formatting the body Flashcards

1
Q

why did edward conkilin use sea squirts (Styella patita) to study developmental patterning

A

because the blastomeres of very early embryos shows a yellow pigment that is easy to follow

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2
Q

what did the yellow pigmented cells of the Styella partita develop into

A

the posterior muscle elements of the tail

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3
Q

how can we track specific cells in development to create fate maps

A

Inject fluorescent dye into a few cells, use a laser to activate v small number of cells (5) so only they are labelled with the dye, then have a fate map

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4
Q

differences between development of human vs mouse embryos

A

Human epiblast turns into a disk whereas mouse develop as a cup

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5
Q

what is the first thing to form in an embryo

A

the posterior to anterior axis with the formation of the primitive streak

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6
Q

what is Hensons node and where does it form

A

aka primitive node - a thickening at the cranial/anterior end of the primitive streak - will be the organiser (in a chick embryo)

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7
Q

what occurs when you transplant pieces of the primitive streak from and early and late embryo donor into another organism eg quail to chick

A

the graft from the early embryo will turn into a more complete structure with a wider combination of donor and recipient cells used (greater ability to induce)
the graft from the later stage embryo will only induce a more specific structure (eg just the trunk) and be mainly made up on donor cells

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8
Q

how would you experimentally induce a human axis in a recipient embryo

A

Take pluripotent human embryo cells, induce with Wnt + activin (organiser fate) and graft into a donor chick embryo

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9
Q

how does the head process form in a chick embryo

A

once hensons node has reached the most anterior part some cells will carry on under the epiblast and form the head process

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10
Q

what determines the A-P streak in the chick

A

via gravity (embryo rotations cause the heaviest elements to go to the bottom to begin the posterior ingression of the primitive streak)

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11
Q

describe the conversion of radial symmetry to bilateral symmetry in chick embryos

A

As the ovum passes through the hen’s reproductive tract, it rotates. This spinning, shifts the yolk such that its lighter components lie beneath one side of the blastoderm.
This imbalance tips up one end of the blastoderm, and that end becomes the posterior marginal zone (PMZ), adjacent to where primitive streak formation begins.

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12
Q

what ultimately determines left right asymmetry in the chick

A

Nodal and PitX (only expressed on the left side

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13
Q

describe the signalling cascade that determine left right symmetry in the chick

A

Shh is expressed from the node
on the left side: Shh activates cerebrus, which activates BMPs, which activates Nodal and PitX
on the right side

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14
Q

describe the signalling cascade that determine left right symmetry in the chick

A

Shh is expressed from the node
on the left side: Shh activates cerebrus, which activates BMPs, which activates Nodal and PitX
on the right side: Shh expressed causing activin expression, inhibiting Fgf8 which inhibits cerebrus so there is no downstream signalling of nodal or pitx

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15
Q

what determines A-P axis formation in the Xenopus

A

site of sperm entry

(cortical roation and definintion of the animal and vegetal pole then organiser formation at the site of entry)

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16
Q

what structures form when you transplant a portion of the dorsal lip from young and advanced gastrulas

A

young dorsal lip = anterior structures

later stage dorsal lip = more trunk peices

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17
Q

what is the next step after axis formation

A

segmentation

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18
Q

what transcription factors confer identity to the segments

A

Hox genes

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19
Q

what is Hox gene collinearity

A

relates the gene order of the Hox cluster in the chromosome (telomeric to centromeric end) with the serial activation of these genes in the ontogenetic units along the Anterior-Posterior embryonic axis

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20
Q

the 3 and 5 prime ends of the hox cluster determine what

A
3' = head
5' = posterior structures
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21
Q

invertebrates how many clusters of Hox genes are there

A

4 or more

mouse 4 chick 7

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22
Q

hox genes have a sharp __________ boundary and a more diffuse ____________

A

sharp anterior boundary and more diffuse posterially

23
Q

what is homeotic transformation

A

Homeotic transformation is a transformation of tissues in which the developmental fate of an tissue is changed to that of another caused by misexpression of developmental/ Hox genes

24
Q

if a hox gene is knocked out what occurs

A

the more anterior hox gene continues its expression

25
what are somites
precursor populations of cells that give rise to important structures associated with the vertebrate body plan and will eventually differentiate into dermis, skeletal muscle, cartilage, tendons, and vertebrae.
26
where are osmite derived from
paraxial mesoderm (presomitic mesoderm)
27
what is somitogenesis
a highly regulated process that determines “what, when, where, and how many” somites an organism makes. Anterior to posterior direction. – blocks of somites in the mesoderm on either side of (flank) the neural tube in the midline - regulated periodic budding of somites
28
where do somites form
on either side of the midline (neural tube)
29
somitogenesis occurs simultaneously with________
the closing of the neural tube
30
the mesoderm is partitioned into four distinct zones, what are they
lateral plate mesoderm, intermediate mesoderm, paraxial mesoderm and chordamesoderm
31
the type of mesoderm is determined by .....
relation to the midline
32
paraxial mesoderm differentiates into head and somite. somite differentiates into what 5 things and what do they develop into
``` sclerotome (cartilage) syndetome (tendons) myotome (skeletal muscles) endotome (endothelial cells and dorsal aorta) dermatome (dermis, skeletal muscles) ```
33
what provides the signals that induce the somite lineage
the surrounding tissues: Signalling from lateral plate, notochord (Shh) and ectoderm (Wnt)
34
what are the somite called when they are formed, forming and not yet formed
S1 formed S0 is being formed S-1 soon to be formed
35
clock genes are components of what three signalling pathways
notch, fgf and wnt
36
how are clock genes expressed
cyclic genes expression in an oscillatory pattern
37
what direction does the wavefront move
anteriorly - moves from the posterior to anterior
38
what direction are somites formed
anterior to posterior
39
what system works in conjunction with the clock genes
a gradient system - the wavefront
40
what opposing gradients control the wavefront/determination front
: retinoic acid in the anterior decreasing towards posterior, FGF and Wnt higher in the posterior moving anterior – where they intersect is where you get the wave front where the somites will form
41
the intersection of what gradients is the location of somite formation
retinoic acid and fgf&Wnt
42
what ways do the clock genes interact
The clock genes oscillate out of phase with the other clock signalling pathways – and also work in conjunction with each other
43
what types of signalling is the notch pathway
juxtacrine signalling - physical contact between the cells is required
44
briefly describe the notch singalling pathway
physical contact between notch receptor on one cell and ligand on another cell causes cleavage that allow the notch intracellular domain to induce expression of the target gene
45
which end of the axis is retinoic acid highest
the anterior
46
which end of the axis is fgf highest
in the posterior
47
describe the process of somite boundary formation
Notch expressed in the presumptive somite activates Mesp2 in this area, downregulated in the caudal part just being expressed in the rostral (lower/posterior) part -> induces ephrin (ephrinA4) leading to epithelialisation (morphological boundary develops)
48
what are the different timescale in somite formation in 4 vertebrates
In zebrafish = every 30 mins In chick = every 90 mins In mouse = every 2.5 hours in human = every 5-6 hours
49
when is the temporal order/identity of the somite determined
before somitogenesis early in development
50
what confers identity of the segments
Hox genes
51
what experimentation showed when somite identity is determined
transplanting presomitic mesoderm and flipping it, still showed the correct ordering of the development of somites take some presomitic mesoderm transplant into a different position and you get the same structure it would originally be
52
what causes segmental defects in humans
when somites arent formed in the synchronous fashion at the right times you get a mismatch of somites and vertebrae - caused by mutations in notch and other related signalling pathways
53
whats structures other than the spine are segmented
skull and brain