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Developmental Biology
Chapter 16
I. Evolutionary significance
A) All animals and plants do
sexual reproduction the same way
B)Gamete nuclei fuse
(fertilization) to form a zygote
C) Embryo grows from zygote by
mitosis
II. Vertebrate Zygotes undergo:
1.Cell division: mitosis & cytokinesis
of heterogeneous cytoplasm
2.Cell differentiation: specialization
of structure & function
3. Morphogenesis: development of
form by organizing cell types into
tissues & organs
III. Cytoplasmic Determinants:
substances in eggs, influence development
A. cytoplasmic mRNA & proteins
unevenly distributed in egg
B. After 1st cytokinesis…
nuclei of diff. cells exposed to diff.
cytoplasmic determinants
C. cytoplasmic determinants
influence gene expression &
thereby differentiation
IV. Cell Differentiation (specialization)
A) Determination: molecular events
determine what differentiation will take
place (pre-determined in protostome)
B) Differentiation
1. expression of tissue-specific genes
2. sets of genes sequentially expressed
3. tissue-specific proteins give the cell its
characteristic structure & function
4. transcription control most important

(induction of transcription factors)
C) Skeletal Muscle example

1. determination creates myoblasts by
activating ‘master genes’ (example myoD)

2. these regulatory genes create
regulatory proteins called…
(transcription factors) that activate groups
of tissue specific genes


3. muscle specific version of genes for
contractile proteins create lots of
a. actin
b. myosin
 4. cells fuse to form multinucleate elongate
muscle cells
V. Embryonic Induction:
A) an interaction btwn an (inducing) tissue
and another (responding) tissue
B) direct timing of developmental steps &
differentiation
C) most important mechanism leading to
differences between cells & to the
 organization of cells into tissues & organs.
D) caused by
 1) direct contact btwn cell-surface proteins
 2) secreted growth factors (signal mol.)
Vertebrate camera eye development
VI. Apoptosis: programmed cell death
(morphogenesis mechanism)
A) signal transduction pathways activate
cascade of suicide proteins
B) cell ‘blebs’: partitions into vesicles.
C) vesicles engulfed by phagocytes
D) genetic similarity in apoptosis genes
indicate its evolution early in eukaryote
line (yeast, animals)
V. Pattern Formation: correctly place
tissues (morphogenesis)
A. 3 major body axes
 1. anterior-posterior

(head – tail)
 2. dorsal – ventral

(back – belly)
 3. left – right
B. pattern formation is determined
 1. before fertilization by…

a. Maternal cytoplasmic determinants

b. control anterior/posterior

c. control dorsal/ventral
 2. After fertilization pattern formation

controlled by Homeotic genes
D. morphogen gradient hypothesis
 1. maternal effect genes make mRNA
that is concentrated in one region of egg
 2. mRNA makes its pattern forming
protein (morphogen) after fertilization
3. High concentration of that morphogen
at one end causes diffusion toward
opposite end of embryo setts up gradient
4. cell determination governed by
relative concentrations of morphogens
E) Embryonic Genes Take over
 1. after ant/post and dors/vent have
been established
 2. mRNA of egg-polarity genes broken
down by miRNA
 3. embryo’s own genes take over

a. homeotic genes
 b. transcription factor regulatory genes
play major role in pattern formation

c. evo-devo …evolutionary
developmental biology
VI. Cloning
A. Organism develops from single cell
 1. no meiosis
 2. no fertilization
 3. genetically identical to 1st cell
 4.first done with carrots
 a. differentiated plant cells can
dedifferentiate and give rise to all types
of cells

b. totipotent cells can become any cell
B. Differentiated Animal cells

1. don’t divide in culture

2. can not make other cell types
C. Nuclear Transplant

1. dedifferentiates nucleus

2. nucleus placed in enucleated egg

3. egg develops into organism

4. Dolly
D. Reproductive cloning problems

1. high embryo mortality
 2. DNA methylations affect gene
regulation
 3. Telomeres not restored =
premature aging
E. Therapeutic Cloning – stem cells to
treat disease (eggs donated IF clinics)
 1. nucleus from person with disease
used for nuclear transfer

a. cells to study

b. cells to treat patient
 2. Ethical issues
VII. Stem Cells: reproduce indefinitely &
can differentiate into specific cell types

