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MBB262 > Casson (Developmental genetics) > Flashcards

Casson (Developmental genetics) Flashcards

1
Q

How much complexity must be dev from a single cell?

A
  • ≈10-50 trillion cells of >200 cell types
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2
Q

What diff patterns can form in an organism?

A
  • apical-basal polarity (top and bottom)
  • dorsal-ventral polarity (back and front)
  • bilateral symmetry (2 mirror halves w/ single plane)
  • radial symmetry (division into equal portions from centre)
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3
Q

By what processes does 1 cell generate such complexity?

A
  • cell proliferation –> increase in cellular no. via cell division
  • cell specialisation –> cell differentiates to acquire specific cell fate/role in certain position
  • cell interaction –> cell behaviour coords w/ that of neighbours
  • cell movement –> rearrangement of cells to form structured tissues/organs
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4
Q

In what organisms does cell movement not occur, why and what do they do instead?

A
  • plants
  • cells essentially fixed
  • so achieve dev by regulated division pattern
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5
Q

What would happen if cell divides w/o specification?

A
  • get clones, so never get any differentiation
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6
Q

How can 1 cell give rise to diff daughter cells w/ diff identities through intrinsic asymmetry?

A
  • DIAG*
  • component becomes polarised in mother cell prior to division
  • unequal distribution leads to daughter cells w/ diff fates
  • not always physical asymmetry of division –> can both be same size but contain diff determinants
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7
Q

How can 1 cell give rise to diff daughter cells w/ diff identities through extrinsic asymmetry?

A
  • DIAG*
  • diff fates gen by signalling between cells, from surrounding cells or from precursor cell
  • signalling only acts upon 1 cell
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8
Q

When does asymmetric division occur?

A
  • often at v beginning of embryo dev, when fertilised egg divides to give daughters w/ diff fates
  • in assoc w/ stem cells (in animals and plants), where division regens daughter w/ stem cell activity and 2nd daughter w/ new fate
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9
Q

How does extrinsic asymmetry cause diff fates to occur?

A
  • lateral inhibition
  • DIAG*
  • 2 cells both inherit determinant x after cell division
  • x acts on neighbouring cell to inhibit prod of x
  • transient bias creates slight symmetry –> stochastic
  • +ve feedback amplifies diff
  • bistability –> all or none alt outcomes, gen opposite but relatively stable states
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10
Q

How can short range cell-to-cell signalling quickly gen increased complexity w/in a dev tissue?

A
  • DIAG*
  • B signals to A, resulting in new cell type C being specified
  • C signals to A and B, to gen D and E, respectively
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11
Q

Do cell autonomous decisions occur too, and when?

A
  • yes
  • examples where cells in culture undergo specific no. divisions before differentiating
  • but much harder to prove in an in vivo cellular env
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12
Q

What is a morphogen?

A
  • signalling molecule that acts directly on cells to prod specific cellular responses, dep on its local conc
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13
Q

What type of molecules can morphogens be?

A
  • TFs
  • hormones
  • signalling molecules
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14
Q

How do morphogens gradients work?

A
  • morphogen prod in 1 region and diffuse from source creating grad
  • responses w/in grad occur at threshold levels
  • so cells acquire diff fates dep where lie in conc grad
  • DIAG*
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15
Q

How can morphogen grad be represented as a circle?

A
  • DIAG*
  • greatest conc at centre
  • decreases as diffuses outwards
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16
Q

How can morphogen activity be key to output, instead of conc?

A
  • DIAG*
  • morphogen uniformly distributed
  • inhibitor has conc grad
  • inhibitor interacts and -vely regulates morphogen activityU, resulting in opp grad of morphogen activity
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17
Q

Using an inhibitor to control morphogen activity is more complex than a conc gradient, so why bother?

A
  • sometimes may wish to limit activity of morphogen and this allows more control than just relying on morphogen distribution
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18
Q

If morphogen is a TF, what would we expect expression pattern to look like for a gene w/ high or low affinity, across a changing morphogen conc?

A
  • high = activated fairly evenly across whole domain , as sites bound even at low concs of morphogen
  • low = when morphogen conc decreases, expression quickly turned off
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19
Q

What functional classes of genes is early Drosophila dev dep on?

