1. how do different cytoplasmic structures have different structure and function when all are made by the same nucleus and all have protein, lipid content

2. membrane lipid: kinds, membrane domains, function, physical characteristics of lipids allowing their function, fluidity, charge

3. proteins in membranes: structure, hydrophobic, assymetry in membrane, domains and charge, receptors, attach to cytoskel and ECM, prim, sec, tert, quat structure, assoc with lipid

4. What factors can change membrane content? Exo- and endo-cytosis, synthesis, degradation, exchnage, kinds of membrane proteins- receptors, ion channels, pumps, structural connections. What does detergent do to membrane

5. cytoskeleton: factors influencing actin assembly and structures such as mesh or fibers or gel. Components other than actin: microtubules, MAPS. Polarity in both actin MF and MT

6. Control of protein structure : binding domains for ATP, Ca++, kinases, phosphatases; structure of pro-pre-protein, SH, protease, tertiary, quaternary, folding

7. striated muscle, sarcomere, microfilament content and control, physical p[roperties of muscle proteins, cisterna, T-tubules, polarity of MF and large filaments. Anchor proteins. Mechanism of contraction. Rigor mortis

8. Smooth muscle and non-muscle movement and control . MLC kinase, calmodulin. Myosin I and II.

9. Amoeboid movement: pushing versus pulling. Ca++ and pH effects on polymerization and myosin. Cytoplasmic streaming in plants, chloroplasts and actin.

10. Cilia and flagella and vesicular transport: axoneme, dynein arms, spokes, nexin, 9+2, bending, centriole, motors:dynein to center of cell, kinesin to outside

11. receptors and second messengers: cAMP, IP3, DAG, cADPribose, Ca++;ion channels, enzymes, Gproteins, kinases, phosphatases, cGMP

12. synapse, neuromuscular junction, action potential, patch clamp, drugs, neurotransmitter, breakdown enzymes, endocytosis

13. Inhibitory synapse

14. gene expression, upstream control, inhibitory, stimulatory, growth factors

15. energy charge, metabolic control, hormones, kinases, phosphatases, different receptors on liver and fat and muscle.

16. growth factors, SRC homology domains (SH2 and SH3) on recpetors bind second messenger proteins with SH2 or SH3, GRB, RAS, hookup to MAPkinase path, effect transcription, cytoskeleton, oncogenes.

16a. Types of receptors; Gprotein, phosphorylation, ion channels, second messenger pathways.

17. Cell cycle, serine-threonine kinases, tyrosine kinase, MPF, cyclin, wee-1, CSF,

18 meiosis control- CMOS-activates protease for CMF, or CDC25 kinase which turns off MPF, lower cAMP, PKA; Ca++ inactivate CSF which protects MPF, recombination control genes, synaptonemal complex, small nRNA nick DNA with L protein

19. mitosis and cytokinesis- mechanics of division; spindle, centrioles, centromeres, kinetochore, vesicles, Ca++, MAPS, motors, tension, contractile ring, myosin, actin, pro-meta-ana-telo-phase

20. cancer- oncogenes-types of loss of control

21. transcription control, cytoplasmic determinants, rescue, reporter genes, contructs, DNA binding protein, affinity columns, maternal control genes, gap, segmentation, homeobox

22. cell adhesion; receptors, ECM, protein domains, cell polarity, CAMs, cadherens, fibronectin, collagen, loss in cancer, change in devel

23. vesicular transport-coatamers, epitope receptors, cargo receptors, sorting domains, lipid involvement, phospholipases

24. Immune system, cell interactions, types of cells, types of receptors and function of MHC receptors, interleukins, cytokines; clonal selection, gene rearrangement.


What have been our main objectives in the course?

To understand how cells do their functions: division, motility, response to stimuli, communication, maintain homeostasis.

To learn what control mechanisms there are for allowing cells to change between different states of the above functions.

This includes membrane cycling, assembly and disassembly of cytoskeleton, synthesis of new material to be incorporated into old. We emphasized those control mechanisms initiated by external factors rather than nuclear control from within as in maintainance and repair.

To recognize the functions of the cell membrane components, cytoskeleton components, cell motor components.

To understand how all of these things are thought to occur at the molecular level by changing which things are bound or released: ions such as H+,Ca+,Mg+, Na+, K+, Cl-; high energy molecules such as ATP, GTP, cAMP, cGMP; extracellular factors such as hormones, growth factors, neurotransmitters, extracellular matrix, antigens or antibodies; level of phosphorylation resulting from cAMP, cGMP, DAG, IP3 production and activation of protein kinases or phosphatases.

