Lecture 2 Flashcards

1
Q

How can bacterial store their genomic information?

A

Mostly circular, but occasionally, linear chromosomes and plasmids.

Bacteria can have one or multiple chomosomes.

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2
Q

What range of bacterial genome sizes exist?

A

0.14Mb to 14.3Mb

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3
Q

What usually underpins bacteria having larger genomes?

A

Needing more genes because you live in more complex environments

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4
Q

What is the common bacterial genome size?

A

Between 2 and 6Mb

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5
Q

How do bacterial genomes acquire new genes?

A

Genes that are remnants of phage attack can be found in bacterial genomes

Bacteria will naturally take up DNA form their environment (are transformable)

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6
Q

What is the core genome?

A

Core genome - Genes that are seen in all strains of the species

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7
Q

What is the dispensable genome?

A

Genes that are present in two or more strains

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8
Q

What are unique genes?

A

Genes that are specific to an individual strain

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9
Q

What is the pan-genome?

A

The pan-genome is the full complement of genes in a clade.

Made up of the core genome, dispensable genome and unique genes.

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10
Q

What is reductive evolution?

A

Loss of genes that are no longer required

e.g. Evolution of extracellular bacteria that have become intracellular; in which they lose genes that are now superfluous in their new environment.

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11
Q

What are pseudogenes?

A

Genes which have lost their ability to be expressed; an outcome of reductive evolution

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12
Q

What can cause rapid emergence of genetically uniform pathogens form variable ancestors?

A

Genetic bottlenecking

Individuals acquire new trait which makes them more likely to survive. Outcompete other individuals untill only pathogen with that trait surviving

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13
Q

Why are the genomes of pathogenic bacteria commonly smaller than non-pathogenic bacteria?

A

Narrower functional range

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14
Q

What stages does a bacteria go through from being free-living and extra-cellular to being an organelle?

A

From free-living and extracellular to facultative intracellular, to obligate intracellular, to obligate intracellular mutualist, to organelle.

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15
Q

Where do enteric pathogens live?

A

In the gut

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16
Q

Where are the potential carbon sources in the gut?

A

Host glycans on mucin proteins

From the digested food

17
Q

How are host sugars taken up by enteric pathogens?

A

Anaerobic residents in the lower bowel digest polysaccharides and liberate free sugars. These monosaccharides can then be used by the enteric pathogens. Some enteric pathogens can’t use the polysaccharides.

18
Q

What has been shown about the sugar comsumption of commensal and pathogenic E.coli?

A

Both are very flexible and can use a wide range of carbon sources. But commensal (MG1655) and pathogenic (EDL933) have differential use of these C-sources. With preferences about which order they use them in.

19
Q

What will E.coli use as a carbon source last?

A

After all sugar has run out the E.coli will use acetate

20
Q

Which sugars were shown to be more timportant to the EDL strain than the MG strain?

How?

A

Galactose and Mannose

Knockout mutants of EDL strain for catabolism gene of each sugar grew less in mouse model then wild type. Effect not as large in MG strain.

21
Q

Which sugar was shown to be more important to MG strain?

A

Sialic acid

22
Q

What effect does secondary infection with a commensal strain have on a mouse already infected with a different commensal strain?

A

The numbers of the first strain slightly decrease but stay high, the numbers of the second strain increase to match that of the first strain. The two can have different niches; and not effect each other.

23
Q

What effect does secondary infection with a commensal strain have on a mouse already infected with a pathogenic strain?

A

The pathogenic strain is unable to accumulate and the numbers decrease soon after infection - therefore the commensal strain appears to protect the mouse.

24
Q

What is the function of the VPI-2 in vibrio cholerae?

A

Conatains a series of metabolic genes which can release sialic acid from host proteins and consume it.

NanH encodes a sialidase which can cleave sialic acid from host mucin proteins

25
Q

Which gene from the VPI-2 has been shown to be important in earrly colonisation of mouse models?

A

The nanA gene

Loss of the gene by deletion causes a signicant decrease in the number of CFU’s in early colonisation

26
Q

What effect can anti-biotic treatment sometimes have?

A

Removes infection by initial bacteria however can cause infection from other bacteria due to loss of microbiota and hence more space and more nutirents for the enteric pathogens to grow in. E.g. clostridium difficile

27
Q

What was the initial hypothesis of the Sonnenburg paper?

A

Post-antibiotic treatment the microbiota that usually comsume the free monosaccharides from mucin proteins are gone. Therefore the pathogenic bacteria, C.difficle and salmonella trphimurium, have more esy access to the monosaccharides.

28
Q

What is a gnotobiotic mouse?

Why are they useful?

A

A mouse with no microbiota. Breed under controlled conditions.

Can add single organisms that you are interested in with no interference. Similar conditions to those seen in anti-boitic treated individuals.

29
Q

How did Sonnenburg use gnotobiotic mice to identify salmonella genes?

A

Mice were monoassociated with Bacteriodes thetatiotaomicron, to model a microbiota that is susceptible to pathogenic emergence. Model and germ-free mice were give S. typhimurium and then the caecal contents were collected five days later and sujected to transcriptional profiling using a S.typhimurium gene chip.

30
Q

What did the gene chip show about salmonella gene expression?

A

Genes expression of nan, fuc and pdu operons were higher in Bacteriodes thetatiotaomicron infected mice then in germ-free mice and in-vitro studies. Nan operon for sialic acid transport and catabolism. Fuc and pdu operons for fucose transport and catabolism.

31
Q

How were these increases gene expression checked?

A

qRT-PCR of in vitro results of germ-free free and Bacteriodes thetatiotaomicron pre-treated culture

32
Q

What effect did loss of nanA and fucI have on the salmonella growth?

A

Resulting strains cannot grow on either as thier sole carbon source

33
Q

What was shown by the competition index of effect of Bt on growth of nanAfacI salmonella mutants?

A

nanAfucI mutant has significatn disadvantged to the wild type on days 1&2 after infection when Bt is present but not when Bt is absent

34
Q

What efect does Bt have on sialic acid?

How was this seen in the paper?

A

Bt has a sialidase to cleave the sialic acid but no catabolic genes to catabolise it.

In presence of Bt there was an increase of sialic acid in caecal matter, this was not seen when mutant of Bt lacking it sialidase activity was used.

35
Q

What does the paper argue the Bt cleaves the sialic acid for if its not going to catabolise it?

A

Release of the sialic acid allows the Bt to access the carbohydrates it is actually interested in which lie below the sialic acid.

No evidence of this claim

36
Q

What effect was Bt infection shown to have of C.difficile?

A

Increased expression of nan genes and more CFU’s.