Leaf Development & Evolution- 4 lectures Flashcards

1
Q

indeterminate meristem function

A

leaf primordium and SAM in the middle

made up of ‘zones’ and ‘layers’, made up of different cell types

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2
Q

function of the SAM

A

to produce a stem cell population, and produce derivatives which give rise to organs

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3
Q

reduced meristem phenotype

A

wuschel

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4
Q

enlarged meristem phenotype

A

clavata 1,2,3- more cells in the central zone

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5
Q

WUS and CLV interactions

A

wus ptomotes clv expression

clv inhibits wus - feedback loop which maintains an appropriately sized SAM

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6
Q

chimera

A

mutation in a plant which leads to 2 different cell types- can use these to look at how different cell types organise themselves

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7
Q

how can you do lineage analysis by manipulating the SAM?

A

irradiate different bits, and look at what doesn’t develop- e.g. as a proportion of the leaf, can go back to how many cells are likely to have been present at that point

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8
Q

KNOX genes

A

knotted1-like homeobox genes, involved in the switch from indeterminate to determinate development

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9
Q

KNOX mutants:

A

-have no SAM (loss)
-have extra cell divisions (gain)

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10
Q

KNOX expression

A

on in the meristem, off in the primordium

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11
Q

what turns KNOX genes off where it isn’t needed?

A

rs2- shows a similar mutant phenotype to KNOX gain of function, and possibly mutually exclusive domains- suggests inhibition

ARP genes also

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12
Q

when did leaves develop first?

A

around the devonian

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13
Q

KNOX evolutionary consevation

A

seems to be similar expression in KNOX in lycophyte and eudicot models- but no direct orthology

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14
Q

experiment which looked at KNOX evolutionary conservation

A

cross-species complementation experiment between a lycophyte and a eudicot- seems like it can rescue, so probably does have the same function

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15
Q

4 phyllotactic patterns

A

alternate- 180
opposite- pairs at 90
whorled- multiple leaves at the same point on the stem
spiral- 137.5

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16
Q

phytomer

A

repeated unit along the stem

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17
Q

how does patterning work at the meristem?

A

the stem cells are at specific points, and cause the merustem to bifurcate

18
Q

what seems to be responsible for leaf initiation?

A

PIN1- create directional flow of auxin, which then promotes growth- both required

19
Q

PIN1 polarity

A

regulated by microtubule orientation, and creates auxin maxima

20
Q

leaf axes

A

proximo-distal (up/down)
medio-lateral (across)
adaxial-abaxial (top and bottom)

21
Q

features of the ab/adaxial axis

A

patterns of stomata, arrangement of xylem and phloem, position of organs (one side will be closer to the meristem)

22
Q

adaxialisation/abaxialisation protein

A

Phb- adaxialise
Kan- abaxialise (K and B come before P and D)

23
Q

regulation of ad/ab axis

A

RNAi- miRNA expressed on the abaxial side to take out Phb

24
Q

when and how is the SAM established?

A

heart stage- STM and CUC expression, STM defines SAM and CUC establishes the boundaries of it in a feedback loop where STM restricts CUC

25
Q

medio-lateral specification- important genes

A

WOX and NOX
>WOX suppressed NOX, in monocots

WOX expands the leaf blade by promoting auxin biosynthesis

26
Q

words for equal/unequal growth

A

isotropic- equal growth in all directions
anisotropic- expansion in a different orientation

27
Q

what induces ectopic lobing?

A

KNOX turning off GA, creating lobing
gives you auxin maxima at the tips of the outgrowths

28
Q

gene expressed in lobe sinuses

A

CUC2- forms a growth-restricted boundary

29
Q

KNOX and compound leaves

A

overexpression seems to lead to overcompounding

30
Q

hormone responsible for compounding alongside KNOX

A

cytokinin- overexpression creates compound leaves

31
Q

3 functions of auxin maxima

A

precedes leaf initiation, leaflet initiation, lobe initiation

32
Q

KNOX in simple vs compound leaves

A

gets turned off in simple leaves after primordium initiation, but turns back on in compound leaves

33
Q

how can KNOX be repressed at the leaf margins?

A

LMI1 TF- repressed KNOX at leaf margins
RCO- a LMI1 duplicate which is only present in compound leaves- mutants seem to have less compound-ness, but not none

> changes in which proteins are required in different plants

34
Q

LFY

A

alternaitve to KNOX for compound leaf development- also used in flower development, both seem to be able to be used for leaves though

35
Q

trichome

A

outgrowths on plants/algae- hairs, scales etc, vary in structure and function

36
Q

model of trichome expression

A

GL1, GL3, TTG transcription complex activates GL2 which initiates expression. also activates TRY, which represses GL2 expression in nearby cells, creating a spaced pattern

37
Q

how is spacing maintained?

A

lateral inhibition- activator and inhibitor both being activated so you get spacing automatically

38
Q

trichosome development in roots vs shoots

A

in shoots- lateral inhibition- in roots, not as random, only cells next to cortex cells are activated

39
Q

alternative to GL1

A

WER- derived from an older pathway

40
Q

what determines vein structure?

A

the adaxial-abaxial patterning in the primordium

41
Q

canalisation

A

causing a flow of auxin into the leaf primordium, increasing flow further down