If you've seen differences in the distribution of phenotypes in Tm4 over-expressing B35 cells versus control B35 cells, describe these differences. Formulate a hypothesis with regards to what changes on the molecular level may have occurred due to the over-expression of Tm4 that lead to morphological changes that you have observed Lab 6 - Cytoskeletal Exercise
- I opted to count the number of primary nuerites projecting from the nucleus-associated compartment. I defined a primary neurite as neurite whos origin is from the nuclear associated compartment only and not shared with that of another neurite/projection. Ie: Neurites in a branched conformation or with poorly defined basal decrimination were counted as being one neurite only.
Although my exact data set was lost/handed in with other Lab work it was observed that the median number of primary neurites between phenotype groups A and B was signifcantly different (I didn't get time to work out the mean before the dataset was lost)
- Median primary neurite number; A=3(40% of dataset) B=2(39% of dataset)
- Hypothesis: without knowing the identities of the control b35 and Tm4 OE's it is difficult to formulate an explaination as to whether Tm4 overexpression results in an increased or decreased neurite number but the data is suggestive that mannipulation of Tropomyosin(4) expression may result in a tendency of cells to form semi-differentiated dentritic-type structures (or not do so).
Mark, more information would be useful to better formulate a response in this section(help!?)
Intermediate filaments Lecture
The layer between the straum basale and granulosum is the stratum spinosum. This layer is dense in intermediate filament bundles and adhesion junctions/desmosomes. The structure of this layer imparts a flexible yet strong mesh-work to the comparatively brittle hardened keratin layer above it. Thus the spinosum layer imparts an equivlent of elastic strength to the epidermal structure.
'Though I didnt find the exocytosis lecture particularly difficult the funtional duality of the smooth and rough ER regions is interesting... Although both are within the same functional membranous compartment they are treated as two distinct structures- not merely to specialised portions of a larger whole. My question would then be is there any overlap between the function regions? Ie: is it possible to have both lipolysis and glycosylation in proximity to eachother? if so, what is the restrictive factor preventing enzymes/substrates from straying from thier respective functional compartments. (i can fathom that the enzymes are likely protein bound much like the ribsomes, what of the substrates? is there a membrane-bound carier protein involved?)
Lecture 4 - Nucleus
I found "Protein Postcodes" to be an interesting concept; in order for proteins to reach their appropriate sites for post-translational changes to occur, the mRNA is first translated by cytoplasmic ribosomes. The initial amino sequence determines whether the mRNA-Amino-ribsomal complex remains in the cytoplasm or is translocated and becomes fixed in the Rough ER. Normal translation occurs from here using local ribosomes(be they cytoplasmic or reticular) and, in the case of ER translation, Peptide products are ejected from complex into the ER lumen for further post-translational modification.
Cell Adhesion Lecture
- I-CAMs are intracellular adhesion molecules
- N-CAMs are neural cell adhesion molecules
- Ng-CAMs are Neurone glia cell adhesion molecules
- L-CAMs are liver Cell adhesion molecules
Cellular processes requiring increased mitochondrial number;
- Electron transport Chain/oxphos
- Citric Acid Cycle
- Heat generation in brown adipose tissues; "futile" electron transport processes
- Apoptotic functions
- Cellular metabolism regulation
- some calcium signaling
- many tissue-specific functions