More specifically, SOD1 activates a MAPK pathway which results in hyperphosphorylation and in turn, inhibits its ability to facilitate anterograde transport (Fig 1). Normally, mitochondria are recruited for transport via the adaptor protein Milton which also binds the Miro protein discussed above - allowing calcium dependent binding of the mitochondria to kinesin. In wild type neurons, influxes of calcium allow Miro to bind to kinesin without the help of Milton, preventing axonal transport and keeping the mitochondria in place in areas requiring high energy needs. However, in the presence of mSOD1, the increased membrane permeability due to degeneration leads to an unneeded influx of calcium, as stated earlier, which then facilitates the Milton/Miro pathway, preventing mitochondrial anterograde movement, even when other areas of the neuron require energy. On the other hand, the specifics of mSOD1’s inhibition of the retrograde transport of mitochondria remain murky, although it has been postulated that the protein somehow interacts with the dynein-dynactin complex to prevent transport. In addition to all of this, mutant SOD1 proteins tend to form aggregates on the microtubules of mitochondria, acting as physical barriers to axonal transport as well. In either case, a lack of mitochondrial transport to areas of high energy demand within the neuron such as synapses and nodes of Ranvier results in diminished neuronal functionality and eventual stress-induced apoptosis (Ping et al. 2010).
Through the Methods Project, I was able to learn how to decipher my own observations from the inferences that are made because of these observations coordinated with previous knowledge. Previously, I did not understand the concept that inferences were made through observations. I never put much thought into the topic, and mistakenly thought that observations made were one in the same as the inferences derived from observations. During the Methods project for our Results section, we had to exclusively point out the different observations that were made looking from our original figure to the replicate figure. It was only in the discussion section that I was to infer what exactly may have been different during the timing of the photos taken for the two figures. These inferences I made for my discussion section was a direct product of the differences I observed for my results section. This exercise was able to teach me how to grasp the concept of observations and inferences being different from one another.
ACD2 is a protein in cells that is used to regulate programmed cell death (PCD) in plants. ACD2 is activated when plant cells are under an environmental stress and are triggered to kill off certain cells. These cells may include those that are infected with a pathogen, for example. In the absence of ACD2, the plant would be molecularly triggered to kill off those cells and other cells that the pathogen may have spread to. This would lead to the plant rapidly killing off numerous cells and it would start to phenotypically die, becoming yellow and wilted. ACD2 works as a regulator to slow down the process of PCD and only kill of those cells that are absolutely necessary in order to ensure the plants survival and acclimation. ACD2 is triggered by the breakdown of chlorophyll and works to eliminate the free radicals generated by the active light-dependant processes that chlorophyll breakdown product produces.
The overall methodlogical approach of this study was to place mice in different contexts and measure their fear response. Mice respond to fearful situations by freezing. This is a measurable behavior, since mice cannot verbally communicate that they are afraid. One aspect of emotion is that it is filtered through emotional expression. They are using an emotional response, a fear memory. In this case the fear memory is the room that the mice were shocked in. In this case the researchers used the protien c-fos. When neurons are really active they turn on c-fos. The researchers make use of c-fos by putting the promoter for c-fos downstream of the promoter. For th two contexts they had mice in room A. Room A is essentially a chamber with no smells. Context B is room B. This chamber is similar to room A but it has different color walls, different scents, ect. They let the mice explore room A. Then they let the mice explore room B. In room B the mice are shocked. The researchers turn on the neurons using c-fos when they put the mice back in room A. They can then measure the mouses response. This way they can ask if the mice remember being in room B. This is synthetic because they are forcing neurons to be on when they normally wouldn't be. In this way they are able to ask what does the mouse remember?
Some of the weaknesses of this study include the small sample size of patients, the variability in amputated limbs such as the arm and the leg, and the different times of amputation. Some of the amputees had their arm or leg amputated much more recently than others. All of these variables could lead to significant differences in their results. The results however, do seem valid since the results showed that the patients with phantom limb pain had areas in their thalamus that remained active while those that didn’t feel anything had that area rearranged; the results showed a general trend among all of the patients.
Genetics Update Terminology
Genome - The total genetic content contained in a haploid set of chromosomes in eukaryotes, in a single chromosome in bacteria, or in the DNA or RNA of viruses.
Promoter - a region of DNA that initiates transcription of a particular gene.
Transcription Factor - In molecular biology and genetics, a transcription factor (sometimes called a sequence-specific DNA-binding factor) is a protein that binds to specific DNA sequences, thereby controlling the movement(or transcription) of genetic information from DNA to mRNA.
5’ and 3’ UTR’s - 5’ can contain elements for controlling gene expression by way of regulatory elements. 3’ the section of messenger RNA (mRNA) that immediately follows the translation termination codon.
Exon - any nucleotide sequence encoded by a gene that remains present within the final mature RNA product of that gene after introns have been removed by RNA splicing
Introns - any nucleotide sequence within a gene that is removed by RNA splicing while the final mature RNA product of a gene is being generated.[
Splicesome - a complex of snRNA and protein subunits that removes introns from a transcribed pre-mRNA (hnRNA) segment. This process is generally referred to as splicing.
shRNA - A small hairpin RNA or short hairpin RNA (shRNA) is a sequence of RNA that makes a tight hairpin turn that can be used to silence target gene expression via RNA interference (RNAi)
siRNA - Small interfering RNA (siRNA), sometimes known as short interfering RNA or silencing RNA, is a class of double-stranded RNA molecules, 20-25 base pairs in length. siRNA plays many roles, but its most notable is in the RNA interference (RNAi) pathway, where it interferes with the expression of specific genes with complementary nucleotide sequence.
sncRNA - a functional RNA molecule that is not translated into a protein. the term “small” typically refers to short bacterial ncRNAs
lncRNA - similar to sncRNA, as it doesnt contain coding for proteins, only these are large and in eukaryotes
RISC - The RNA-induced silencing complex, or RISC, is a multiprotein complex that incorporates one strand of a small interfering RNA (siRNA) or microRNA (miRNA). RISC uses the siRNA or miRNA as a template for recognizing complementary mRNA.
Gene silencing - a general term describing epigenetic processes of gene regulation. The term gene silencing is generally used to describe the "switching off" of a gene by a mechanism other than genetic modification.
Genetic “Dimmer” mechanism - The gene Foxp2 acts like a "genetic dimmer switch" that regulates wiring in the developing brain. It does this by controlling the products of other genes, resulting in changes in the length and number of connections between brain cells
What are the advantages and disadvantages of using wood for biomass fuel?
A. What is Biomass fuel?
1. fuel that came from organic materials, a renewable source of energy used to create e electricity or other forms of power
2. a renewable source of fuel because waste residue will always exist
B. Why is wood a good biomass fuel source?
1. wood is a renewable source, so there is a dependable, sustainable amount
2. the amount of carbon produced while burning wood is 90% less than fossil fuel
3. wood has very tiny amounts of metal and sulfur
4. not a threat to acid rain and particulate emissions can be handled
5. economically wood costs significantly less than competing fossil fuels
The experimenters showed that in patients with phantom sensations, there is a thalamic representation of that missing limb that continues to be active thus causing the sensations and pain felt in the missing limb. Another conclusion is that the loss of the limb caused the thalamic representation of the stump to expand (in some patients more than others). Yes, the conclusions follow logically from the design of the experiment and the results. They tested for receptive fields and then looked at the projected fields and noticed mismatches.