In the presence of a β lactam transglycosylation

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In the presence of a β-lactam, transglycosylation proceeds normally, but the glycan strands are not crosslinked, so the PG becomes weaker. The PG lysis reactions also proceed normally, so the balance is shifted toward breakdown of the cell wall. The cells eventually lyse due to osmotic pressure, because bacteria often live in environments that are less concentrated than their cytoplasmic contents. How do β-lactams kill bacteria?
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Resistance to β-lactams is often mediated by enzymes called β-lactamases , which break the ring and inactivate the antibiotic.
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Different bacteria have characteristic cell shapes, which are generated by the shape of the PG layer. How are these shapes maintained during growth and division?
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PBP3 or ftsI was identified genetically, in a screen for f ilamentous, t emperature-s ensitive mutants ftsI mutant 30°C ftsI mutant 42°C PBPs help to generate characteristic cell shapes
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By knocking out one or several PBP genes at a time, investigators have found several effects on cell shape: WT ΔPBP2 ΔPBP3 ΔLMW PBPs ( E. coli ) death, no effect, or ΔPBP1 PBP2 synthesizes lateral cell walls PBP3 synthesizes septa
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PBP localization coincides with predicted functions: FtsI (PBP3) is located at division septum PBP2 is located preferentially In lateral cell walls PBP1 is found in both septa and lateral walls
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