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UT BIO 326R - Stress Response and Antibiotic Resistance
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BIO 326R 1st Edition Lecture 28 Outline of Last Lecture I. Motility continueda. Swimming, Twitching, Swarming, Glidingb. Memoryc. TaxisII. Stressa. Recognition and gene expressionb. RpoSOutline of Current Lecture I. Stress Responsea. Generalb. SpecificII. Antimicrobialsa. Traitsb. Historyc. Basic sitesd. Penicilline. Other cell wall inhibitors Current LectureStress Response- General stress responseo RpoS- Specific stress responseo Bacterial 2 component regulatory system Inner membrane cytoplasmic protein- Signal received by sensor kinaseo Kinases phosphorylateThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute. Soluble cytoplasmic protein- Transcriptional regulator, response regulatoro Only active when phosphorylatedo Steps to regulatory system Sensor kinase sense stress signal and phosphorylates itself at the histidineresidue Sensor kinase then phosphorylates the response regulator Response regulator is now activated and alters transcriptiono Mycoplasm= obligate human bacterium 0 two component systemso E. coli= 30-35 two component systemso Pseadomones= over 50 two component systemsAntimicrobials- Antibiotics, disinfectants- Bacteriostatic antibioticso Stops bacteria growth (does not kill) and lets the immune system take over- Antibiotic traitso Minimal side effectso Low molecular weight Easily diffusible, solubleo Low toxicityo Stops growth or kills bacteriao Naturally occurring- Historyo 1888—Freudenreich, pyocyanase Killed bacteria, but killed humans tooo 1908—sulfa drugs Inhibit folic acid biosynthesis, red Problem: allergies, ~3% of population allergico Ancient Egyptians—put moldy bread on woundso 1928—Flemming discovers penicillin Accidental discovery-- noticed bacteria didn’t grow where mold was Flemming was not capable of isolating the active ingredient Lots of people began working on this and purified the active component—penicillin- Basic target sites—first three are most commono Cell wall Peptidoglycan or other membrane componentso Protein synthesis 30s, 50so Nucleic acid synthesis RNA, DNAo Antimetabolites- Penicillin—most used around the worldo Beta- lactamo Preference for gram + No outer membraneo Minimal toxicityo Very high resistance mediated by genetic exchange Gene that encodes beta- lactamase enzyme that cleaves penicillin-  high resistance Augmentin—can give if allergic to penicillin- Beta-lactam + cavulanic acid (beta-lactamase inhibitor)- Antibiotic relationshipso Synergistic—greater than additive Together they give a better result than the individual results of each Two different targets typically (ex: DNA synthesis and PG synthesis)o Antagonistic—activity of one interferes with the other The activity of one antibiotic interferes with the other—the antibiotics areworse together than if taken individually o Beta lactam antibiotic only works against growing bacteria Because peptidoglycan synthesis is only needed when growing- Other cell wall inhibitorso Bacitran—only kills gram +o Polymixin—detergent that dissolved membranes Mostly gram-- Assessing antibiotic activityo Typically done in vitroo More on this next


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UT BIO 326R - Stress Response and Antibiotic Resistance

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