Bacterial Motility Flashcards
Brownian motion
random movement of molecules suspended in a fluid due to the collision with the fast moving particles in the fluid
why don’t all bacteria move in a culture on a slide
stuck to the slide, run out of energy, dead
types of flagella
monotrichous, amphitrichous, lophotrichous, peritrichous
monotrichous
one flagella
amphitrichous
2 flagella - one on each end
lophotrichous
more than one flagella at each pole - mono or bipolar
peritrichous
have flagella protruding all over
motility pattern of bacteria
alternating between running for a few seconds and tumbling for a fraction of a second
running movement description
motor turns anti clockwise, flagellar filaments with left handed helices form a bundle and propel the cell in a new direction
tumbling movement description
quick reversal of motor to clockwise rotation -> twist into right handed helix - bundle falls apart rapidly - causes bacteria to move in a random direction
Aerotaxis
movement towards oxygen
chemotaxis
movement usually towards nutrients but also away from toxins
bacteria sense changes in nutrient conc in the environment
magnetotaxis
movement along lines of magnetism - certain bacteria with iron in cells -> find iron to make energy from
phototaxis
movement towards light
tactic responses (4 types)
chemotaxis, phototaxis, magnetotaxis, aerotaxis
tactic responses - response to attractants and repellents
bacteria sense changes in nutrient conc in environment
when capillary with chemical attractant inserted into culture -> lots of bacteria accumulate inside and around the capillary tube
when capillary with repellent -> v little bacteria found in or around it
function of methyl-accepting chemotaxis proteins (MCP) or transducer proteins
detect and measure changes in the environment - for very specific compounds, and interact with cytoplasmic proteins: CHE proteins
function of Che proteins
interact with rings of the motors - regulating direction in which it turns: dictates running or tumbling by switching the direction from ccw to cw
chemotaxis full mechanism description
1) MCP interacts with sensor kinase CheA -> autophosphorylates
2) attractant: decreases CheA-P
repellent: increase in CheA-P
3) CheA-P phosphorylates CheY -> CheY-P binds to flagellar motor (not CheY)
4) CheY-P change ccw to cw -> tumble
5) CheZ, a phosphatase - dephosphorylates CheY-P -> continue ccw
6) attractants decrease CheY-P due to less CHeA-P = less switching and longer runs. repellents increase CheY-P as there is more CheA-P formed -> more tumbles
chemotaxis - methylation adaptation explanation
- over time cell integrates attractants/repellents via constant methylation of MCP by CheR
- fully methylated MCP is insensitive to attractant
- CheA-P phosphorylates CheB (methylesterase) -> CheB-P -> demethylates MCP
- Low conc attractant: high CheA-P, High CheB-P = demethylation of MCP increase sensitivity to attractant = longer runs
- high conc attractant: low CheA-P, low CheB-P = high demethylation of MCP = insensitive to attractant -> increase autophosphorylation of CheA -> more likely to tumble to not swim out of the favourable environment
how many transducers are in E. coli
5 - each detect different compounds
bacterial memory
methylation of MCP
methylation of MCP effects
high conc attractant - methylated MCP (more CheA-P = shorter runs and more tumbling to stay in good environment
high conc repellent - methylated MCP less CheA-P = longer runs and less tumbling to leave bad environment
(essentially the CheA-P released is reversed after the MCP becomes methylated by CheR)
traits of mcp receptors
sequences of cytoplasmic domains of all these receptors are highly conserved
sequences of periplasmic sensing domains vary significantly from species to species and from receptor to receptor
each receptor binds diff ligands
each species have diff optimum niches
example of gliding motility in bacteria
F. johnsoniae - latex spheres added to it bind to and are rapidly propelled along cells = suggests that adhesive molecules move laterally along the cell surface during gliding
which genes control the ability to glide?
Gld genes:
3 Gld proteins are components of an ATF-Binding-Cassette (ABC) transporter
5 Gld proteins are lipoproteins in the cytoplasmic membrane or outer membrane
disruption of these genes = loss of motility but ups resistance to bacteriophages that infect wild type cells + loss of the ability to digest the insoluble polysaccharide chitin
what is gliding?
moving without flagella, cell pulls along slime extruded on the outside
how does twitching motility work?
type IV pilus
- extends from the cell surface then is retracted, drags the cell along the surface
- powered by ATP hydrolysis
- retraction proteins control the direction of movement
how does a cell move using gas vesicles, and which kinds of cell?
planktonic bacteria e.g. cyanobacteria, and some archaea
- protein vesicles contain gas -> cell = buoyant
- float up to oxygenated water + light
- vertical migration in aquatic systems like lakes
what are fimbriae/pili?
surface appendages - multi subunit proteins + not flagella!
what are fimbriae/pili needed for?
- host-pathogen interactions
- colonisation + virulence
- host and tissue specificity (tropism)
- biofilm formation
- adhere to other cells and surfaces
- aid resistance in immune cell phagocytosis
- act as antigens
- agglutination
- specialised pili: genetic exchange between bacteria
most important types of pili/fimbriae?
type I and IV
structure + size of fimbriae/pili?
thinner and shorter than flagella
2-5 micrometers long
hundreds to thousands per cell
How does the immune system recognise pathogenic bacteria?
fimbriae are antigenic - called Colonisation Factor Antigens (CFA)
- secretory antibodies (IgA) block bacterial colonisation
- circulating antibodies (IgG/IgM) lead to phagocytosis
What is the process for invading host tissues?
fimbriae/pili loosely associate + adhere to mucosal membranes, invade into or through submucosal epithelial cells
explain the process of fimbriae/pili assisted adhesion -> colonisation
TYPE iv PILI WITH ADHESIVE TIP PROTEIN
- pili establish initial contact to host cell (membranes are negatively charged: avoid electrostatic repulsion, resist flushing by moving contents of intestine/urine)
- the pilus’ adhesive tip protein binds to a receptor (glycolipid/glycoprotein)
- type IV pili depolymerise and shortens
- pulls bacterium close to host cell
- additional adhesins bind to host cell
- colonisation can begin!!
