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Physiology of Organisms > Microbes > Flashcards

Microbes Flashcards

1
Q

What are some features of all bacterial cells/

A

Cell wall (peptiglycan)
Ribosomes
Cicular loop of DNA
Protoplast membrane

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2
Q
A
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3
Q

What are features of just some bacteria cells?

A

Pili - protein filaments (enable transport and binding as well as attachment)
Micro-capsule/capsule (polymer of sugars and amino acids) - protection from noctus substances. Useful for nitrogen fixing bacteria which are oxygen sensitive
Granules - storage
Flagellum
Photosynthetic membranes (cyanobacteria)

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4
Q

What are the 4 stages of bacterial growth?

A

Lag
Log - exponencial growth
Stationary phase - growth stops due to lack of nutrients
Death phase - loss of cells as products of metabolism become toxic

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5
Q

What strategies may bacteria have to obtain nutrients from their environment?

A

Active transport/Cotransport with protons
Release of enzymes to degrade polymers
Release of toxins
Chemotaxis (adaptive response)

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6
Q
A
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6
Q

How do bacteria get iron?

A

Fe concentration is low in natural environments, and its availibility frequently limits bacterial growth
Bacteria release siderophores that bind to iron with high affinity before being activley transported back into the cell

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7
Q

Describe gram postive bacterial cell wall and its permeability

A

Thick cell wall made of peptidoglycan
Freely permeable to molecules with low molecular rate
Many nutrients can pass through, limited only by rate of diffusion

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8
Q

Describe gram negativebacterial cell wall and its permeability

A

Thin cell wall with a 2nd, outer membrane
Permeability through this outer membrane is facilitated by the presence of specific protein transporters
2nd membrane contains lots of liposaccharides, making it very impermeable

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9
Q

Describe the structure of peptidoglycan

A

Amino acid chain + carbohydrate
Gram positive ~ 50 sheets
Gram negative ~ 3-5 sheets

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10
Q

How is peptidoglycan synthesised? (for bacteria growth)

A

Balance between activity of two enzymes:
Autolysins hydrolyse outer peptigoglycan layers
Biosynthetic enzymes cross link new inner layers

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11
Q

How does penicillin kill bacterial cells?

A

Inhibits activity of biosynthetic enzymes while autolysins remain active
so peptidoglycan is broken down without being replaced

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12
Q

How may bacteria signal to each other

A

Quorm sensing: monitor their own population density through the release of chemical signals
Rapid electrical signalling: bacteria can form communities called biofilms

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13
Q

Describe electrical signalling in biofilms

A

Cells at the centre of the biosilm will lack glutamate and so activate K+ ion channels
This activates K+ channels in neighboring cells causing a wave of of extracellular K+ that inhibits glutamate uptake at the edge of the biofilm, leaving more for those at the centre

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14
Q

Give some examples of unicellular fungi

A

(Only make up about 15 of the fungal kingdom)
Includes both budding and fission yeast

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15
Q

What are the cell walls of fungi like?

A

Made of layers of glucan and chitin

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16
Q

What are some features of mutlicellular fungi?

A

Specific growth form: the hypha, which emerges from a spore
Hypae are usuallly divided into compartments by cross walls.
Continuity between cells are provided by pores/septa which may be blocked by woronin bodies

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17
Q

How are spores produced by fungi

A

Asexually or sexually produced from hyphae

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18
Q

How may fungi grow from spores?

A

After germination, the fungus is commited to polar growth. Tropisms allow the fungus to grow towards a food supply (such as amino acids)

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19
Q

How do fungi grow?

A

No universially accepted model and they only grow from the apex
Wall components and enzymes to catalyse wall formation are continuously delivered to the tip of a hypae in vesicles
Vesicles are directed to the the apex by the cytoskeleton, where they fuse with the plasma membrane and enzymes released by exocytosis
Cell wall begins to be synthesised and hydrostatic pressure ‘pushes’ out the tip

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20
Q

How may vesicles (that contain enzymes to catalyse fungi cell wall synthesis) be delivered to the right location

A

SNARE proteins (like in ACh release)
High Ca2+ concentration also simulates exocytosis

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21
Q

What is exoenzyme secretion and why do fungi do it?