A. Adult Stem cells – from fully
developed organism
 1. can differentiate into a few cell types
 2. can reproduce indefinitely
B. Embryonic Stem cells –from blastula
 1. blastula (blastocyst in humans)
 2. hollow ball of about 150 cells
 3. Pluripotent = differentiate into many
types of cells
C. iPS – induced pluripotant stem cells
 1. adult cells given stem cell ‘master
genes’
 2. genes inserted by retro-virus
 3. very similar to embryonic stem cells
 4. potential to make genetically
identical repair tissues
 5. genetically engineer cells &
reintroduce to body
 6. NO egg NO embryo No problem!! 
VII. Cancer & gene regulation
A. Somatic cell mutations can =cancer
 1. caused by chemical carcinogens
 2. high energy radiation
 3. ex. translocation

a. chromosome breakage & relocation

1. moved near very active promotor

2. broken gene inactive
 4. ex.gene amplification(many copies)
 5. ex. gene mutations
B) Proto-oncogenes = normal genes
 1) if mutated become oncogenes
 2) code for proteins that stimulate cell
division
 3) ras gene example (30% of cancers)


a. codes for a G protein called ras
G protein review (p 110) (p325)
G proteins use GTP energy
 G proteins send signals from receptor
proteins to transduction cascade
 not working = too much or too little
signal
4) ras G-protein relays growth hormone
signal to cascade of protein kinases.
 a) transduction of signal results in
production of protein that stimulates cell
cycle

b) mutated ras gene is an oncogene
 c) mutated ras protein constantly
triggers cascade of protein kinases
regardless of presence of growth factor
 d) protein product stimulates cell
division (p 325, fig. 16.17)
C. tumor-suppressor genes
 1. some code for DNA repair proteins
 2. some code for adhesion proteins
 3. some code proteins that inhibit cell
division
 4. example:p53 tumor-suppressor gene

a. 50% of cancers show this mutation

b. p53 codes for transcription factor

that promotes production of

cell cycle inhibiting proteins
 c. p53 transcription factor activates
several different genes
 1. gene p21 makes a protein that
binds cyclin-dependent kinases, stopping
cell division

2. miRNAs activated by p53 inhibit c.c.

3. genes for DNA repair also activated
 4. activates apoptosis genes if DNA
can not be repaired

D. Multi-step model
1. More than one somatic mutation
needed to produce cancer cells
2. Explains increased cancer risk
with age
E. Inherited Cancer Risk
1. inheriting one oncogene or mutated
tumor suppressor gene
 a. won’t automatically cause cancer
 b. puts you one step closer
2. BRCA1 and BRCA2 are inherited
mutations associated with Breast Cancer
 a. second most common cancer in USA
 b. tumor suppressing genes
 c. DNA tests developed
F. Virus caused Cancers
1. implicated in 15% of cases
2. Human Papillomavirus

a. cervical cancer

b. vaccination
G.Cyclin Dependent Kinase Review
CDKs =enzymes. turn on or off
processes in cell division
CDKs only active when bound to cyclin
proteins
Different cyclins activate different CDKs
at each stage of cell division
Tumor suppressor genes may activate
genes that block CDK action
Mutated CDK or Cyclin genes can be
oncogenes
H. Check points – regulated by CDKs
1) G1 checkpoint – cycle initiation

a)controlled by cell size

b) growth factors

c) environment
2) G2 checkpoint – transition to M

a) DNA replication complete

b) DNA damage/mutations
3) M-spindle checkpoint

a) spindle attachment
 Embryonic induction = timing
 Homeotic genes = pattern formation in late embryo
 Hox genes = animal homeotic genes (very highly conserved
 Morphogenesis = gives organism its shape