A

Axis formation:
- egg-polarity genes

Segment identity:

  • gap genes
  • pair-rule genes
  • segment polarity genes
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20
Q

Why couldn’t segment identity gene expression in Drosophila be reg by other zygotic factors?

A
  • 1st turned on when zygotic transcrip initiates

- must be factors already present in zygote to direct their expression

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21
Q

How did Nusslein-Volhard carry out a mutant screen which resulted in identification of several maternal effect genes?

A
  • looked for mutant phenotypes in progeny of females from a homozygous mutant pop
  • as females defective in maternal effect gene dont show mutant phenotype, as from egg form heterozygous female, but offspring do
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22
Q

What general effect do mutations in maternal effect genes have on Drosophila dev?

A
  • large scale deletions of body plan
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23
Q

What is the structure of a WT Drosophila embryo?

A
  • DIAG*

- acron, head, thorax, abdomen, telson

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24
Q

What are the diff phenotypes of Drosophila w/ mutations in maternal effect genes?

A
  • bicoid –> deletions in anterior region (head and thorax)
  • nanos –> deletions in posterior region (abdomen)
  • torso mutant –> terminal deletions
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25
Q

When axis polarity determined in Drosophila oocyte?

A
  • not yet determined in unfertilised oocyte in egg chamber, assoc w/ Nurse cells and follicle cells
  • determined just prior to fertilisation
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26
Q

How is axis polarity determined in Drosophila oocyte?

A
  • bicoid mRNA at anterior pole and nanos mRNA at posterior pole of oocyte
  • this positioning dep on formation of microtubule network, req for targeting of bicoid and nanos mRNAs to their respective poles (this is unfertilised egg so all factors have origin in maternal tissue
  • gurken also assoc w/ oocyte nucleus and precedes bicoid/nanos –> essential for establishing dorsal-ventral and anterior-posterior patterns
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27
Q

How was it shown that bicoid determines head structure dev, and what did this prove?

A
  • bicoid mRNA cloned and in vitro transcribed, before injecting into various regions of bicoid mutants or WT embryos
  • wherever injected, head prod, then thorax
  • proving bicoid bicoid is anterior determinant and confers head identity to regions where most conc
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28
Q

How do conc of bicoid, nanos, hunchback and caudal change between mRNA and translation to protein?

A
  • DIAG*
  • hunchback and caudal mRNAs distributed evenly throughout early embryo
  • in proteins they have similar distributions to bicoid and nanos
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29
Q

How do bicoid and nanos affect protein concs of caudal and hunchback?

A
  • bicoid represses translation of caudal –> by binding to 3’ UTR of caudal transcript
  • nanos represses translation of hunchback –> by decreasing length of polyA tail of hunchback mRNA
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30
Q

How does nanos differ from bicoid, hunchback and caudal?

A
  • all TFs capable of activating/repressing gene expression

- except nanos, which is RNA binding protein

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31
Q

What does bicoids role as a regulator inc?

A
  • binds bicoid recognition element (3’ UTR) and recruits cap protein
  • this cap binding protein diff to 1 req for normal translation (so can’t recruit ribosome)
  • reg hunchback
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32
Q

In what way is bicoid an unusual regulator?

A
  • v rare eg. of TF that can bind DNA and RNA using same domain
  • mutation of Arg54 (determines RNA binding) sufficient to abolish translational inhibition of caudal, but no bicoids transcriptional activity
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33
Q

Why is hunchback classified as a maternal effect gene and a GAP gene?

A
  • 1st present as maternal transcript

- but due to reg by bicoid, alos get zygotic expression

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34
Q

What is a syncytium?

A
  • multinucleate structure w/o cellular boundaries

- env that morphogen grads working in

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35
Q

How does early embryo dev from a syncytium to cellular blastoderm stage?

A
  • rapid nuclear divisions

- nuclei migrate to periphery, where cellular boundaries form

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36
Q

How are Drosophila segmented?

A
  • 16/17 physical segments
  • parasegments relate to gene expression domains and don’t perfectly align w physical segments –> but often match regions actually deleted in mutants
  • GAP genes define broad regions of embryo (mutants have large scale deletion similar to bicoid/nanos)
  • pair rule genes define alt segments, so mutants lack every other segment
  • segment polarity gene mutants show defects in every segment –> may appear as deletions, duplications or polarity reversals
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37
Q

What level of affinity for bicoid do the sites found in hunchback have?