A

Filamentous fungi secrete an array of enzymes to degrade insoluble external substrates (cellulose, lignin, chitin) so that they can be absrobed.
Exoenzymes are only secreted as they are needed (eg. if a fungi is grown in glucose, secretion of carb digesting enzymes would be inhibited)

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22
Q

What does neurospora arginine metabolism show?

A

Fungi generally halt metabolism once it becomes unessesary
If a fungi is grown on arginine, the pathway of arginine synthesis would be inhibited (arginine itself inhibits)

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23
Q

What does 50% of fungal ATP go towards?

A

H+ ATPases to set up a proton electrochemical gradient
Fungi run on a proton economy

24
Q

How may fungi control the uptake of nutrients? (example of glucose)

A

Varying the expression of hexose transporters on the fungal cell membrane
HXT2 and HXT4 are high affinity glucose transporters and are mainly expressed in low glucose environments

25
Q

What are the three zones of fungal hypae?

A

The absorption zone
The storage zone
The senensence zone - vacuoles release hydrolyic enzymes to breakdown old cells

26
Q

What does it mean that many fungal hypae are autotrophic?

A

When one hypha senses another, it will grow away from it

27
Q

How do fungi reduce/manage nutrient depletion zones?

A

As depletion increases, growth in these regions is switched off
Means that unlike bacteria or yeast colonies, teh mycelium is not limited by rate of diffusion of substrate into the colony

28
Q

How does metabolic flexibility help fungi?

A

Glyoxylate cycle
- under low C conditions, glyoxylate cycle is switched off
- in a phagosome (nutrient poor environment) the fungus upregulates glyoxylate cycle enzymes, producing more TCA products for growth

Oxygen
- most fungi are aerobes
- some are facultaive aeobes (increased survival chances). This means they can anaerobically resipire in low oxyxgen conditions

29
Q

Where might pathogens infect a plant?

A

Leaf niche environment = phyllosphere (generally a harsher environment)

Root = rhizosphere (more nutrient rich)

30
Q

What is amensalism?

A

The presence of one microbe diminishing the ability of another to colonise
- eg. ethanol produced by yeast can limit bacterial growth

31
Q

What are two possible nutrition strategies of plant pathogens?

A

Necrotophs: kill plants and utilise the dead tissue.
Biotrophs: feed on living tissue of plants

Also, some necrotrophs may be be able to use saprotrophy and feed on already dead material

32
Q

Given an example of a fungal biotroph and how it operates

A

Powdery mildew fungus
Developes specialised feeding structures within host cells (similar to myocorrhizal arbusucle - plasma membrane is not breached)

33
Q

How are viruses transmitted between hosts and between cells?

A

As particles called virions: simple structures of viral nucleic acid (RNA) + a protein coat

Symplastic movement between cells is symplastic: through plasmodesmata. Can also move through phloem if reached and will follow the movement of photosynthates.

34
Q

How may pathogens be transported between plants?

A

Insects and other invertebrates act as vectors
May also be carried on/as fungal spores

35
Q

How do bacteria exploit the plant to gain entry?

A

May enter through wounds or stomata etc.

36
Q

How do uromyces appendiculatius (aka. rust fungi) enter plants leafs?

A

If a germ tube growing over a leaf comes into contact with stomata, it will form an appressorium (bulbous structure over stomatal pore from which an infection hypae can grow into the plant)

37
Q

How does the rust fungi recognise stomata?

A

Germ tubes are thigmotropic: can sense and react to changes in the surface contor of leaves

Cation channels (K+ and Ca+) open when tension is experienced and this activates appressorial swelling
ALSO Gd3+ can block these channels, therefore inhibiting apressorium formation.

