BIOL 461 Lecture Notes - Lecture 23: Homeobox, Primordium, Sepal
29 Apr 2018
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BIOL 461 – Lecture 23 – week 13 Wednesday 11/04/2018
- ABC model and how these regulatory genes can
establish the identity of the 4 different whorls in the
developing flower
- Their expression pattern that determines the whorls
- Code include these homeotic genes – gees ho’s
expression determines the identity of the cells in the
whorl, and the establishment of these 3 fields of the
expression of these homeotic genes, is what
establishes the differentiation of the whorls into the
flower parts
- Whorls can be transformed from one to the other
- Can make very messed up double mutants, that can
then confirm the model
The genes were cloned
- Mechanism/Expression turns out to be
analogous of homeotic genes
- In the whorl, the flower primordium as
its developing you start to get the
expression of these genes in their different
fields (second row, last 3) which gives that
pattern of ABC fields – when you look at
the mutant their function is required there
- Code for identity is due to localized
expression of these MADS bo gees kid of hoeoo gees ut the do’t hae a
homeobox) (MADS box binding motif)
MADS box transcription factors bind DNA. Promoters, regulate
target genes
- Each of these genes encodes a TF that can activate
downstream genes to express the proper combination of
genes to make the sepal, petal, carple, stamen
- Depending on the combination of MADs box genes that
you get, get a different TF complex that forms at each of
the different whorls, that activates different target genes,
and the expression of different target genes, those downstream genes that give different
proteins that lead to the differences between the different organs of the flowers
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2
- Also other mutants identified
- Superman – a regulator of the homeotic genes
- Somehow those genes have to be expressed properly there,
to establish the pattern
- A WT flower, and below is a superman mutant (got all male
parts)
- Superman limits the expression of P1 and AP3 to the second
field – prevents the expression of those genes from
extending over into the end of the C field
- In the mutant this field gets bigger, and PI and AP3 are now
expressed further out covering the whole region of the C
field
- Does’t hage the ode, the idetit gees – ou’re
changing a gene that is required for limiting their expression
- Superman is limiting the expression, and you can see
this genetically
- If you take an AG mutant that spreads the AP2 field
through fields A and C, then
- Superman spreads the B field !!!
- Changing the identity of the field
- If you have a supermam mutant which lacks the PI and
AP3 all together, it does’t do athig lose the idetit of
the B field altogether) – but because there are no AMDS box
genes functioning there to miss-epress the C field, it’s ot
going to have an effect (no phenotype)
- All of the transformations and then adding superman
are consistent with the very simple thing of just overexpending this expression of the B field into
the C field
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3
Inheritance patterns
- Homologous recombination
- Uniparental or cytoplasmic inheritance
- Look at inheritance patterns instead of phenotypes
- Genetic Recombination:
o Homologous recombination
o Site-specific recombination
o Illegitimate recombination
- Homologous recombination:
o Crossing over
o Gene conversion
o Postmeiotic segregation
- This science of homologous recombination is one type of recombination that is under the
general classification of genetic recombination which involves breaking and joining DNA
- Homologous recombination happens between sequences that are very similar (homologous)
Homologous recombination occurs in meiosis 1
- Homologous chromosomes, after DNA replication, they
pair and when they line up at the metaphase plate, they
undergo breaking and joining the shuffle the genes
between the maternal and paternal chromosomes
- To generate variability in the progeny
Chiasmata
- Chiasmata: everytime a
recombination occurs, youll have these connections between the
chromosomes (a bivalent – 2 chromosomes attached)
- Chiasmata is where the recombination occurs
- Attachment sites are broken at anaphase when theyre pulled
appart
- Chiasmata are important because the tension on the spindle
is the checkpoint that says the chromosomes are lined up and
ready to go
- At the site of exchange, we have a tetrad
- In the S phase is generates a copy of each of the
chromosomes to generate homologous chromosomes
- 2 blue = sister chromatids
- Blue + red = homologous chromosomes
- Breaking and joining happens in G2, after this recombinatino occurs
- Only 2 of these 4 chromosomes are affected by this homologous recombination
- Each of these chromosomes, all 4, have each 2 strands of DNA so in total 8 strands (2 x 2 x 2)
- How does this breaking and joining occur to make the shuffling in homologous recombination?
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