A
  • in hunchback, 3 high affinity sites

- others don’t match bicoid consensus binding site as well so bound lower affinity

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38
Q

What is the effect having diff affinity binding sites for bicoid?

A
  • reporter genes under control of high affinity sites have expression widely across anterior domain
  • those w/ low affinity only in much smaller anterior domain
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39
Q

What is the signif of having high and low affinity bicoid sites, as demonstrated by Gao and Finkelstein?

A
  • orthodenticle (GAP gene) has 3 low affinity bicoid binding sites and is expressed in tight anterior domain (much smaller than that of hunchback
  • demonstrating how bicoid conc grad can be decoded to give diff expression patterns
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40
Q

Why is hunchback also expressed at posterior?

A
  • due to transcrip activation by GAP gene tailess
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41
Q

How is GAP gene expression defined by a dynamic regulatory network?

A
  • bicoid central as initiates network
  • genes can have binding sites for various TFs w/in promoters –> having both +ve and -ve regulatory effects
  • restricted expression domains crucial for correct patterning
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42
Q

When is segmentation initiated by pair rule genes?

A
  • begins after syncytium undergone 13 nuclear division cycles and cells begin to form at periphery of embryo
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43
Q

How do pair rule genes initiate segmentation?

A
  • expression pattern initially fuzzy, but becomes distinct v rapidly (strips across embryo)
  • 1° pair rule genes build striped expression pattern de novo
  • 1° reg 2° pair rule genes to define their boundaries
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44
Q

What are the 3 1° pair rule genes?

A
  • hairy
  • even-skipped (eve)
  • runt
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45
Q

What is the structure and function of the eve pair rule gene?

A
  • large, approx 20kb
  • regulatory regions extend up and downstream of coding seq, and composed of distinct modules
  • each module determines expression in specific stripe and contains binding sites for maternal effect and GAP proteins –> allowing enhancers to dictate eve expression in each diff stripe
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46
Q

How was it demonstrated indiv enhancer module determines stripe specific expression for eve?

A
  • cloning module in front of reporter gene, eg. LacZ
  • can then visualise expression domain by histochemical staining w/ X-Gal
  • eg. stripe 2 enhancer cloned in front of LacZ, giving expression of this receptor in single domain, as opposed to 7 stripes dictated by full regulatory region
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47
Q

How does eve control expression of ftz (a 2° pair rule gene)?

A
  • before cell cycle 13, ftz expressed broadly though embryo
  • eve expressed at same time and acts as repressor
  • wherever eve expressed, ftz isn’t
  • so expressed in alt segments to each other
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48
Q

What is counted as basic segmentation?

A
  • everything up to and inc pair rule genes (not segment polarity genes)
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49
Q

Are bicoid homologs found in other species?

A
  • only in close relatives
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50
Q

Are segment polarity gene homologs found in other species?

A
  • yes, their discovery had major impact on dev bio, esp in higher euks
51
Q

When does the change to cell-to-cell signalling occur, and what can now be determined?

A
  • cellular blastoderm stage, free nuclei now enclosed w/in cells
  • cell fate determination begins
52
Q

How were segment polarity genes identified?

A
  • mutational studies
53
Q

What is WT for hair in Drosophila, and how do mutants differ?

A
  • variety of hair types across segment
  • -> 1° = denticles (in overlapping paraseg)
  • -> 2° = smooth
  • -> 3° = small, thick hairs
  • -> 4° = fine hairs
  • mutants lack differentiation and have single cell type
54
Q

How does expression pattern of segment polarity genes compare to pair rule genes?

A
  • much narrower expression domains –> single rows of cells in ring around embryo
55
Q

What are the expression patterns of engrailed, hedgehog and wingless segment polarity genes?

A
  • engrailed expressed immediately posterior to wingless

- hedgehog expressed in same cells as engrailed

56
Q

How is tight gene expression pattern achieved in segment polarity genes?

A
  • hierarchical system
57
Q

How is expression of segment polarity genes controlled by pair rule genes?