So in looking back over this list ask yourself on each part of the sentence How does it work, what controls it, how is important for normal cell function? For example for division in the very first sentence above. How does the cell divide- what machinery is involved? How does a cell know when to divide- what control mechanisms are there and what kinds of external factors can alter the control mechanisms? What kinds of signal transduction are involved and wwhat happens at the molecular level to initiate, to assemble the machinery, to provide energy for the work which is done, to stop when finished.

You should ask these same questions of all topics in the syllabus and ask yourself how they are interrelated. For example how is the membrane involved in each of the topics? Are there receptors involved, ion channels, membrane potentials, G-proteins, lipid breakdown, membrane cycling? How is the cytoskeleton involved in each of the topics? What second messengers and molecular controls are used for each topic?

You see, now we are trying to relate all the topics we have learned about rather than keeping them as isolated compartments of knowledge and that is what the final exam will test, your ability to do that.


1. How can one cell influence another to move or divide or stop dividing?

2. How can the extracellular environment influence a cell to move or divide or stop moving or dividing?

3. What kind of cell membrane components or receptors are involved? Is there an effect on the cytoskeleton?

4. How is cell adhesion related to cell division, cell motility, extracellular matrix? What are some of the molecules involved?

5. What do we mean by recognition molecules and how is that related to cell differentiation and how is it related to the immune system?

6. What kinds of molecules are in the extracellular matrix, and how do they differ between tissues for support. What are the proteoglycans, glycoseaminoglycans, glycoproteins involved?

After you answer these questions try to think of other possible answers. Always have experimental proof of your statements, or examples.


1. What kinds of cells fuse?

2. How can viruses fuse with cells?

3. What are some mechanisms working in cell fusion?


cell adhesion molecules


4. How are these related to vesicular fusion with different membranous compartments?


1. Describe how some molecules transport targets one side of the cell and others target the opposite side.

2. What is the difference in endocytosis and exocytosis?

3. What is the difference in constitutive and regulative secretion?

4. How is secretion and vesicular transport important in nerve transmission of impulse?

5. What kinds of motors and cytoskeletal elements are involved- give specific examples in cells.


What do we mean by:

1. Heavy and light chains:

2. constant and variable regions.

3. different heavy chains for 5 types




7. helper T cells


9. clonal selection theory



What kinds of factors can influence filament formation of myosin? Where is the presence of bipolar filaments of myosin important for function? How can myosin stabilize actin filaments?

What is the difference between myosin I and II?

What kinds of actin structures are present in microvilli or stereocilia of ears? How does the acrosome filament form in sea urchins? How are actin filaments important to fertilization in both sperm and eggs in sea urchins?

What are the subunits of microtubules? What are MAPS? How can MAPS control assembly or disassembly of MT? What is the difference between + and - ends of MT? What kinds of things influence + end, - end? What is the effect of Ca++ on MT, and does that involve calmodulin; effect of cold on MT? How does EDTA influence this? Make a chart of control proteins for MT like we had for Microfilaments. What is the difference between control proteins for cilia and flagella and for spindle and vesicular transport (this will be on second midterm)?

What do we mean by motor protein? Is the sliding filament model for MT movement, just interaction of MT, or are there other proteins involved as we saw with myosin and actin sliding?

Does endocytosis or secretion ddepend on cytoskeletal events? Are there cases where MT of tubulin act as skeletal elements or stabilizers as do stress fibers of actin?

What is the significance of having families of genes for actin, myosin, tubulin present in cells? Could there be domains for control or binding of control proteins specific for different functions?

Is MT motion important in amoeboid movement, and how do you know? Is actin and myosin important in spindle movement, and how do you know?


nexin between adjacent doublets

tektin on alpha subunits of doublets, help form shared wall

spokes extend to inner sheath

sheath projections from central pair to spokes

tubulin acetyl transferase modifies amino acids- acetylates lysine in assembled flagellum, another enzyme does opposite

detyrosinating enzyme removes terminal tyrosine, cell cytoplasm, works on assembled MT another enzyme does opposite

HMW MAPS bind along entire length, many phosphorylated.

MAP 1 axons and dendrites

MAP 2 only dendrites

both form crossbridges between MT and also InterFil

TAU -low MW ". MT form thick bundles. In nerve.



dynein extend between doublets moves to - end


kinesin drives outward to + end