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
Q

what are somites

A

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
Q

where are osmite derived from

A

paraxial mesoderm (presomitic mesoderm)

27
Q

what is somitogenesis

A

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
Q

where do somites form

A

on either side of the midline (neural tube)

29
Q

somitogenesis occurs simultaneously with________

A

the closing of the neural tube

30
Q

the mesoderm is partitioned into four distinct zones, what are they

A

lateral plate mesoderm, intermediate mesoderm, paraxial mesoderm and chordamesoderm

31
Q

the type of mesoderm is determined by …..

A

relation to the midline

32
Q

paraxial mesoderm differentiates into head and somite. somite differentiates into what 5 things and what do they develop into

A
sclerotome (cartilage)
syndetome (tendons)
myotome (skeletal muscles)
endotome (endothelial cells and dorsal aorta)
dermatome (dermis, skeletal muscles)
33
Q

what provides the signals that induce the somite lineage

A

the surrounding tissues: Signalling from lateral plate, notochord (Shh) and ectoderm (Wnt)

34
Q

what are the somite called when they are formed, forming and not yet formed

A

S1 formed
S0 is being formed
S-1 soon to be formed

35
Q

clock genes are components of what three signalling pathways

A

notch, fgf and wnt

36
Q

how are clock genes expressed

A

cyclic genes expression in an oscillatory pattern

37
Q

what direction does the wavefront move

A

anteriorly - moves from the posterior to anterior

38
Q

what direction are somites formed

A

anterior to posterior

39
Q

what system works in conjunction with the clock genes

A

a gradient system - the wavefront

40
Q

what opposing gradients control the wavefront/determination front

A

: 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
Q

the intersection of what gradients is the location of somite formation

A

retinoic acid and fgf&Wnt

42
Q

what ways do the clock genes interact

A

The clock genes oscillate out of phase with the other clock signalling pathways – and also work in conjunction with each other

43
Q

what types of signalling is the notch pathway

A

juxtacrine signalling - physical contact between the cells is required

44
Q

briefly describe the notch singalling pathway

A

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
Q

which end of the axis is retinoic acid highest

A

the anterior

46
Q

which end of the axis is fgf highest

A

in the posterior

47
Q

describe the process of somite boundary formation

A

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
Q

what are the different timescale in somite formation in 4 vertebrates

A

In zebrafish = every 30 mins
In chick = every 90 mins
In mouse = every 2.5 hours
in human = every 5-6 hours

49
Q

when is the temporal order/identity of the somite determined

A

before somitogenesis early in development

50
Q

what confers identity of the segments

A

Hox genes

51
Q

what experimentation showed when somite identity is determined

A

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
Q

what causes segmental defects in humans

A

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
Q

whats structures other than the spine are segmented

A

skull and brain