A
  • engrailed reg by pair rule genes
  • -> indirectly activated by eve and directly activated by ftz
  • -> so always expressed in last cell rows of a segment
  • -> active in posterior cells and activates hedgehog
  • wingless repressed by eve and ftz, and req hedgehog for its expression
58
Q

Why is it important that wingless and hedgehog are secreted factors, and what does this result in?

A
  • can diffuse to nearby cells and form conc grads from cells where transcribed and translated
  • hedgehog binds to receptors on neighbouring cells and activates signalling pathway to activate wingless
  • hedgehog –> wingless
    wingless –> hedgehog/engrailed
  • this is +ve reinforcement and stabilises expression boundaries
59
Q

What is the role of homeotic genes?

A
  • reg structures that dev on each segment of adult fly
60
Q

What do mutations in homeotic genes cause?

A
  • don’t get deletion

- get conversion of segment to a diff identity

61
Q

What was the 1st homeotic mutant isolated

A
  • ultrabithorax

- T3 had identity of T2, so dev 2 pairs of wings

62
Q

What is the phenotype of an antennapedia mutant?

A
  • legs instead of antenna
63
Q

What did the isolation of a no. of homeotic mutants suggest?

A
  • that initially insects w/ multiple legs/wings and dev leg/wing suppressing genes to achieve body plan now observed in Drosophila
64
Q

How are homeotic genes organised in Drosophila?

A
  • all 8 on chromosome 3
  • organised into 2 groups = antennapedia complex and bithorax complex
  • seq corresponds to order expressed in along body axis
65
Q

What enables diff homeotic genes to be expressed in specific domains?

A
  • reg by gap and pair-rule genes, so determine where each homeotic gene is initially expressed
66
Q

How is activation of homeotic genes achieved by gap and pair-rule genes?

A
  • promoters have high and low affinity binding sites for activating TF
  • differing combo of these binding sites can determine where gene expressed in grad
67
Q

Using an example, how do interactions between homeotic genes can provide an additional level of control?

A
  • antennapedia gene expression repressed by genes of bithorax complex (= homeotic genes posterior to it in genome arrangement and expression
  • prevents expression expanding into T3 and further into abdomen
  • so expression of Antp confined to T2
68
Q

How can the phenotype of ultrabithorax mutants be explained?

A
  • by interactions between homeotic genes

- deletions of Ubx result in Antp expression domain extending towards posterior end of fly, as no longer repression

69
Q

What is epistasis?

A
  • alleles of 1 gene masking or cancelling effects of a 2nd gene
70
Q

What is the epistatic relationship in homeotic genes, and what does this mean mutations cause?

A
  • homeotic genes are epistatic to their anterior neighbours

- so losing function of gene results in gene anterior to it being expressed in that domain

71
Q

What did a series of experiments show, which placed wither Antp or Ubx genes under control of heat shock promoter?

A
  • Antp specifies PS4 identity and Ubx specifies PS6 identity
  • so when early embroys heat shocked it resulted in their expression throughout embryo
  • for Antp all PSs anterior to PS4 took on PS4 identity and all posterior remained WT
  • similarly, for Ubx all PSs anterior to PS6 took on PS6 identity and all posterior remained WT
  • shows posterior dominant and stops expansions
72
Q

How is the phenotype of the antennapedia mutant not what we woudl expect, and why is this?

A
  • if Antp defective would expect Scr to be expressed in Antp domain
  • not the case, as mutant has all correct organisation, except legs instead of antenna
  • mutant phenotype is caused by dominant mutation, causing Antp to be expressed ectopically in head region
73
Q

What did Struhl’s experiments into antennapedia mutants show?

A
  • mutagenised this dominant antennapedia mutant and looked for revertants –> to isolate recessive allele of Antp gene
  • these adult recessive antp mutants had antenna instead of leg on T2
  • due to Antp having important function in repressing Homothorax and Extradenticle genes that are req for antenna dev (represses these genes in leg segments)
  • appears leg dev is default pathway, as Antp not specifically a ‘leg determinant’ –> it blocks certain head fates in thoracic region, leading to acquisition of default leg state
74
Q

What are common features of all Drosophila homeotic genes?

A
  • all TFs containing a homeodomain
  • have 60 AA DNA binding domain (and occasionally RNA too, eg. bicoid)
  • so reg structures by regulating genes that specify tissue/organ primordia
75
Q

Are all homeodomain genes homeotic genes?

