Devo Lect 11 - Neural tube and Vision

Question 2

Main changes in differentiation in ectoderm

Answer 2

Macroscopic changes, tissue level changes, cellular level changes

Question 3

Macroscopic

Answer 3

3 areas (primary vesicles): forebrain, midbrain, hindbrain; divide: forebrain (telencephalon and diencephalon, midbrain (mesencephalon0, hindbrain (metencephalon, myencephalon);

Question 4

5 secondary vesicles

Answer 4

Telencephalon, diencephalon, mesencephalon, metencephalon, myelencephalon (most anterior to posterior)

Question 5

Adult derivatives of telencephalon

Answer 5

Olfactory, hippocampus, cerebrum

Question 6

Adult derivatives of diencephalon

Answer 6

Retina, epithalamus, thalamus, hypothalamus

Question 7

Adult derivatives of mesencephalon

Answer 7

Midbrain

Question 8

Adult derivatives of metencephalon

Answer 8

Cerebellum, pons

Question 9

Adult derivatives of myencephalon

Answer 9

Medulla

Question 10

Cells of neural tube

Answer 10

Ventricular zone: neural stem cells; Intermediate layer: gray matter; marginal zone: white matter. Still present in adult (with other nuclei)

Question 11

Neural stem cells

Answer 11

We still have them as adults! But they can’t migrate or there aren’t enough to repair damage to brain

Question 12

Chick-Quail chimera (brain)

Answer 12

Nicole le Douarin: View brain development and fate map; can be viewed under microscope

Question 13

Chick-Quail crowing pattern chimera

Answer 13

Mesencephalon/diencephalon graph, changed crowing pattern; that part of brain is involved in that function; affects behaviour

Question 14

Development of vertebrate eye

Answer 14

Forms after neural tube (from diencephalon); neural tube bulges out (evagination) to form optic vesicles; about day 30 in humans; optic cup (retina), epidermis invaginates to form eye pit; at day 33, pit has pinched off, will become lens, epidermis on outside will be cornea; completed around day 60 (stage 23)`

Question 15

Holoprosencephaly

Answer 15

Abnormal outpouching of diencephalon; telencephalon and diencephalon don’t divide and hemispheres don’t separate normally; usually results in death or mental defects

Question 16

Cyclopia

Answer 16

Diencephalon doesn’t split into two eyes;

Question 17

Pax6 phenotypes

Answer 17

+/+: normal; +/-: small or malformed eyes; -/-: no eyes, brain development

Question 18

Aniridia

Answer 18

Human condition, Pax6 +/-, no iris

Question 19

Role of pax6

Answer 19

Highest in presumptive invaginating lens; not expressed in completed eye, therefore it is implicated in development of the eye

Question 20

Refresher on in situe hybridization

Answer 20

Complementary nucleic acid probe for mRNA, fluoresces; put directly on tissues

Question 21

What type of molecule is Pax6?

Answer 21

Transcription factor, binds to promoter regions of crystalline genes

Question 22

Promoter vs enhancer

Answer 22

Promoter regions are close and in front of genes, turn genes on or off; enhancers are often further away, serve to amplify

Question 23

Drosophila homologue to Pax6?

Answer 23

Eyeless, very similar to human pax6 (almost interchangeable! - ectopic experiments on flies).

Question 24

Other animals with pax6?

Answer 24

Squid, flatworms, C. elegans, jellyfish, tunicates, many of them don’t even have eyes! Affects sense organs in anterior part of C. elegans - anterior central nervous system

Question 25

Eye types

Answer 25

Simple eye: one lens, formed from brain and epidermis (vertebrates); Compound eye: many tiny lenses (or omatidia), almost all from epidermis (arthropods); simple: all from epidermis (cephalopod)

Question 26

Photoreceptors in different eye types

Answer 26

Simple vertebrate: axons face out then back through optic nerve; compound and cephalopod: axons face back

Question 27

Pax6 origins

Answer 27

Only in animals; arose in cambrian; first animals didn’t have eyes, so it was probably in nervous system - head development (new structures like feeding, eyes, etc)

Question 28

Master control gene

Answer 28

“Help start the ball rolling” to create major structures; Pax genes, Hox genes; early in development, TF (cascade),

Question 29

Induction of lens placode

Answer 29

By optic vesicle, release growth factors (which are initiated by pax6), lens folds inwards

Question 30

Induction of cornea

Answer 30

By the lens; causes epidermis to form cornea

Question 31

Why are Cornea and Lens clear?

Answer 31

No pigment, no blood vessels; both have living cells, but most cells are dead and full of crystallin proteins for rigidity and clarity

Question 32

Cataracts

Answer 32

Clouding of lens; crystallins clump together and denature; caused by metabolic disorders, age, trauma, heredity; treated by replacing lens with plastic (can’t focus close but can wear glasses)

Question 33

Congenital cataracts

Answer 33

Mutation in crystallin gene; one form is due to one amino acid change

Question 34

Retina

Answer 34

Forms 3 layers: back is photoreceptors; middle is bipolar nerve layer; outer is ganglion, connect to optic nerve; layer below retina has pigment to absorb excess light

Question 35

Vision of infant

Answer 35

Newborns can just make out outlines; by about nine months it is about perfect; early photoreceptors are fat, then start to shrink and increase in number, higher density increases vision