BIOC2306 Bacterial cell wall

who has cell walls

plants, fungi, bact

what is plant cell wall made of

cellulose

waht is bact cell wall made of

peptidoglycan (murein)

role of cell wall

primary function is structual (protect from osmotic pressure) as acts as a scaffold

plus an anchoring point for components of bact that interact with environ

how is bact cell wall important to humans

has key role in its virulence

immune system recognit

antibiotic target

biological interest

structure of peptidoglycan wall

polymer of repeating N-acetlymuramic acid (NAM) and N-acetylglucosamine (NAG) with peptide bridges/crosslinks (betw muramic)

stages of peptidoglycan synthesis

synth in cyto

attach to lipid carrier and transp into extracellular matrix

glycan polymerisation and crosslinking

stage 1 product

UDP-MurNac pentapeptide

stage 2 product

lipid 1 conv to lipid 2

export of lipid 2

req lipid II flipping cat by flippase (MurJ), moves from inner leaflet to outer leaflet of memb by protecting hydrophilic part of lipid II in a aqueous cavity

stage III reactions

transglycosylation

transpeptidation both done by penicilin binding protein

what enzymes are required for peptidoglycan recycling

PG hydrolases, permeases, cytoplasmic enzymes

(other bact rely on scavenging PG instead of synth, uses diff enzymes)

gram positive vs negative

positive only have cyto memb and peptidoglycan wall

negative have outer memb too (thinner PG wall too)

have diff proteins in outermost membs too

external vs internal face of PG cell wall

external has larger pores, allow environ mols to enter

internal has frequent small ones that allow small mols thru whilst maintain strong wall

how can the immune system detect peptidoglycan (uniquely bacterial)

extracellular recognition (proteins on surface)

intracellular recognition by NOD1 and NOD2, that recognit specific

soluble PG recognit mols

beta lactam (e.g. penicillin) antibiotic mechanism of action

are D-ala D-ala substrate analogue (dd on term of PG) so binds penicilin binding protein, causing irrev acetylation of transpeptidase domain

when PG hydrolases cleave peptide bridges of PG network for expansion, can no longer reform

gradual weakening off PG network (futile cycle) suseptible to environ

how do all beta lactams work

target PG syth

so normal PG hydrolases that break down network for growth cause weakening of network, make suseptible to environ (lysis)

hydrolase work in expansion of network in own growth or when try to divide

mechanism of vancomycin (glycopeptide)

binds d-ala d-ala therefore prev crosslink formation

(primarily aff transglycosylation but also transpeptidation)

which bacterial strain is vancomycin inaffective against and why

gram negative as have outer memb that prev access PG network