A
  • no, eg. bicoid and caudal

- and not all homeotic genes contain a homeodomain

76
Q

In what way is embryonic gene expression transient?

A
  • genes show spatial and temporal control –> not expressed throughout lifetime, only in specific place and time
  • eg. some expressed from early embryogenesis to late embryo dev, some expressed early then either gradually reduced in expression or rapidly switched off
77
Q

What kind of control do gap and pair rule genes show, that is similar to homeotic genes?

A
  • spatial and temporal control
78
Q

What is the phenotype of an extra sec combs (Esc) mutant?

A
  • all segments transformed into abdominal segments
79
Q

What was observed in an experiment probing giant salivary gland chromosome w/ antibody to Polycomb (Pc)?

A
  • saw Polycomb protein bound to various genome regions, inc antennapedia complex and bithorax complex
80
Q

How is pattern prod in homeotic genes locked in after gap and pair-rule genes switched off?

A
  • chromatin regulation

- through Polycomb genes and trithorax genes

81
Q

How do Polycomb genes help lock in the pattern through chromatin regulation?

A
  • Pc and Esc are components of 2 multimeric complexes called PRC1 and PRC2 (polycomb repressive complexes)
  • Pc part of PRC1 and Esc part of PRC2
  • PRC1/2 target polycomb responsive elements (PREs) in reg region of Pc target genes
  • PRC1/2 can’t bind DNA themselves and are guided into PRE by other DNA binding factors
  • once there, complexes methylate histones flanking PRE, condensing chromatin, making it inaccessible to transcriptional machinery
  • this silencing maintained stably in adults and correct pattern of homeotic expression domains maintained
82
Q

How do trithorax genes help lock in the pattern through chromatin regulation?

A
  • for genes that need to stay switched on
  • maintain gene activity and antagonise polycomb genes
  • so also maintain correct homeotic expression domains
83
Q

What is the hedgehog signalling pathway?

A

HH (ligand) —-I Patched (receptor) —-I Smoothened (signal transducer) —-> Ci (gene regulator) —-> transcrip of gene targets (Wg)

84
Q

What is the role of Ci (cubitus interruptus), ie. when does activate transcrip and when does it repress it?

A
  • in HH absence, tethered to microtubules, where phosphorylated by kinases, resulting in its cleavage, part of cleaved protein translocates into nucleus and acts as transcrip repressor
  • when HH present, smoothened inhibits kinases that phosphorylate Ci, so full length Ci protein moves into nucleus, acts as transcrip activator
85
Q

What hedgehog equivalents are found in vertebrates and what roles do they have in dev?

A
  • sonic hedgehog = limb dev, neural differentiation, facial morphogenesis
  • desert hedgehog = spermatogenesis
  • indian hedgehog = bone growth
86
Q

How did studies into chick limb dev point towards sonic hedgehog (shh) being a morphogen?

A
  • shh expression found at posterior region of bud
  • if surgically remove shh expressing region from 1 bud and transplant it to anterior pole of another, whilst leaving posterior pole intact, get mirror image duplication of digit pattern in wing
  • suggest shh is morphogen and its conc along grad affects decisions –> highest conc assoc w. digit 4 fate etc.
87
Q

How does shh play a role in mouse limb formation?

A
  • polydactyl w/ no digit identity is default
  • digit no. and identity determined by shh grad –> results in changes in ratio of GLi3 forms between active and repressive (Gli3R)
  • another eg. of epistasis, as gli3 mutant masks phenotype of shh/gli3 mutant, indicating Gli3 activity req for shh action
88
Q

Where was it seen shh was expressed by looking at chick embryos, and what is its role?

A
  • gut, limb buds, spinal cord and dev brain
  • important role in ventral induction (2nd stage of brain dev, when most structures formed, eg. cerebrum, which is sep into 2 hemispheres
89
Q

What is the result of loss of shh on brain dev?

A
  • leads to ventral induction defects and forebrain can fail to divide
  • shh expressed at ventral centre, so structures derived from here can be absent
  • mild to severe holoprosencephaly
  • forebrain dev linked to aspects of facial dev, so loss of Shh at certain point in dev can lead to undivided eye field = cyclopia
90
Q

In what species is cyclopia often seen, and why is this?

