Discussion
Based on the results recorded, it is fair to say that the hypothesis was partially supported. Both the methylene blue and phalloidin stains showed how there are distinct morphological changes between the untreated and treated cells. This part of the hypothesis was fully supported by the data collected.
Although there were distinct morphological changes between the treated and untreated cells, there was not a distinct change between the amount of GFAP and β-Tubulin between the cells. It was expected that there would be none of the GFAP and β-Tubulin in the untreated cells and a significant amount of these proteins in the treated cells. This was expected because retinoic acid treatment forces a cell to differentiate and GFAP and β-Tubulin are indicative of a neuron. Because these proteins were found in both the treated and untreated cells, it is inferred that the aspect of gene expression related to protein production was ultimately unchanged in the treated cell because it did not mutate in a way that effected the production of the neuron specific proteins. Instead of the neuroblastoma having a lack of neuron specific proteins it contains roughly the same amount as the treated cells. The treated cells however experienced a higher active potential and a higher sodium spike which shows how the treated cells have more sodium ion pumps than the untreated cells. Even though both cells have the GFAP and β-Tubulin, which are responsible for a neurons ability to transfer electrical signals, the untreated cells were unable to do so as efficiently as the treated cells. This leads to the conclusion that the treated cells experienced a change in gene expression that allowed these sodium ion pumps to work more efficiently than those in the untreated counterparts.
This is more characteristic of a neuron which when coupled with the morphological changes makes it fair to conclude that there was a change in the cells treated with retinoic acid. Since the hypothesis is only partially supported it is important to understand the differences between the treated and untreated cells in terms of GFAP and β-Tubulin production. Both cells had about the same amount of these proteins that are specific to neurons. The most likely cause is that the proteins are present but not able to be used efficiently by the cells which is shown in the conductivity test. In the treated cells there is most likely a gene change that allows these cells to have a better active potential within the cell and also a better sodium spike which are both characteristics of a neuron.
Although there were distinct morphological changes between the treated and untreated cells, there was not a distinct change between the amount of GFAP and β-Tubulin between the cells. It was expected that there would be none of the GFAP and β-Tubulin in the untreated cells and a significant amount of these proteins in the treated cells. This was expected because retinoic acid treatment forces a cell to differentiate and GFAP and β-Tubulin are indicative of a neuron. Because these proteins were found in both the treated and untreated cells, it is inferred that the aspect of gene expression related to protein production was ultimately unchanged in the treated cell because it did not mutate in a way that effected the production of the neuron specific proteins. Instead of the neuroblastoma having a lack of neuron specific proteins it contains roughly the same amount as the treated cells. The treated cells however experienced a higher active potential and a higher sodium spike which shows how the treated cells have more sodium ion pumps than the untreated cells. Even though both cells have the GFAP and β-Tubulin, which are responsible for a neurons ability to transfer electrical signals, the untreated cells were unable to do so as efficiently as the treated cells. This leads to the conclusion that the treated cells experienced a change in gene expression that allowed these sodium ion pumps to work more efficiently than those in the untreated counterparts.
This is more characteristic of a neuron which when coupled with the morphological changes makes it fair to conclude that there was a change in the cells treated with retinoic acid. Since the hypothesis is only partially supported it is important to understand the differences between the treated and untreated cells in terms of GFAP and β-Tubulin production. Both cells had about the same amount of these proteins that are specific to neurons. The most likely cause is that the proteins are present but not able to be used efficiently by the cells which is shown in the conductivity test. In the treated cells there is most likely a gene change that allows these cells to have a better active potential within the cell and also a better sodium spike which are both characteristics of a neuron.