L4- Evolution of parasitism Flashcards

1
Q

What is the “arms race”?

A

A series of escalating mutual counter adaptations by the 2 lineages to exploit or inhibit exploitation by the other

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2
Q

What is coevolution?

A

Continuous fine tuning of the host parasite relationship

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3
Q

Describe 3 types of symbiosis?

A

Commensalism – no metabolic dependence
Mutualism – obligatory relationship – both benefit
Parasitism – one partner benefits, metabolic dependence, may cause harm to host

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4
Q

Features of nematode phyla?

A

Species richness
Numerical abundance
Ecological omnipresence

Estimated to be 1 to 10 million nematode species on earth.
Nematodes can exceed 1 million individuals per meter squared.
Fresh water, marine, terrestrial, extreme environments.
Range of ecological niches: Free living, predators, parasites.

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5
Q

What are the 3 main principles in the evolution of parasitism?

A

Loss of otherwise essential genes through mutualisitic relationship with bacterial endosymbiont

Horizontal gene transfer

Parasitic features evolving under free living conditions - the concept of pre-adaptation (while the nematode was free living and that gave it an advantage in a parasitic relationship)

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6
Q

What’s strange about the different types of nematodes?

A

They look the same but some are parasitic and some aren’t.

Most are just parasitic for some part of their life.

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7
Q

What suggests some characteristic of nematodes that favours evolution of parasitism?

A

Molecular phylogenetic approaches – show parasitism evolved at least 7 times in nematodes!
4 groups animal nematode parasites
3 groups of plant nematode parasites.

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8
Q

Brugia malayi – animal parasite

Life cycle?

A

Have female parasite which have eggs which develop into microfilariae. It’s these microfilariae that circulate in the host. The mosquito take up the microfilariae and there’s a devlopment stage within the mosquito. And then mosquito will infect the host again.

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9
Q

Meloidogyne incognita – plant parasite. Life cycle?

A

Eggs in root system of host. J2 (juvenile stage 2) develops in egg. J2 penetrates plant root; migrates between cells; induces multinuclear cells. Moults x3 to adult.

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10
Q

Pristionchus pacificus -beetle associated. Necromenic. Life cycle?

A

Pristionchus makes an association with a beetle. Very similar life cycle to C. elegans.
Pristionchus lays eggs. The eggs hatch and become L1s then L2s. Then very interesting- the L2 can either arrest into a Dauer larva under times of stress, or it can carry on to L3 then l4 in normal pathway.

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11
Q

Loss of otherwise essential genes- example? (detailed)

1st principal of evolution of parasitism

A

Brugia malayi – major human filarial parasite (animal parasite transmitted by mosquito)

Genome analysis – 20% of gene predictions are B. malayi specific - indicates huge pool genes involved in nematode defending itself in its habitat.

However, Genome shows loss of genes encoding enzymes required for biosynthesis of purine, heme and riboflavin. These are essential for its survival. 9/10 of the genes needed to make puring are absent. 6/7 of genes encoding in enzymes encoding haem are absent. And all of the genes to make riboflavin are absent.

Brugia malayi has evolved so it can source these things from a host or endosymbiotic bacetia Wolbachia. So this has become reliant on the host to survive.

Do remember- it appears simple but parasites often genomic complexity

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12
Q

Brugia malayi survival?

A

It has lost otherwise essential genes. So can’t make purine, haem and riboflavin. So it sources these from a host or endosymbiotic bacteria- Wolbachia.

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13
Q

Meloidogyne incognita and M. hapla?

A

Plant parasites are of agricultural importance
Life style very different to animal parasites
All have a stylet to puncture plant cell wall to provide multinucleated plant cells which worms feeds on.
Called “Root-knot nematodes”

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14
Q

Horizontal gene transfer in Meloidogyne incognita and M. hapla?

A

Genomes of the two species are rich in cell wall degrading carbohydrate-active enzymes (CAZymes) (eg cellulases, xylanases).

This is odd. No counterpart in most other animals, absent from free-living nematodes , most similar to genes of bacteria, so the hypothesis is that horizontal gene transfer occured from bacteria also in the roots of plants were transferred to these nematodes and then selected for retention of parasitism enhancing genes.
(from rhizobia)

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15
Q

Explain the concept of pre-adaptation?