A
  • lambs and other grazers of genus Veratrum
  • plant prod cyclopamine
  • inhibits smoothened by binding directly to it, so prevents activation of pathway, even in HH presence
91
Q

What can happen when HH signalling pathway is constitutively activated?

A
  • patched is tumour suppressor gene and assoc w/ Gorlin syndrome (basal cell carcinomas)
  • believed BCC origins are undifferentiated epithelial cells in hair follicle
  • so mutations in patched may lead to constitutive activation of Gli targets
92
Q

What are the Gli family in humans orthologs of in Drosophila?

A
  • Ci
93
Q

How is Gorlin Syndrome inherited and how is it treated?

A
  • autosomal dominant, so single copy of defective patched gene increases risk of dev symptoms
  • 1 treatment is cyclopamine or an analog of it, as inhibits pathway
94
Q

What is the wingless signalling pathway?

A

Wg (Wnt) —-> Frizzled —-> Dishevelled —-I Axin, APC, GSK3, CK1 —-I Armadillo (β-caterin) –> Wg (Wnt) targets

95
Q

What mutation of wingless signalling pathway causes constitutive activation?

A
  • KOs of Axin/APC/GSK3/CK1
96
Q

What is the phenotype of colorectal cancer, and how is this caused by mutation of APC?

A
  • colon covered in 100s of tiny projecting polyps, w/ high prob of 1 progressing to become malignant
  • this phenotype caused by mutation/deletion of APC gene, hereditary syndrome in humans
  • not all colorectal cancer is hereditary and can be caused by spontaneous mutation of APC gene
97
Q

How was blocking of wingless signalling pathway shown by looking at urogenital dev in mice?

A
  • Wnt4 expressed in dev kidneys and gonads

- when KO, kidneys fail to dev and ovaries start to synthesise testosterone, so take on male characteristics

98
Q

Together, what are the antennapedia and bithorax complexes known as?

A
  • HOM-C complex
99
Q

How does HOM-C equivalent in mouse and humans differ, and how is it similar?

A
  • 4 copies of Hox complex
  • organisation achieved by various dups and deletions
  • generally genes are HOM-C homologs and order matches that in Drosophila
  • also show anterior-posterior expression
100
Q

Why is it harder to solve whether Hox expression domains correlate w/ vertebrae in vertebrates than in Drosophila?

A
  • easy in Drosophila as each homeotic gene is unique
  • harder in vertebrates as often multiple homologs in diff Hox clusters
  • -> problem of redundancy
  • -> if KO single Hox gene, other family members can counter loss, so unlikely to prod phenotype
101
Q

So how was the question of whether Hox expression domains correlate w/ vertebrae solved for vertebrates, and how were these results explained?

A
  • gen KO mice in single genes and crossed them to gen triple KO mice by homologous recomb (in hox10 and hox11 families)
  • triple hox10 KOs = lumbar vertebrae replaced by thoracic vertebrae (hox9 replaced hox10)
  • triple hox11 KOs = sacral vertebrae replaced by lumbar vertebrae
  • in Hox genes posterior genes repress activity of anterior genes (like Drosophila)
  • so if KO all hox10 family members, expression domain of hox9 family expand in posterior direction
102
Q

How is Polycomb function in humans similar to Drosophila?

A
  • BM11 —-I CDKN2A —-I cell cylce
  • BM11 is human homolog of Psc, it is an oncogene overexpressed in B cell lymphoma, gen unreg cell growth
  • CDKN2A is a cell cycle regulator that inhibits G1 progression
103
Q

How has studying Drosophila been important for humans?

A
  • have dev whole fields of dev and disease bio as result of 1st studies
  • many genes identified as having sig roles in Drosophila dev have homologs w/ similar function in vertebrates, inc humans
  • can use info gained form Drosophila to predict functions of these genes in vertebrates, eg. homeotic genes and vertebrate specification
104
Q

What can be seen in a dev plant by the time it reaches the heart stage?

A
  • apical-basal polarity
  • bilateral symmetry
  • shoot and root meristems defined and organised
105
Q

What is the importance of shoot and root meristems?

