Some terms you should be familiar with:

fertilization, egg activation, holoblastic and meroblastic cleavage, morula, blastula, mid-blastula transition, blastocoel

gastrulation, epithelium, mesenchyme, archenteron, blastopore, invagination, involution, ingression, epiboly, primary germ layers, epiblast, hypoblast, Hensen's node, inner cell mass, trophoblast

induction, progressive determination, cytoplasmic determinants

Lecture 1 Intro and control of gene expression

1)What is meant by the developmental fate of a cell?What is an embryonic fate map?

2)What is a cell autonomous determinant?What is meant by induction as applied to embryos?

3)What kinds of experimental evidence show whether or not the fate of a particular blastomere or tissue is already autonomously determined?

4)What kinds of experimental evidence indicate that the fate of a particular blastomere or tissue is determined by subsequent induction?

5) What is a promoter? What happens at a promoter site?

6) What are enhancers and silencers?  How do they differ from promoter elements?

7) How do transcription factors regulate transcription?

8) How can enhancers/silencers function at large distances from the promoter?

9) Why do enhancers work in some cell types and not others, and what is the significance of this in development?

10) What is meant by "combinatorial control of transcription"?

11) What is the significance of combinatorial control in determination and differentiation?

12) What are the four major classes of transcription factors, and how are they named?  Can you name an example of each?

Lecture 2: Signaling

1)  Define autocrine, paracrine, endocrine, and juxtacrine.

2)What are the components of the Wnt pathway, and what do they do?

3) What are the components of a typical RTK signal transduction pathway and how are receptor tyrosine kinases (RTKs) activated by growth factors?

4) What is required for conversion of the hedgehog ligand precursor to its active form?

5)  Can you name four TGF-b-related growth factors that are important in controlling embryonic development?

6) How do extracellular matrix (ECM) components affect paracrine signaling pathways?

7)Name an ECM component that can serve as a signaling ligand.  What are the cellular receptors for ECM ligands called?

8) What type of signaling system do Notch and Delta participate in, and how does the Notch receptor regulate transcription?

9)What are cadherins and how do they function?

10) What molecule has the potential to provide integration/cross-talk between cadherins and Wnt signaling? 

11)  What is meant by multiplexing of signaling pathways? What is its significance in cell determination and differentiation?

Lecture 3 - Fertilization and Cleavage

1) What is the acrosomal reaction, and what are its consequences?

2) How does mammalian sperm bind the egg?  What happens to prevent polyspermy?

3) Explain the relation between amount and distribution of yolk and cleavage patterns.

4)How are the orientations of cleavages determined (i.e. anterior-posterior, left-right, etc.)?

5)If a cell has just divided with an A-P orientation, what will be the default orientations of the cleavages of its two daughter cells?

6) How does the blastocoel form during cleavage?

7)What three things happen at the mid-blastula transition in amphibian embryos?Do all embryos have a mid-blastula transition?  Explain.

Lecture 4 - Gastrulation  -- cellular mechanisms

1)List the important distinguishing characteristics of epithelial and mesenchyme cells.

2) What is the first event in amphibian gastrulation?Where does it occur, and how does it proceed?

3) What are the roles of cell adhesion molecules, specifically cadherins, catenins, and CAMs, in the formation and behavior of epithelia?

4)Define homophilic and heterophilic binding and give examples of each.

5) What happens to the blastocoel during gastrulation?

6)How does the archenteron form, and what does it become?

7) How is chick cleavage different from amphibian cleavage and human cleavage?

8) How does the primitive streak originate, and what structure does it terminate as?  What structure is this similar to in amphibian?

9) Define what is meant by invagination, ingression, involution, and epiboly and explain how they contribute to gastrulation.

10)  Name the different kinds of mesoderm that are formed during gastrulation, and indicate the order in which they are formed.

11) How does the human embryo separate into the inner cell mass and trophoblast?  What do each of groups of cells give rise to?

Lecture 5  --  Induction and establishment of the embryonic axes and mesoderm

1)  What was the early evidence that different regions of the frog ectoderm become progressively determined during early embryogenesis?

2) Where does the signal come from that induces animal cap cells in a frog embryo to become mesoderm?Describe the experiments that provided the answer to this question.

3) What is the evidence that this signal is a small diffusible molecule, and how can this signal be assayed in culture?

4) What is the evidence indicating that activin can act as a morphogen for mesoderm induction?

5)  Describe the Spemann-Mangold experiment.  What key aspect of the experiment showed that induction was occurring, i.e. that the transplant was changing the normal cell fates of the surrounding tissues?

7) At the time, Spemann called this phenomenon "primary induction;" why is this term inappropriate?

8  What is the initial cue that determines which side of a frog egg will become the dorsal side of the embryo, and how is this cue transmitted?

9) What is the evidence that cortical rotation produces a dorsalizing signal? 

10)  What is the Nieuwkoop center; what does it induce, and what is the evidence that it acts by induction?

Lecture 6 --  Molecules involved in induction

1)  What is the molecular basis for the initial dorsalizing signal produced by cortical rotation?

2) Through what signaling pathway does this signal have its effects?

3) How does the mesodermal layer become patterned prior to gastrulation?  What are the three principal signals responsible for this patterning, and what do each of them do in the three-signal model?

5)  Name four functional properties of the cells in the Spemann organizer, i.e. what they do in development before, during, and after gastrulation. What is the master transcriptional regulator that initiates these organizer functions?

6)  What is the default fate of Xenopus dorsal ectoderm? What is the molecular mechanism by which the organizer causes dorsal ectoderm to adopt a neural fate rather than epidermis?

7) What is the molecular mechanism by which the anterior head and brain are specified?

8) What other signals contribute to anterior-posterior patterning of the neural ectoderm?

Lecture 7 -- Axis formation 

1)  How do the mechanisms for D/V patterning in chick and mammals differ from D/V patterning in Xenopus?

2) Describe the factors that help to pattern the A/P axis in chick, mammals and Xenopus.

3) Describe the Hox genes and their significance in A/P patterning.

4) What are some standard left/right asymmetries, and what is unique about the establishment of the L/R axis?

5)  What is the first molecule to show a L/R asymmetry in Xenopus?  In chick?

6)  What is the sequence of events at a molecular level that leads to the establishment of the L vs. R side?  You should be able to name 3 molecules for each side.

7)  What kinds of experiments indicate that the asymmetric expression of these molecules is important for L/R establishment?

8)  In mammals, what is the evidence suggesting that there is a mechanism directing flow of molecules to the left?