38
Q

Can pathogens force themselves into plants?

A

Only filementous fungi are capable of forcing themselves through plant cell walls. This may require the use of exoenzymes to degrade the cell walls

39
Q

How does the rice blast fungus enter plant cells?

A

Germ tube secretes hydrophobins from its apex. This allows it to adhere to the leaf surface.
Appressorium begins to form and glycerol accumulates to drive water into the fungus, driving cell wall expansion.
Pressure builds and eventually a penetration hypae can force itself into the plant cell.

40
Q

How do we identify what is causing pathogenity?

A

Knock out suspect gene and still if it can still infect

41
Q

What are some physical barriers that plants have as defences?

A

Waxy cuticle, antimicrobial chemicals

42
Q

How are potential pathogens identified by a host plant?

A

Leave chemical traces which are characteristic of a particular pathogen: Pathogen-Associated Molecular Patterns (PAMPs)

43
Q

What might be a plants reaction to PAMP recognition

A

Generation of ROS that triggers localised synthesis of antimicrobial compounds
Known as PAMP triggered immunity (PTI)

Known as ‘non-host’ resistance and is enough to reject most non-virulent pathogens

44
Q

How may plants react to virus attack?

A

RNA silencing is first line of defence
Eukaryotes can produce Dicer-like nucleotides which ‘dice’ RNA
RISC enzymes silence RNA

45
Q

What are virulent pathogens?

A

Pathogens that have evolved to become compatible with a host by overcoming non-host resistance (PTI)

46
Q

How do virulent pathogens overcome non-host resistance?

A

Produce effector proteins
Bacteria/fungi effectors damage/modify host signalling
Virus effectors interfer with RNA silencing

47
Q

Describe how pathogens and plants could be coevolving?

A

‘Arms race’ between plant and pathigen populations in the evolution of effector genes and plant genes that can prevent damage by effectors.
These plant resistance genes are clled R genes and their proteins are called R proteins.

48
Q

How are R genes different to PTI

A

Much more specific response
Can result in programmed cell death of infected cells

49
Q

What name is given to the response of a plant to a pathogen

A

Hypersensitive response or Effector-triggered immunity

50
Q

What is the result of the hypersensitive response?

A

Spread of defence signals through a plant
Known as systemic aquired resistance
Synthesis of salicyclic acid increases

51
Q

What is the effect of increased synthesis of salicyclic acid in a plant?

A

Plant hormone
Stimulates production of many pathogenesis-related proteins (these do not have antiviral capabilities though)

52
Q

How may pathogens effect photosynthesis (biotrophs)

A

Fungi, such as powdery mildew) can block photosynthesis by shading a leaf with fungal spores
Viruses (TMV) inhibits photosystem II and causes chlorosis in leaves)

53
Q

How do nectrotrophs damage plants?

A

Mainly through the production of toxins

54
Q

How does the tabtoxin damage plants?

A

Causes tissue chlorosis
Inhibits glutamine synthetase so that glutamine synthesis cannot take place
This leads to a build up of ammonium ions (also needed for glutamine synthesis)
The ammonium ions disrupt membrane integrity and cause chlorosis

55
Q

Why is there increased oxygen uptake of plants infected with necrotrophs and biotrophs?

A
  • Pathogen toxins may act as uncouplers
  • Increased activity of oxidative pentose phosphate pathway
  • Oxygen uptake due to activity of non-cytochrome oxidases
  • Biosynthesis for the defense response and replacements of metabolites that have been removed by the pathogen
56
Q

How may pathogens induce changes in host biosynthetic pathways?

A

Shikimic acid pathways is a major defence response of a plant
Can provide carbon skeltons for salicyclic acid synthesis (?????)

57
Q

How may pathogens change carbohydrate translcaion

A

Are sometimes able to ‘reprogramme’ plant metabolism so more photosynthetic products are fed to the leaves they are in

58
Q
A

Physiology of Organisms (10 decks)

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