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Unformatted text preview: BIOLOGY 205/SECTION 7 DEVELOPMENT-LILJEGREN Lecture 6
1. Neurulation is the formation of the nervous system.
Many of the same cell movements that occur during gastrulation are involved
in neurulation, such as invagination and convergent extension.
In animals, nervous system & epidermis both derived from ectoderm--i.e.
CNS is derived by invagination of subset of ectoderm.
In vertebrates, this entire process of setting aside precursors of nervous
system= neurulation 2. The PROCESS of neurulation.
a. Dorsal ectodermal cells divided into 3 sets.
i. Dorsal-most are cells (purple in ppt) called the neural plate which will go
on to form the neural tube
ii. Adjacent to the neural plate are the cells (green) which will form the
iii. Even more ventral cells (blue) go on to form the epidermis
b. The neural plate forms - epidermal cells change their cell shape and become
c. central neural plate cells (purple) constrict apically, leading to invagination
d. neural plate begins to buckle, creating a neural fold with a neural groove in the
middle. This process along with neural plate formation result in part from shape
changes in cells. Convergent extension is important.
e. The neural folds elevate and converge at the midline to begin neural tube
f. Eventually the neural tube pinches off to become a separate structure, the
epidermis above it fuses, and the neural crest cells at the fusion point (green)
leave epithelium and migrate to become peripheral nervous system and skin
pigment cells. g. Changes in cell adhesion properties help the neural tube separate from the ectoderm. The outer ectoderm expresses E-cadherin, while the invaginating
neural plate ceases E-cadherin expression and instead expresses N-cadherin.
When the neural tube has formed, the neural crest cells between it and the
ectoderm express neither of these cadherins.
h. Neural tube closure usually starts in the middle and moves both anterior and
i. IF the neural tube does not close properly on the posterior side, the condition is
spina bifida. IF neural tube does not close properly on the anterior side, a fatal
condition called anencephaly can occur that severely affects brain development
(usually forebrain is absent). Neural tube defects are not rare (1 in every 500
live births). Folic acid is crucial for neural tube closure, and it is recommended
that all women of childbearing age take 0.4 mg of folate daily because the
development and closure of the neural tube are normally completed within 28
days after conception, before many women are aware that they are pregnant. Teratogens
1) Teratogens are substances in the environment that cause birth defects. They were first
recognized by the realization that the pesticide DDT destroyed bird eggs and caused
problems with reproduction and that a drug called thalidomide given to pregnant women
caused severe birth defects. Rachel Carson’s book Silent Spring (1962) eventually led to a
nationwide ban on DDT and other pesticides.
2) Fetal alchol syndrome. Alcohol is a teratogen associated with congenital mental retardation.
1/650 children born are thought to be affected, and the average IQ is 68. Studies of alcohol
exposure in developing mice have demonstrated the craniofacial abnormalities associated
with this syndrome, ranging from anterior neural tube defects to characteristic changes in
the nose and lip areas. Magnetic resonance imaging has shown that mice exposed to
alcohol have missing olfactory bulbs and inappropriated fused cerebral hemispheres. Signaling
1) Setting up a signaling gradient: the role of the fruit fly wingless gene
a) Fruit fly maggot is segmented; segmentation is easily seen in the cuticle, which is the skin.
b) On the ventral side of the embryo, each segment has an anterior patch of hairs, and
naked cuticle in the posterior.
c) To set up this repeating pattern, the fly uses the product of wingless gene to specify the
posterior fate. wingless encodes a secreted protein, a cell:cell signaling molecule.
d) A segment starts with 4 cell rows in the anterior/posterior dimension.
e) The 3rd row of cells in each segment expresses wingless protein and secretes it into
f) wingless protein then diffuses in both directions.
i) wingless protein concentration is highest near cell that secretes it & is lower and lower
the further away one travels.
g) All cells have receptors for wingless proteini) cells that see low levels of wingless protein make hairs
ii) Cells that see high levels of wingless protein make naked cuticle.
iii) Notice that cells have different fates depending on how much wingless they see
h) Experimental support: remove wingless by mutation.
i) All cells see low (zero) levels of wingless. Result: All make hairs! [Armadillo is a protein
downstream of wingless with the same mutant phenotype—if lose wingless signaling, get
hairs in posterior portion of segment.]
ii) In contrast, if experimentally create flies in which all cells see high, uniform levels of
wingless Result: all cells make naked cuticle. i) Wingless signal transduction pathway revealed through genetics
j) Conservation of wingless signaling pathway across species: inappropriate signaling
of the Vertebrate relative of Wingless (Wnt1) causes colon cancer. One of 5
signaling pathways that influence virtually all cell fate decisions in all animals.
5. Signaling at a distance: steroid hormones & insect metamorphosis
a) Insects have a series of juvenile larval stages. The larva undergoes a series of molts
(shedding the cuticle) as it becomes larger. The stages in between these molts are called
instars. The # of molts before becoming an adult is characteristic of a certain species. Ie.
egg >1st instar>2nd instar>3rd instar> 4th instar>5th instar> metamorphosis>adult
metamorphosis=transition from larval to adult stage b) Types of metamorphosis: hemimetabolous=gradual, larval instars resemble adult,
holometabolous=sudden, larva go through a complete transformation during the pupal stage
and become adults with little resemblance to the larva
c) Blood-borne hormones regulate these developmental switches
Experiment#1: Decapitate and fuse 1st instar larva to molting 5th instar larvae
Result: induces 1st instar larva to molt into very small adult. Signal in blood tells
it to become a young adult.
d) other hormones prevent metamorphosis
Experiment#2: Remove important gland (corpus allatum) associated with the brain
from 3rd instar larva
Result: induces 3rd instar larva to molt into small adult. (instead of molting
Conclusion: something produced by this gland prevents metamorphosis
Experiment#3: transplant corpus allatum from 4th instar into 5th instar larva
Result: blocks metamorphosis, 5th instar larva > large “6th instar larva” which
would never form normally
Conclusion: corpora allata has signal to remain juvenile
e) so what are these hormones? a complex cascade of hormones regulates insect
i) Molting process initiated in the brain, where neurosecretory cells make the peptide
hormone PTTH in response to environmental or other signals, which is released in insect
equivalent of “blood”.
-PTTH stimulates prothoracic gland to make steroid hormone ecdysone
-ecdysone then modified to become the active molting hormone 20E
-pulses of 20E in the “blood” initiate molting. Do this by stimulating epidermal
cells to synthesize enzymes that digest the cuticle.
ii) corpora allata secrete juvenile hormone (JH)
-As long as JH presesent, the 20E-stimulated molts result in a new larval instar.
-last larval instar: JH levels drop. 20E with low levels of JH results in pupal
development. (New mRNAs synthesized).
-later on 20E in absense of JH, pupa develops into adult
f) steroid hormones like 20E can pass across the plasma membrane and bind to nuclear
receptors, then hormone/receptor complex binds DNA
-these activated transcription factors cause expression of new genes, which results in
changes in cell fate
f) insectide precocene (targets bugs not us) produced by plants kills corpus allatum (which
produces juvenile hormone), so insect larva prematurely form small adults, which are sterile. ...
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This note was uploaded on 05/26/2011 for the course BIO 205 taught by Professor Reed during the Spring '11 term at UNC.
- Spring '11