sporulation Flashcards

1
Q

what is a diaspore

A

a type of spore found in some bacteria as well as plans and fungi. it has a dispersal mechanism after sexual reproduction

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2
Q

what is an endospore

A

a type of spore in bacteria which is metabolically inert and is designed to survive harsh conditions and periods of starvation

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3
Q

why is sporulation a last resort

A

is it energetically costly, takes a long time and is irreversible. it only occurs if stationary phase is not enough to enable survival

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4
Q

what is the transition phase

A

bacteria has entered stationary phase but has not yet committed to sporulation

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5
Q

which three transcription factors are responsible for controlling sporulation

A

AbrB, CodY and SpoOA.

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6
Q

what is the role of AbrB

A

it represses stationary phase genes during exponential phase

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7
Q

what does CodY do

A

it represses early- stationary and sporulation genes. it is only active when bound by GTP so is indicative of nutrient levels

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8
Q

what does SpoOA do

A

it is the master regulator or sporulation. at low SpoOAP (monomer) it represses transcription but at high SpoOAP (dimer) it activates transcription of sporulation genes. it regulates 121 genes

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9
Q

how is SpoOA phosphorylated

A

by a relay of Pi via 5 sensor kinases (Kin A-E), SpoOF, SpoOB, then the D region of SpoOA. the steps allow greater levels of control and sporolation will only occur when there is a threshold amount of SpoOAP dimer present

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10
Q

what upregulates and downregulates phosphorylation of SpoOA

A

it is upregulated by KipA and downregulated by sda

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11
Q

what unregulated and downregulates transcription of SpoOA

A

it is promoted by sigma H and is repressed by CodY

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12
Q

what is the role of RAP phosphatase

A

it removes Pi from SpoOF-P, preventing the formation of SpoOA-P. this is done at a high concentration of bacterial cells which is detected by the movement of small peptides in and out of cells

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13
Q

what is the role of SpoOE

A

it encodes a phosphatase which dephosphorylates SpoOA-P. this is done at a low, constant rate to prevent accidental build up and premature sporulation

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14
Q

how does the FtsZ ring cause cell division in normal vegetative division

A

it is positioned in the centre of the cell by proteins DivIVA and MincD. it forms a septum to split the cell into two discrete cells

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15
Q

how does the FtsZ ring cause asymmetrical cell division

A

more FtsZ is produced so it coils. this coil splits and forms two rings- one at each pole. one of these forms a septum to divide the cell, assisted by SpoIIE phosphatase

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16
Q

what is the role of sda in asymmetrical cell division

A

it senses whether DNA replication is incomplete. if so, it inhibits phosphorypation of KinA and therefore prevents sporulation

17
Q

what is the role of SirA in asymmetrical cell division

A

is displaces DNAA from the OriC (if located there it will initiate replication). this prevents replication being initiated again within the prespore

18
Q

what promotes transcription of SirA

A

SpoOA-P

19
Q

how do chromosomes enter the presopore

A

they are stretched into a filament due to attraction of SopOJ (bound close to OriC) to DivIVA (located at the poles). only 1/3 is trapped in the prespore at the initial division

20
Q

how is the whole chromosome moved into the prespore

A

DNA translocase SpoIIE forms a two channel pore. the two arms of the chromosome are pumped in simultaneously

21
Q

which sigma factors are active at asymmetrical division

A

sigma E in the mother and sigma F in the prespore

22
Q

which sigma factors are active at engulfment

A

sigma K in the mother and sigma G in the prespore

23
Q

how sis activation of sigma F controlled

A

it is inactive when bound by anti sigma factor SpoIIAB. it is active when bound by anti anti sigma factor SpoIIAA

24
Q

when is SpoIIAA active and inactive

A

it is inactivated when phosporylated by SpoIIAB (also a kinase). it is active when dephosphorylated by SpoIIE (located in the Z ring)

25
Q

why is SpoIIAA only active in the prespore, not the mother

A

there is the same exposure to the Z ring but a much smaller volume. the SA to volume ratio is greater

26
Q

why can’t SpoIIAA and SpoIIAB both bind to sigma F

A

steric displacement. they bind to the same region so the binding or one will displace the other

27
Q

how is sigma E synthesised and activated

A

it is synthesis as pro sigma E. the inhibiting protein domain is cleaved by GA protease once it has located in the septum and been activated by the binding of SppoIIR on the presopre side

28
Q

how is sigma G synthesised and activated

A

it is synthesised inactive due to being bound by SpoIIAB. this is cleaved by SpoIIIJ (produced in the mother) which localises in the septum, cleaved SpoIIAB and activates sigma G

29
Q

how is sigma K synthesised and activated

A

to be synthesised the Skin region which divides the gene has to be removed by a SpoIVCA site specific recombinase to produce pro sigma K. this is activated by SpoIVB protease (mediated by sigma G in prespore) cleaving SpoIVFA and BofA protein off pro sigma K, activating it

30
Q

how is the prespore dehydrated

A

low weight proteins eg dipicolonic acid enter the prespore along with Ca2+ which causes water to move out of the cell