6W: Ectoderm-Endoderm

Question 1

What is the first step of gastrulation?

Answer 1

Formation of the Primitive Streak

Question 2

What is special about day 17 formation?

Answer 2

Notochord is present. Notochord and primitive streak never overlap!

Question 3

Formation at day 19

Answer 3

Early Neurulation

• Neural plate is induced (neuralized) by underlying notochord (neuroectoderm) and prechordal mesoderm
• notochord and prechordal mesoderm secrete noggin, chordin, and follistatin to “dorsalize the ectoderm”

Question 4

How do levels of BMP4 effect cranial neurulation?

Answer 4

BMP4 is a ventralizer
High BMP4: ectoderm become epidermis
Medium BMP4: neural crest is induced
Low BMP4: ectoderm become neuralized (to form the neural plate)
- with low BMP4, noggin, chordin, and follistatin from the notochord, prechordal mesoderm, and node are antagonizing the BMP4

Question 5

Neural folds form what later structures?

Answer 5

Forebrain (proencepahlon), Midbrain (mesencephalon), and Hindbrain (rhombencephalon)

Question 6

Formation at day 20

Answer 6

Neural Fold Formation

• elevation of later portions of the neural plate to form the neural folds
• depressed midline = the neural groove

Question 7

Formation at day 22

Answer 7

Cranial and Caudal neuropores are still open to amniotic cavity.

• fusion occurs in the middle first and then moves out bidirectionally cranially and caudally
• areas still open (not yet fused) are called neuropores
• mesoderm somites are forming which will later become vertebrae

Question 8

Formation at day 23

Answer 8

Pericardial bulge (from the lateral plate mesoderm) starting to form. Which will later become the heart

Question 9

Formation at day 28

Answer 9

Completion of Neurulation

• neuropores close cranially at day 25 and caudally at day 28
• neural tube now comprised of spinal cord and brain vesicles
• other ectodermal thickenings (lens and otic placodes) are apparent

Question 10

Ectodermal Derivatives

Answer 10

• CNS
• PNS
• Sensory epithelium or ear, nose, and eye
• Epidermis, hair, and nails
• Mammary, pituitary, and subcutaneous glands

Question 11

Anencephaly and Spina Bifida

Answer 11

Anencephaly
- when the baby does not have a head
- caused by the cranial neuropore not closing
- high levels of alpha fetoprotein in the maternal serum or amniotic fluid are indicators of failure of neuropore closure. (follow this up with ultrasound)
- can be prevented by maternal use of folic acid (Vitamin B9) prior to and during pregnancy
Spina Bifinda
- neural tissue and/or meninges protrude through the vertebral arches and skin
- caused by failure of the posterior neuropore
- can be prevented by maternal use of folic acid (Vitamin B9) prior to and during pregnancy

Question 12

Neural Crest Cells

Answer 12

• found at the crest/border of the of the non-neural and neural ectoderm
• exit the neural tube at head and trunk regions.
• multipotent
• transient (only found in the embryo)
• unique to vertebrates

Question 13

What do the neural crest cells give rise to?

Answer 13

melanocytes, craniofacial cartilage and bone, smooth muscle, preaortic ganglia, sympathetic chain, Schwann cells (glial cells in PNS)

Question 14

How do neural crest cells exit the neural tube in the TRUNK REGION?

Answer 14

• only leave once the neural tube closes
• as the neural folds fuse, NCCs undergo epithelial-to-mesenchymal transition in order to leave and enter the mesoderm
• note that the ectoderm has to then come together to cover over the neural tube

Question 15

How do neural crest cells exit the neural tub in the HEAD REGION?

Answer 15

• cells leave before neural tube is closed
• NCCs migrate into the pharyngeal arches (1-4, 6)
• NCCs can form craniofacial seleton and cranial ganglia

Question 16

What structures to NCCs form in the head/ neck that they don’t anywhere else? Why don’t they form these anywhere else?

Answer 16

Cartilage, bone, and connective tissue. Because it is so important for the head to develop, that they go ahead and form these. Everywhere else, these tissues are mesodermal derivatives (while NCCs are ectodermal derivatives).

Question 17

What are possible neural crest related cranio-facial defects?

Answer 17

Treacher Collins Syndrome
- small mandible and malformed ears
DiGeorge anomaly
- craniofacial defects such as low-set ears and widely-spaced eyes
Robin sequence
- small mandible
Hemifacial microsomia
- lower half of one side of the face is under-developed; ex: ears, mouth, mandible

Question 18

Hox genes

Answer 18

• responsible for patterning the body plan along the A/P axis
• code for transcription factors that activate gene cascades regulating segmentation identity (i.e. what structures form from what segments)
• genes present in clusters on multiple chromosomes
• the lower the number (i.e. 1 or 2) are expressed anteriorly and early while the high numbers (i.e. 12 and 13) are expressed posteriorly and later
• lower numbers are more susceptible to retinoic acid/oxidized Vitamin A

Question 19

Define:

a. gene cluster duplication

b. paralogous groups

Answer 19

a. clustering of Hox genes on a chromosome
ex: all of the Hox-A genes are clustered on one chromosome
b. genes that encode for the same temporal and spatial expression on different chromosomes
ex: all of the Hox-(N)1 genes, N being A, B, C, or D, are a paralogous group

Question 20

relation between Hox genes and the hindbrain

Answer 20

Hox genes encode positional information about the A/P axis within the hindbrain
- segments the hindbrain into rhombomeres, which are segments along the A/P axis that them develop different functions such as chewing or breathing

Question 21

Gut formation from the endoderm and cephalocaudal folding

Answer 21

• cephalocaudal folding promotes the endoderm-lined cavity to be incorporated into embryo body (gut formation)
  foregut (anterior): bounded by buccopharyngeal membrane until rupturing in the 4th week
  midgut: temporarily still connected to the yolk sac
  hindgut (posterior): terminates temporarily at the cloacal membrane until it ruptures during the 7th week

Question 22

Lateral folding

Answer 22

• results in rapid somite growth
• pinches off cranially and caudally, but the midgut stay connected to the yolk sac
• how the amniotic cavity goes from being above the embryo to surrounding the embryo

Question 23

Vitelline duct

Answer 23

midgut connection with the yolk sac as lateral and cephalocaudal folding occurs that becomes long and narrow

Question 24

Why is the Vitelline duct important in gut formation?

Answer 24

because as our intestines grow, there isn’t enough room inside the embryo. So, our gut herniates out through the Vitelline duct and are in the umbilical cord for awhile

Question 25

Defects of failed lateral folding

Answer 25

Ectopia Cordis: ectopic heart
Bladder Exstrophy: failure of pelvic region to close causing eversion of the bladder
Gastroschisis: intestines stay in the Vitelline duct, causing herniation of the intestines through the abdominal wall
Cloacal Exystrophy: failure of pelvic region to close

Question 26

Role of epithelial-mesenchymal interactions and Hox genes

Answer 26

• interactions between the mesenchymal cells expressing Hox genes and epithelial (endodermal) cells expressing SHH stabilizes the segments so they retain their “identity” of where they are supposed to go (being segmented.

Question 27

How are the esophagus and trachea formed?

Answer 27

The respiratory diverticulum/lung bud is an outgrowth from the ventral wall of the foregut and about 4wks. of development. the Tracheoesophageal septum later divides the foregut into the dorsal esophagus and the ventral trachea + lung bud
so… foregut = esophagus respiratory diverticulum = trachea and lung buds