Lecture 3 - Cell wall Flashcards
Where is the bacterial CW located in G+ve vs G-ve?
Outermost of G+ve, under OM of G-ve
What are the 4 functions of the CW?
- Shape
- Anchor flagella
- Prevent cell bursting in hypotonic
- Contributes to pathgenicity
Describe the overall structure of the CW - protein, formation, repeat molecules, links
- Peptidoglycan/murein
- Peptidoglycan sacculus both strong and elastic
- N-acetylglucosamine (NAG), N-acetylmuramic acid (NAM)
- beta-1, 4 glycosidic bonds
Describe the cross-linking patterns of peptidoglycan in the CW - location, aa’s, unique aa’s not in proteins
- To NAM’s carboxyl groups by tetrapeptides of D and L aa’s
- D amino acids protect from peptidases which recog L aa’s
- D-glu, D-ala, meso-diaminopimelic acid (DAP) not in proteins
Compare G-ve vs G+ve cross-linking with bacteria examples of each
- G+ve = peptide interbridge eg % Gly residues in S-aureus
- G-ve = direct cross-linking eg DAP to D-ala in E. coli
Compare G+ve and G-ve CW - thickness, % cross-linked, components
- G+ve = 20-80nm thick, 70% NAMs cross-linked, -ve charge from aa’s and phosphate groups,
- G-ve = 2-7nm thick, 25% NAMs cross-linked, no teichoic acid
Describe the components of teichoic acid and list its 5 functions
- Polymers of phosphate, glycerol, side chains eg D-ala, glucose
1. Taxonomy = antigenic from varied R groups
2. Anchor PM and wall for structure
3. Bind pathogenic bacteria to host
4. Protect from chemicals
5. Ion uptake and cell division
What is the function of lipoteichoic acid?
Covalently bound to PM lipids = anchor wall to PM
Describe the differences in Gram staining results for G+ve vs G-ve in terms of CW structure
- G+ve = ethanol shrinks pores so violet dye retained
- G-ve = larger pores allow violet dye to be removed
Describe the 8 step process of CW synthesis and where each step occurs
- UDP derivatives of NAM and NAG made in cytoplasm
- aa’s added to UDP-NAM = NAM-pentapeptide in cytoplasm
- NAM-pentapeptide moved to BP phosphate by pyrophosphate to make lipid 1 in PM
- UDP moves NAG to BP-P-P-NAM-pentapeptide and interbridges made to make lipid 2 in PM
- Bactoprenol moves NAG-NAM-pentapeptide across PM by flippase enzyme and BP-P-P embedded in PM
- Autolysins murein hydrolase and endopeptidase make gaps in peptidoglycan for transglycosylation in periplasm
- Bactoprenol moves back across PM and loses 1 phosphate
- Peptide cross-links made by transpeptidation via transpeptidases to remove terminal ala to make tetrapeptide in periplasm
What are the 2 types of antibiotics inhibiting CW synthesis and give examples of each.
- Penicillins (PCs) = penicillin, ampicillin, methicillin for growing bacteria
- Cephalosporins = cephalothin, cefoxitin, cefaperazone
How do antibiotics inhibit CW synthesis? How do PCs specifically inhibit CW synthesis?
Bind transpeptidases by imitating pentapeptide to block peptidoglycan/murein cross-linking = elongates without cross-linking = weakened to osmosis
How do PCs specifically inhibit CW synthesis?
PCs = growing bacteria = transpeptidases (blocked), autolysins (triggered) like endopeptidase are PBPs = dysregulated so imbalance between synthesis and destruction of PG bonds
Where are lysozymes found and how do they affect CW structure in what type of bacteria?
- Sweat glands and mucous membranes
- Break beta-1, 4 glycosidic bonds between NAM and NAG
- Growing and non-growing bacteria
What are protoplasts and how do they form?
- Spherical osmotically sensitive G+ve with only PM
- Lysozyme + isotonic solution = protoplast
What are spheroplasts and how do they form?
- Spherical osmotically sensitive G-ve with only PM and some OM and PG
- Lysozyme in water + EDTA to damage OM
What are L-forms, where are they found, and what can they result in?
- Protoplasts and spheroplasts which grow/divide
- Made or in vivo from PCs or lysozymes
- Chronic hard to treat infections bc resistant to wall-acting antibiotics and/or persist and revert to CW version after treatment
