Animal Development & Evolution Flashcards
Ur bilateria?
common ancestor of all bilateria
3 main branches of bilateria?
Deuterostomes
proteostomes:
-ecdysozoa
-lophotrochozoa (annelida, mollusca, platyhelminthes)
ur metazoa?
ancestor of all metazoans (Ur bilateri + non bilateria metazoans)
how do differences in animal structures arise in development?
structure develops due to differences in GENE EXPRESSION/TRANSCRIPTION
e.g. 4 cell stage embryo:
one cell behaves differently from others
- INTRACELLULAR SIGNALLING:
contains certain molecule that others dont that will affect cell behaviour (TFs)
(HOX genes etc…) - INTERCELLULAR SIGNALLING
interaction between cells that determine cell differntiation outcome - cell signals neighbour(s)
e.g. like zpa in developing limb patterning digits across A-P axis)
pathways are complex, but just a few of them (Hedgehog, wingless,fgf, bmp)
these pathways work together in different embryonic development stages
(e.g. one cell expresses one TF, causes it to secrete intercellular signal molecule, influences TF expression in other cell)
TF families in metazoa
most TF families found in all metazoans
meaning
1.most signalling systems are very ancient - evolved in common ancestors and retained in all descendents as they diverged away from each other - traces back to original metazoan
- whats giving rise to diversity between different groups of animals is HOW this shared toolkit of systems is being used
control of gene transcription in eukaryotes?
Cis regulatory elements CREs on chromosome upstream of gene
enhancer - will contain elements that regulate that gene
TFs bind recognition sites on enhancer
will have +ve or -ve effect on transcription
(activator vs inhibitor)
transcription unit - DNA length RNA polymerase will run across to give mRNA transcript
receptor on plasma membrane
signal binds it (e.g. Hh)
signalling cascade from receptor kicked off
activates previously inactive TF in the cell
active TF then binds enhancer
has repressive/activation effect
activation effect may be enough to start trasncription of that gene
signal out of cell leads to internal change in expression
sorts of mutation that can change gene activity
mutation in regulatory region
(affects how/when/where gene is expressed)
mutation in coding region
(affects the action of expressed protein)
coding changes effect
in intron - silent - probably no effect
in coding/exon:
may produce change in protein (codon code??)
-then MAY be significant to affect its function (e.g. TF ability to bind site)
-proteins pleiotropic - one changed protein may affect many different pathways
lots of change likely to be deleterious
regulatory changes effect
will only affect how TFs affect the trasncription of THAT specific gene
hypothesised that mutations in regulatory region are more constricted in their effect than coding region changes
argued that this sort of mutation then may be more viable - so more likely to lead to adaptation (no adaptation when deleterious/inviable)
stickleback pelvis example
add to notes
3 spined stickleback has pelvic spines
marine populations of species have full pelvis and spines
some freshwater lake populations have reduced pelvis and pelvic spines
(MAYBE more advantageous die to different conditions and predators)
used linkage mapping to find that difference is in the Pitx gene (encodes a TF)
has 30kb enhancer
3kb coding region
NO DIFFERENCE IN CODING REGION sequence in spined and spineless pops
no difference in TF itself most likely
BUT big differnce in where it is transcribed in embryo
Pitx1 staining showed:
in developing jaw of both populations
in pelvis of spined marine pops
BUT NOT in pelvis of lake fish
DIFFERENCE is in WHERE it is being transcribed in embryo
narrowed down sequence difference to ~500b
enhancer now called PEL
took that PEL enhancer and coupled it to GFP
GFP on in pelvis of marine fish
so in marine fish PEL turns on Pitx1 in pelvis
causes spines to be developed there
took marine PEL and put it next to Pitx1 coding region
put this constricted gene inyo genome of lake fish which normally spineless pelvis
restores spine development in the FW fish
sequenced the chromosome pitx1 is on in many pops of stickleback
found deletion in 500bp region that would be PEL enhancer
all of the different pelvis spine reduced pops had deletions here
proof of strong selection in lake populaiotns too
-reduced heterozygosity
may have driven spine loss whatever advantage that conferred
drosophila male wing spots example
(add to notes)
some drosophila species males have wing spots
some species’ males dont
male wing spots restricted to certain part of dros phylogeny
single point of origin
(individual species in other part in obscura group has a different pattern of wingspot - different origination)
development of spot:
Yellow gene encodes enzyme in melanin synthesis
gain and loss of an enhancer of this determined spot presence (a species in the spot part lost spots -lost this Yellow enhancer
(simpler spot?)
in D. elegans - SPOT enhancer of Yellow
responds to distal-less (activator)
and engrailed (repressor)
distal-less expressed in distal wing region
so Yellow expressed in distal wing part - distal wing spots
in posterior of wing engrailed is expressed - inhibits Yellow
expression of both causes anterior spot on distal part of wing
(d tristis from obscira family’s spot is controlled by different factors doing same thing)
D. guttifera has different (complex) pattern of spots
can use reporter to see where Yellow gene is active
Yellow expression lines up with spots
also lines up with Wingless (TF) expression
different wingspot patterns via Yellow reacting to expression of different TF signalling pathways in different species
differing promoters the reason
evolution of COMPLEX spot patterns in drosophila
(add to notes)
in d. melanogaster - no complex spots - just melanation around veins in wing
no complex expression pattern
no spots
(No VS, no complex wingless expression pattern)
then having complex wingless expression pattern evolved
AND evolution of novel VS enhancer - complex pattern of it evolved
led to development of complex wingspot patterns
evolution of complex wing spots:
-largely due to changes in gene regulation (not coding sequence changes)
-changes to specific regulatory elements in pathways of genes to change their function differently in different regions in development
bithorax mutation in drosophila?
WT
-wing on T2 - T2 legs…
-haltere on T3 - T3 legs…
bithorax:
T2 and T3 segments both look like T2
segment T3 has been transformed into T2
HOX gene family
gene family (homeotic?????)
NON- identical genes that arose from process duplications of another gene within the family
related by sequence (v similar)
all encode TFs
each gene produces slightly different HOX TF
physically close
in drosophila - side by side on chromosome
order of HOX genes on chromosome corresponds to order that they are expressed/pattern the A-P axis
transcription of Ubx and Distal-less in drosophila
turned on 3hrs into development
at 6hr stage of embryo:
Ubx from T3 segment (patchily) then strongly through rest of abdomen (abdomen is legless)
means that whole part of A-P axis is exposed to Ubx TF
early distal-less expression is important for developing structures that will become legs(ventral)/wings(dorsal)
can’t turn on in abdominal segments as Ubx strongly expressed in abdomen (reason why insects have no legs on abdomen)
can turn on in T1/T2 cause no Ubx
(guessing weaker Ubx in T3 allows distal-less to come on a bit - T3 identiy)
