Leaf Development & Evolution- 4 lectures Flashcards
indeterminate meristem function
leaf primordium and SAM in the middle
made up of ‘zones’ and ‘layers’, made up of different cell types
function of the SAM
to produce a stem cell population, and produce derivatives which give rise to organs
reduced meristem phenotype
wuschel
enlarged meristem phenotype
clavata 1,2,3- more cells in the central zone
WUS and CLV interactions
wus ptomotes clv expression
clv inhibits wus - feedback loop which maintains an appropriately sized SAM
chimera
mutation in a plant which leads to 2 different cell types- can use these to look at how different cell types organise themselves
how can you do lineage analysis by manipulating the SAM?
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
KNOX genes
knotted1-like homeobox genes, involved in the switch from indeterminate to determinate development
KNOX mutants:
-have no SAM (loss)
-have extra cell divisions (gain)
KNOX expression
on in the meristem, off in the primordium
what turns KNOX genes off where it isn’t needed?
rs2- shows a similar mutant phenotype to KNOX gain of function, and possibly mutually exclusive domains- suggests inhibition
ARP genes also
when did leaves develop first?
around the devonian
KNOX evolutionary consevation
seems to be similar expression in KNOX in lycophyte and eudicot models- but no direct orthology
experiment which looked at KNOX evolutionary conservation
cross-species complementation experiment between a lycophyte and a eudicot- seems like it can rescue, so probably does have the same function
4 phyllotactic patterns
alternate- 180
opposite- pairs at 90
whorled- multiple leaves at the same point on the stem
spiral- 137.5
phytomer
repeated unit along the stem
how does patterning work at the meristem?
the stem cells are at specific points, and cause the merustem to bifurcate
what seems to be responsible for leaf initiation?
PIN1- create directional flow of auxin, which then promotes growth- both required
PIN1 polarity
regulated by microtubule orientation, and creates auxin maxima
leaf axes
proximo-distal (up/down)
medio-lateral (across)
adaxial-abaxial (top and bottom)
features of the ab/adaxial axis
patterns of stomata, arrangement of xylem and phloem, position of organs (one side will be closer to the meristem)
adaxialisation/abaxialisation protein
Phb- adaxialise
Kan- abaxialise (K and B come before P and D)
regulation of ad/ab axis
RNAi- miRNA expressed on the abaxial side to take out Phb
when and how is the SAM established?
heart stage- STM and CUC expression, STM defines SAM and CUC establishes the boundaries of it in a feedback loop where STM restricts CUC
medio-lateral specification- important genes
WOX and NOX
>WOX suppressed NOX, in monocots
WOX expands the leaf blade by promoting auxin biosynthesis
words for equal/unequal growth
isotropic- equal growth in all directions
anisotropic- expansion in a different orientation
what induces ectopic lobing?
KNOX turning off GA, creating lobing
gives you auxin maxima at the tips of the outgrowths
gene expressed in lobe sinuses
CUC2- forms a growth-restricted boundary
KNOX and compound leaves
overexpression seems to lead to overcompounding
hormone responsible for compounding alongside KNOX
cytokinin- overexpression creates compound leaves
3 functions of auxin maxima
precedes leaf initiation, leaflet initiation, lobe initiation
KNOX in simple vs compound leaves
gets turned off in simple leaves after primordium initiation, but turns back on in compound leaves
how can KNOX be repressed at the leaf margins?
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
LFY
alternaitve to KNOX for compound leaf development- also used in flower development, both seem to be able to be used for leaves though
trichome
outgrowths on plants/algae- hairs, scales etc, vary in structure and function
model of trichome expression
GL1, GL3, TTG transcription complex activates GL2 which initiates expression. also activates TRY, which represses GL2 expression in nearby cells, creating a spaced pattern
how is spacing maintained?
lateral inhibition- activator and inhibitor both being activated so you get spacing automatically
trichosome development in roots vs shoots
in shoots- lateral inhibition- in roots, not as random, only cells next to cortex cells are activated
alternative to GL1
WER- derived from an older pathway
what determines vein structure?
the adaxial-abaxial patterning in the primordium
canalisation
causing a flow of auxin into the leaf primordium, increasing flow further down
