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MBB262 > Sudbery (Fungal genetics) > Flashcards

Sudbery (Fungal genetics) Flashcards

1
Q

When are fungal infections more likely to be a big problem?

A
  • when IS compromised
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2
Q

Are fungal pathogens big killers?

A
  • yes

- kill more than malaria and influenza together worldwide

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3
Q

What are the characteristics of an Aspergillus infection?

A
  • compact and protected from innate IS
  • can break out of lung and infect brain = lethal
  • causes Aspergilloma
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4
Q

When can Candida albicans be an indicator of AIDS?

A
  • if in mouth
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5
Q

When can Candida albicans be deadly?

A
  • if IS compromised can cross mucosal barrier, gets into bloodstream and causes sepsis
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6
Q

Where is Candida albicans usually found?

A
  • common (≈70%) and usually benign commensal of GI tract and vaginal mucosa
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7
Q

What do Candida albican infections usually result in?

A
  • opportunistic pathogen

- vaginitis, oral-pharangeal candidiasis, systemic candidemia

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8
Q

Who is most at risk of infections from Candida albicans?

A
  • premature babies
  • immuno-compromised, eg. AIDS
  • neutropenia (can be result of immunosuppression therapy after organ transplants and blood cancers)
  • abdominal surgery
  • broad spectrum antibiotics (decreases competition from other bacteria)
  • intensive care patients
  • ill fitting dentures (food trapped –> infections)
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9
Q

What are the diff morphological forms of Candida albicans, and why are these diff forms important?

A
  • can look exactly like S. cerevisiae
  • also forms true hyphae which burrow into epithelial cells
  • ability to switch forms critical to pathogenicity
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10
Q

What happens in cdc42 mutants at a restrictive temp?

A
  • mutants grow but fail to bud
  • fail to polarise actin cytoskeleton
  • fail to form septin ring
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11
Q

Where do Rho type GTPases accum in cdc42 mutants?

A
  • incipient bud sites
  • tips of young buds
  • cytokinetic ring
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12
Q

What is the role of the diff GTPases involved in the activation of cdc42?

A
  • Ras-type -> oncogene
  • Rab –> secretory pathway
  • Rho –> polarised growth and actin cytoskeleton
  • Rac
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13
Q

How is the GTPase cdc42 activated?

A
  • DIAG*
  • GEF is cdc24 (GDP –> GTP)
  • GAPs are Rga2 and Bem3 (GTP –> GDP)
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14
Q

What is the role of sec2?

A
  • GEF for the GTPase sec4

* DIAG*

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15
Q

What is the role of the exocyst complex?

A
  • mediates exocytosis
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16
Q

What methods were used to show physical assoc of diff proteins involved in exocyst complex?

A
  • two-hybrid
  • immune precipitation
  • sucrose density centrifugation
17
Q

Which proteins physically assoc in exocyst complex?

A
  • sec3
  • exo70
  • sec5
  • sec6
  • sec8
  • sec10
  • sec15
18
Q

What happens at the restrictive temp to proteins involved in exocyst complex?

A
  • synthetically lethal w/ each other

- can form active config but can’t function

19
Q

What are the diff forms of the actin cytoskeleton and what are their roles?

A
  • actin cables –> delivery of vesicles to sites of polarised growth
  • actin cortical patches –> endocytosis
  • contractile actomyosin ring –> septum formation (separates mother and daughter after cell division)
20
Q

What is the role of cdc42?

A
  • master regulator of polarised growth

* DIAG*

21
Q

What does cdc42 activate?

A
  • formation of actin cortical patches
  • formation of exocyst
  • formation of septins for cytokinesis
  • formation of actin cables (made of polarisome)
  • mating
22
Q

What activated cdc24?

A
  • cdk1
  • mating pheromone
  • localisation cues and bud site selection
23
Q

What occurs during the late secretory pathway in budding yeast?

A
  • secretory vesicles bleb off golgi
  • membrane of secretory vesicle supplies new membrane to sites of polarised growth
  • in order to leave golgi sec2 activates sec4 (GDP –> GTP)
  • travels along actin cables to sites of polarised growth
  • myosin 2 is motor, assoc w/ mlc1 (a light chain)
  • actin cables made by polarisome
  • in budding yeast, secretory vesicle has most components of exocyst complex, but some already present at cell surface
  • when reaches site of polarised growth, exocyst complete and vesicle can fuse w/ pm
24
Q

How can info from studying budding yeast be used to study hyphal formation?

A
  • looking at env cues that cause cell to switch from yeast to hyphal growth –> many diff signal transduction pathways responding to diff external signals, approx 200 genes triggering transcrip but nothing to suggest they trigger hyphal growth
  • mutant screen –> candida is obligate anaerobe so harder to spot mutants, so fuse GFP to proteins to track movement in cell, saw 2 patterns of localisation (one group of proteins localised in crescent structure at tip and another as point at tip
25
Q

What is the Spitzenkorper?

A
  • apical body
26
Q

Why are proteins assoc w/ secretory vesicles very dynamic?

A
  • continually being delivered and leaving to fuse w/ proteins at cell surface
27
Q

Are proteins at cell surface dynamic?

A
  • no, more stable than those assoc w/ secretory vesicles
28
Q

How can it be tested that proteins are continually arriving and leaving Spitzenkorper?

A
  • FRAP
  • shining laser at spot bleaches it and removes fluorescence
  • fluorescence recovers as new unbleached molecules arrive
  • so can look at rate new molecules arrive at particular place in cell
29
Q

What did FRAP experiments show about the diff proteins?

A
  • sec4 and mlc1 assoc w/ vesicle –> fluorescence recovered quickly (30 secs)
  • exo70 part of exocyst so expect to be stable on cell surface –> recovers much slower (as still replenished but not as fast as proteins assoc w/ vesicles)
  • spa2 part of polarisome –> recovers v slowly if at all
30
Q

Can we model this realistically for hyphal growth?

A
  • use lampshade, represents no. hyphal rings
  • when expand, rings that start off flat gain a height, can calc w/ Pythagoras
  • proposing vesicles fuse w/ hyphal growth according to exocyst density, so amount each ring expands is proportional to density of exocyst
  • so need to measure distribution of exocyst density around hyphal tip
31
Q

What was the initial process carried out for each ring to calc new hyphal shape?

A
  • measure exocyst density from observed normal distribution
  • calc amount of synthase deposited in each ring
  • calc new amount of synthase in each ring
  • calc change in area
  • calc new shape of each ring
  • re-calc new hyphal shape
32
Q

What is systems biology?

A
  • recreating what happens in cell w/ a computer
33
Q

Did the initial model work, and why?

A
  • kind of right idea, but not parallel-sided tube hyphal shape
  • need to account for synthase being taken back into cell in sub-apical regions, where actin patches are
34
Q

What is the structure of a fungal cell wall, from inner to outer?

A
  • chitin (polysaccharide)
  • β-glucan (polsaccharide) –> most visible in light microscope, made by enzymes embedded in cell membrane, which are delivered w/ each secretory vesicle
35
Q

How was the model mod?

A
  • after calc amount of synthase deposited, calc amount of synthase removed by endocytosis from distribution of actin patches
36
Q

Did the mod model work?

A
  • yes, quantified where actin cortical patches were and saw just behind tip where should be

MBB262 (7 decks)

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