A

Change in the ecology of organisms. Changed from free living to parasitic. this requires some changes in the organism.
These transitions are helped by adaptations to the current environment before they are parasitic. So adaptations that may be useful in future to be parasite.

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16
Q

What is the classic definition of pre-adaptation?

A

An adaptation evolved to increase fitness in one ecosystem but which can be exploited for survival in another
(however this is still hypothetical, you can’t see pre-adaptation happening, can only see before and after)

17
Q

In nematodes what do Phoretic associations and Necromenic associations show?

A

They may be pre-adaptations (evidence for this theory of pre-adaptations). Because nematodes who have these associations show tolerance to toxic enzymes,
Adapt to low oxygen concentrations and have an ability to form dauer larvae.

The transition is free-living to Phoretic association to necromenic association to parasite

18
Q

When do you Find phoretic and necromenic associations?

A

In the Dauer stage

19
Q

What is the dauer?

A

specialised, arrested, non feeding stage – specialised for survival and dispersal of free-living nematodes

20
Q

What does phoresy mean?

A

Literally means: used for transport.

So in phoresy the dauer uses insects for transportation. This isn’t species specific.

21
Q

What does necromeny mean?

A

Necromeny-dauer associates with insect host in species specific manner – wait for insect’s death then feeds on microbes growing on carcass. (not quite parasitic)

22
Q

How does the dauer stage provide evidence for preadaptation? How is it similar to parasitic infection?

A

Dauer stage and parasitic infective larvae: both has specialised cuticle; both cannot feed; both can resume development to 4th larval stage; where parasitic nematodes use an infective larvae its almost always 3rd stage, as are dauer larvae

23
Q

Molecular similarities between the dauer and infective larvae?

A

Molecular similarities: a conserved endocrine signalling mechanism involving dafachronic acid (DA) and the NHR DAF-12 (receptor for DA) controls formation of dauer and infective larvae.

24
Q

What is Strongyloides papillosus?

A

Strongyloides papillosus – obligate parasite of sheep and rabbits

25
Q

slide 28?

A

…?

26
Q

Caenorhabditis elegans.

Life cycle focussing on DA-DAF12 signalling

A

Once egg is shed and formation of L2.
L2 has to make decision. Has to decide whether it’s going to grow and develop as free living life style or arrest and form dauer. (by sensing environment).
This dauer has a decision to make. Has to know whether dauer should resume free livign life style and become L4. By sensing environment e.g. temp.
In C. elegans development of the dauer is default developmental behaviour.
This happens when DAF12 is not occupied by the ligand.

When conditions are good- DA binds to DAF-12 to specificy non-dauer larvae.

27
Q

Strongyloides papillosus life cycle

focussing on DA-DAF12 signalling

A

Free living developmental stage has choice between infective larvae (analogous to dauer larvae of free-living nematodes) and non infective larvae.

Exeperiments that were done_> Add DA to S. papillosus larvae. Then you get non infective larvae. Like in c. elegans.

DA -driven switch from infective to non infective larvae is equivalent to C elegans where DA specifies non dauer larva

28
Q

What’s odd about strongyloides papillosus?

A

Has adult parasites inside vertebrate host and free-living adult generation. Half-way house between free living and parasitic life style.

29
Q

Ancylostoma- DA

A

Development of L3 is constitutive. Always becomes infective L3.
So what would happen if we added DA to early larval stages. would that prevent the formation of this?
We don’t know the answer but interesting

30
Q

Pristionchus pacificus (the nechromenic nematode mentioned before) as an example for preadaptation

A

Has nechromenic association with scarab beetle.
Look at sequenced genome. See lots of detoxifying enzymes. also genome rich in genes for glycosyl hydrolases. Good for toxic dead body conditions. Not found in any other non-parasitic nematodes.

(So suggests that nechromany is just one step before parasitism)

31
Q

Extra reading

A

Easy reads:

Dieterich C and Sommer RJ How to become a parasite. Trends in Genetics, 2009, 25, 203-

Viney M. How did parasitic worms evolve? Bioessays, 2009, 31, 496-