Module 1 Lecture 2: Axis Formation and Patterning Flashcards

1
Q

what are the two important axes of an embryo

A

anterior-posterior and dorsal-ventral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the neural fold

A

the boundary between neural plate and outside ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does the gastrula develop into

A

neurula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do the neural folds do during neural tube closure

A

rise up, meet in the middle, and fuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does the notochord develop from

A

organizer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

characteristics of notochord

A
  • mesodermal
  • critical role in D-V patterning
  • transient in vertebrates; contributes to vertebral column (usually reabsorbed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

somites function

A

give rise to vertebrae and other musculo-skeletal elements
- either side of neural tube, mesodermal, segmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neural crest function

A

makes PNS, melanocytes, face cartilate
- migrate away
- vertebrate specific, pluripotent
- born at epidermal-neural boundary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

types of neural tube defects

A
  1. anencephaly
  2. spina bifida
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what causes anencephaly

A

anterior neuropore fails to close
- brain absent or does not complete development
- fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes spina bifida

A

posterior closure fails
- survivable but leads to leg paralysis, loss of bowel and bladder control, hydrocephaly, and learning disabilities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

role of folic acid in neurodevelopment

A

reduces risk of neural tube defects by 50-70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

three primary vesicles

A

forebrain, midbrain, and hindbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

primary vesicles subdivided

A
  • forebrain –> telencephalon, diencephalon
  • midbrain –> mesncephalon
  • hindbrain –> metencephalon, myelencephalon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does the telencephalon subdivide into

A

olfactory lobes, hippocampus, cerebrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does the diencephalon subdivide into

A

optic residue, epithalamus, thalamus, hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does the mesencephalon subdivide into

A

midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does the metencephalon subdivide into

A

cerebellum, pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the myelencephalon subdivide into

A

medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what triggers the development of the prospective forebrain from the ectoderm in the activation-transformation model

A

signal 1, “activation”
- neuralizes and specifies forebrain
- aka neural induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what triggers the development of the midbrain in the activation-transformation model

A

signal 2, “transformation” (caudalizes)
- works in tension with activation & forebrain specification signals to induce more posterior structures
- signal coming from tail end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

characteristics of signals coming from posterior end in activation-transformation model

A

soluble signaling molecules similar to BMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the ultimate goal of the activation-transformation model

A

to change gene expression to specify neural fate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does the shape of the activation-transformation effect depend on

A

interaction between caudalizing signal and dorsal mesoderm cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does Wnt overexpression cause

A

induction of head structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does Wnt inhibition cause

A

severe reduction of the head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how do vitamin A derivatives affect neurodevelopment

A

inhibits forebrain & midbrain development in a concentration-dependent manner
- consistent with a role in posterior neural tube specification

28
Q

what does exposure to retinoic acid (RA) cause

A

craniofacial & brain malfunctions

29
Q

first step of RA metabolism

A

make RA via retinaldehyde dehydrogenase (RALDH)

30
Q

second step of RA metabolism

A

paracrine signaling
- broken by Cyp26

31
Q

types of cell signaling

A
  • autocrine: cell targets self
  • gap junction signaling: cell targets a cell connected by gap junctions
  • paracrine: cell targets a nearby cell
  • endocrine: cell targets distant cell through bloodstream
32
Q

third step of RA metabolism

A

response to RA: RA and retinoid X receptors heterodimerize & bind RA-response elements
- activate gene transcription

33
Q

fourth step of RA metabolism

A

Cyp26 generates the “sink” and breaks RA

34
Q

what is the next step after A-P patterning

A

regionalization
- organisms are not built step by step, but asynchronously in overlapping fashion

35
Q

why is establishing segment identity (aka regionalization) important

A

critical to specification of cranial nerves, development of brain stem, inner ear, branchial arches, and the heart and large vessels

36
Q

homeobox

A

a sequence of 180bp nucleotides which encodes a highly conserved 60aa DNA binding domain: homeodomain

37
Q

what can a single homeotic protein do

A

-regulate (activate or repress) hundreds of different genes

38
Q

what determines the target set of genes in a given cell

A

homeotic proteins mixing and matching with other transcription factors

39
Q

co-linearity principle

A

Hox genes are organized in contigous clusters on chromosomes (eg 2 clusters on Chr3.)

40
Q

how does the physical order of Hox genes on a chromosome map to their order of expression

A

physical order on the chromosome matches their order of expression in the AP axis of a developing animal

41
Q

posterior dominance

A

activity of posterior Hox genes dominates over more anterior ones (if they are co-expressed)

42
Q

homeosis
- or homeotic transformation

A

a variation in body plans in which “something has been changed to the likeness of something else”

43
Q

master regulators

A

homeotic genes; they turn on and off expression of so many genes, enough to reprogram entire body parts
- every animal we know has Hox genes

44
Q

what are Hox genes?

A

clustered, master regulators of gene expression that follow the co-linearity principle across phyla

45
Q

what are rhombomeres

A

transient segments of the developing hindbrain

46
Q

what drives regionalization of rhombomeres

A

retinoic acid-dependent Hox gene expression
- also follow colinearity principle

47
Q

what makes RA

A

somites (RALDH)

48
Q

what shapes the RA gradient

A

rhombomeres (Cyp26)
- shaped by where it is made and broken down

49
Q

what interprets the RA gradient

A

Hox genes

50
Q

result of vitamin A deficiency

A

no RA, Hox1b not expressed, hindbrain “anteriorized”

51
Q

result of Cyp26 dysfunction (more RA)

A

too much RA, expanded Hox1b, hindbrain “posteriorized”

52
Q

what is a morphogen

A

a signaling molecule that 1. acts in a concentration dependent manner 2. on cells other than the source 3. to produce specific responses

53
Q

characteristics of Wnt, FGF, and BMP as morphogens

A

their signaling gradient is shaped by where they are secreted from and where they are inhibited by antagonists

54
Q

when does D-V closure occur

A

soon after neural tube closure

55
Q

what are the 11 classes of neural progenitors set up by

A

expression domains of transcription factors

56
Q

what do expression domains of transcription factors control

A

gene regulation and gene expression patterns
- set up the 11 classes of neural progenitors

57
Q

when is Pax7 (dorsal determinants) most present

A

prior to neural tube closure

58
Q

what genes are involved after neural tube closure

A
  • Pax7 becomes more restricted
  • Olig2 expands
  • Nkx2.2 is established
59
Q

what does removal of notochord cause

A

loss of floorplate and motor neurons in the spinal cord

60
Q

what does transplanting the notochord to the side of the spinal cord do

A

gives you a second floor plate and a second set of motor neurons at the dorsal side of the spinal cord

61
Q

what induces ventral fates in spinal cord

A

notochord, with a diffusable signal

62
Q

what is hedgehog

A

a secreted protein

63
Q

what causes development of Sonic hedgehog (Shh)

A

the notochord induces the floorplate to produce it

64
Q

what happens when cells from intermediate spinal cord are cultured with Shh

A

expression of ventral fate markers

65
Q

what does higher Shh concentration cause

A

more ventral fates

66
Q

is Shh a morphogen?

A

yes

67
Q

what is the DV patterning of the spinal cord established by

A

two opposing morphogen gradients:
1. shift from the ventral side (notochord and floorplate)
2. BMP and Wnt from the dorsal side (epidermis and roof plate)