A
  • stem cells of plants

- whole plant kingdom derived from them

106
Q

How do plants gen a pattern when they have rigid cell walls and no cell movement?

A
  • determined by cell division plane, proliferation and cell expansion
107
Q

How is plant form dep on cell division plane and cell expansion?

A
  • cell divisions that define epidermis occur v quickly

- cells surrounding root meristem and 1 cell embryo show asymmetric divisions

108
Q

Why does the 1 cell embryo in plant formation appear to consist of 2 cells?

A
  • only upper cell goes on to form embryo

- basal cell forms suspensor –> connects embryo to maternal tissue in ovule

109
Q

What is the structure of an Arabidopsis flower, ie. diff whorls?

A
  • several organs arranged in concentric whorls
  • whorl 1 = 4 sepals (OUTERMOST)
  • whorl 2 = 4 petals
  • whorl 3 = 6 stamens (consist of anthers and filament - male part)
  • whorl 4 (female part) (INNERMOST)
110
Q

What floral mutants were identified from large scale mutagenesis screens performed in Arabidopsis, and what did they have in common?

A
  • apetala1 = only carpels and stamen
  • pistillata = only sepals and carpels
  • agamous = only sepals and petals
  • only 2 organs remain and have been replaced in their relative position by 2 remaining organs
111
Q

In the 3 floral identity mutants what conversions had taken place and how was this represented to inform a model?

A 
- apetala1:
sepal --> carpel 
petals --> stamen
- pistillata: 
petals --> sepals 
stamen --> carpels
- agamous:
stamen --> petals 
carpel --> sepals
*DIAG*
- appeared there are 3 domains of fate specification
- domains show regions of gene activity --> NOT morphogen activity
112
Q

In the ABC model what are the diff domains responsible for and what genes have been identified in each?

A
  • A = sepals and petals –> apetala1, apetala2
  • B = petals and stamen –> apetala3, pistillata
  • C = stamen and carpels –> agamous
113
Q

What gene function(s) define dev of each flower structure in the ABC model?

A
  • A function defines sepals
  • AB function defines petals
  • BC function defines stamen
  • C function defines carpels
114
Q

How was the ABC model been refined?

A
  • no sometimes referred to as ABCE model
115
Q

How do A and C gene function affect each other?

A
  • antagonise each other and restrict their respective expression domains
116
Q

How can the phenotype of a mutant lacking A function be explained?

A
  • w/o antagonistic interactions expression of C spreads across all 4 whorls
  • B function remains static
  • so outer whorl defined by C (=carpel), next 2 whorls defined by BC (=stamen instead of petals and stamen) and final whorl retains C identity (still carpel)
117
Q

How can the phenotype of a mutant lacking B function be explained?

A
  • antagonism between A and C remains
  • no petals (AB function) or stamen (BC function)
  • so outer 2 whorls defined by A function (sepals) and inner 2 defined by C function (carpels)
118
Q

How can the phenotype of a mutant lacking C function be explained?

A
  • w/o antagonism A spreads across all 4 whorls
  • B function remains static
  • so get outer whorl of sepals (A), 2 whorls of petals (AB) and central whorl of sepals (A)
119
Q

Floral homeotic genes are not homeodomain TFs, what are they instead?

A
  • MADS domain TFs
  • MADS domain approx 50-60 AAs –> allows these proteins to bind DNA of target genes, resulting in activation or repression of target
120
Q

To what extent is the ABC model applicable to other species?

A
  • A/B/C homologs identified in many other flowering plants and ABC model applies to many of them
121
Q

How does Antirrhinum demonstrate the ABC model?

A
  • mutation of B gene leads to petals –> sepals and stamen –> carpels (like apetala3 in Arabidopsis)
  • plena gene is homolog of agamous, so shows loss of stamens and carpels when KO (as it is a C function gene)
122
Q

What is a poss explanation for floral identity in roses?

A
  • no C function

- as sepals and many petals present

123
Q

Why are other organs not converted to floral identity when A/B/C over-expressed outside the flower?

A
  • ABC MADS domain proteins interact w/ another set of MADS domain proteins called sepallata proteins
  • sepallata genes restricted to floral tissue, so if overexpress eg. agamous in leaves, has no sepallata proteins to bind, so cannot activate carpel dev genes

MBB262 (7 decks)

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