chemotaxis

what is chemotaxis

• movement towards or away from chemical or stimulus

  • bacteria want to get close to nutrient

what are membrane functions

• permeability barrier

• transport

• secretion/biosynthesis

• electron transport

• anchor for fimbriae

• pili & flagella

Three main components of flagella connected to bacterial cell wall

• filament

• hook

• basal body

what are the flagellar arrangements

• monotrichous

• amphitrichous

• lophotrichous

• petrichous

what are the types of motility mechanisms

1. flagella (swimming)

2. type IV pili (twitching motility)

3. Gliding motility

4. ‘Swarming’ phenomenon

5. Alteration of cell shape

6. Ratcheting mech on surfaces

7. Quorum Sensing/Swarming Phenomenon

types of ‘taxis’ (causes to move)

• chemo- (chemicals)

• magneto- (force fields)

• photo- (sunlight)

• baro- (pressure)

who was chemotaxis pioneer and what did he do?

• Howard Berg

  • discovered mech of bacterial flagellar rotation/movement in 1973

what is the structure of filaments

• extend helix several cell lengths long

• attached to cell surface by hook (flexible ‘universal joint’)

• rotated by reversible rotary motor

• direction of motor is regulated in response to changing environ conditions

what are the three rings on flagellar attachment

• L (top)

• P (middle-top)

• M/S (middle-bottom)

• C (bottom)

what are two states of chemotaxis

• run vs. tumble/twiddle

what is the random biased walk and who discovered it

…

is chemotaxis spiral or temporal recognition? why?

…

what is the chemotactic cascade and where does each part occur

• chemo effectors (outside cell)

• Periplasmic Binding Protein’s (periplasm)

• Methyl accepting Chemotaxis Proteins (membrane)

• Cytoplasmic Proteins (cytoplasm)

• Flagellar Rotation Proteins (membrane)

types of chemo effectors

• O2, aspartate, glutamate, ribose, galactose, maltose, glycine, indole, glucose

what is the chemical definitions of chemotaxis? how is this a type of primitive memory?

• variations in state of ‘phosphorylation’ and state of ‘methylation’ result in excitation(run) vs adaptation (tumble)

  • methylation - depend on [ ] of methyl groups of MCP and duration is attacked

steps of chemotaxis

1. chemoeffector is presented to MCO and binds

2. decreases amnt of autophosphorylation of CheA —>decreases autophosphorylation of CheY and CheB

3. increased methylation of MCPs; doesn’t allow CheY to tell FliM to ‘tumble’ (default RUN (ccw) is maintained)

4. when methylation builds up too much and/or no chemoeffectors present, autophosphorylation of CheAoccurs

5. cause autophosphorylation of CheB (demethylation of MCPs) and CheY (in phosphorylated state) will activate FliM

6. causes clockwise rotation = tumble

switching mechanism

1. MCP’s transmit a signal when attractants are absent

2. absence of attractants cause inc in CheA-P

3. increase in CheY-P (diffuible protein)

4. CheY-P binds FliM = tumbling

5. Change from CCW—>CW rot

6. N.B. inc. CH3 = dec. binding affinity

7. binding of an attractant to MCO causes dec. of CheA-P

8. results in a ‘run’ (no interaction of CheY with FliM)

9. inc. methylation of MCP’s

10. N.B. autophosphorylation of CheA occurs when either methylation and/or attractant is present