it’s the only method of HGT that has free DNA. the other two either never leave the cell or are protected by bacteriophages.
how does plasmid transfer via conjugation take place?
F+ x F- = F+ x F+
F+ x F- = F+ x F+
is what kind of transfer
plasmid transfer via conjugation
Hfr x F- = Hfr x F-
is what kind of transfer
plasmid transfer via conjugation
what is the formula for plasmid transfer via conjugation?
Hfr x F- = Hfr x F-
what do we mean by antibiotics?
a compound naturally produced by molds or bacteria that inhibits the growth of or kills other microorganisms
who produces antibiotics?
soil microbes
what do antibiotics act on?
bacterial growth
what do antibiotics not work on?
eukaryotic growth
what is selective toxicity?
causing a greater harm to the pathogen than the host
what are the two main groups of soil microbes
bacteria and fungi
what are the five targets of antibiotic drugs?
great wall!
1. cell wall (peptidoglycan synthesis)
2. nucleic acid synthesis
3. cell membrane integrity
4. metabolic pathways (folate biogynthesis)
5. protein synthesis
how do antimicrobial drugs target the cell wall?
by targeting peptidoglycan synthesis
how do antimicrobial drugs target metabolic pathways?
folate biosynthesis
how to calculate the therapeutic index?
lowest dose toxic to the patient / dose typically used
which is safer, a drug with a therapeutic index of 2, or one with a therapeutic index of 100?
- larger TI = safer drug.
given the choice between a therapeutic index of 2 or 100, why would a doctor use a drug with a therapeutic index of 2?
because the 100 wasn’t working.
what’s one way that antimicrobial drugs target cell wall synthesis?
B-lactam drugs
what is the target of B-lactam drugs?
peptidoglycan synthesis
what does penicillin bind to?
penicillin-binding proteins, aka PBPs
what is transpeptidase?
a penicillin-binding protein
what do B-lactam drugs do in general?
inhibit cell wall synthesis
how do B-lactam drugs inhibit cell wall synthesis?
by inhibiting the enzymes that form cross links between adjacent glycan chains. if penicillin can’t form to PBP, new peptidoglycan can’t be formed, so you’ve got chains but no linkage and they fall apart.
what eventually happens to a cell that’s been personally affected by B-lactam drugs?
the cell membrane gets bigger but the cell wall doesn’t, so eventually the cell explodes!