The mostly likely cause of this result was degradation of cDNA and PCR reagents at the time the gel was performed for the HU treated cells (as shown by the dimmer band when it should have been as bright as the untreated lane). Alternatively, the T. therm cells were extracted from different samples, so the untreated vs HU treated samples may have had significantly different cell concentrations that could have caused the band intensities to differ.
Because my gene was down regulated after DNA damage was induced, I could conduct an experiment in the future where Hymelc expression was purposefully unregulated in order to study its potential affects on different stages of DNA damage repair. Protein localization could also be done to study where Hymelc localizes in the cell when it is expressed and study its potential functions based on those results. Gene knock out would also be interesting to see how losing Hymelc expression entirely could affect cellular processes compared to the downregulation that occurred in this experiment.
You state that no further research should be done, is that because it is not involved at all in the pathway? What about gene knock-in and gene knock-out mechanisms?
No further research should be done in terms of Hymelc’s role in this part of the DNA damage response pathway. I made this conclusion after Hymelc was down regulated after DNA damage was induced. If Hymelc contributed to the DNA damage response pathway, its expression would have increased. That being said, other experiments like gene knock out could more definitively support this conclusion and possibly expose Hymelc’s function in other aspects of DNA damage repair (we only studied the initiation of DNA damage response, so Hymelc might be expressed later or under different types of DNA damage – double stranded vs single stranded breaks)
Nice job! Do you think your findings will have any implications in the field of medicine? Do you think hymelc is a good organism for studying and understanding DNA repair in other organisms?
Studying the DNA damage response pathway and any gene involved in it are crucial to understanding and developing treatments for neurodegenerative diseases and cancers that target this pathway. Although I don’t believe that Hymelc is one of those genes involved in this response pathway, my findings will help further narrow down the list of potential T. therm genes being studied in this pathway. Hymelc also could potentially be studied further to determine if it may have any alternative functions later on in the pathway or if it can modify other gene’s expression patterns. For the purposes of this class’s research, though, genes that were unregulated after DNA damage was induced are much better candidates for further study involving their role(s) in DNA damage response.
Why do you think ftt18 showed a decrease in expression?
The mostly likely cause of this result was degradation of cDNA and PCR reagents at the time the gel was performed for the HU treated cells (as shown by the dimmer band when it should have been as bright as the untreated lane). Alternatively, the T. therm cells were extracted from different samples, so the untreated vs HU treated samples may have had significantly different cell concentrations that could have caused the band intensities to differ.
What other experiments could be done to learn more about hymelc expression?
Because my gene was down regulated after DNA damage was induced, I could conduct an experiment in the future where Hymelc expression was purposefully unregulated in order to study its potential affects on different stages of DNA damage repair. Protein localization could also be done to study where Hymelc localizes in the cell when it is expressed and study its potential functions based on those results. Gene knock out would also be interesting to see how losing Hymelc expression entirely could affect cellular processes compared to the downregulation that occurred in this experiment.
You state that no further research should be done, is that because it is not involved at all in the pathway? What about gene knock-in and gene knock-out mechanisms?
No further research should be done in terms of Hymelc’s role in this part of the DNA damage response pathway. I made this conclusion after Hymelc was down regulated after DNA damage was induced. If Hymelc contributed to the DNA damage response pathway, its expression would have increased. That being said, other experiments like gene knock out could more definitively support this conclusion and possibly expose Hymelc’s function in other aspects of DNA damage repair (we only studied the initiation of DNA damage response, so Hymelc might be expressed later or under different types of DNA damage – double stranded vs single stranded breaks)
What do you think could be some of the benefits from doing the further research not related to DNA damage response?
Nice job! Do you think your findings will have any implications in the field of medicine? Do you think hymelc is a good organism for studying and understanding DNA repair in other organisms?
Studying the DNA damage response pathway and any gene involved in it are crucial to understanding and developing treatments for neurodegenerative diseases and cancers that target this pathway. Although I don’t believe that Hymelc is one of those genes involved in this response pathway, my findings will help further narrow down the list of potential T. therm genes being studied in this pathway. Hymelc also could potentially be studied further to determine if it may have any alternative functions later on in the pathway or if it can modify other gene’s expression patterns. For the purposes of this class’s research, though, genes that were unregulated after DNA damage was induced are much better candidates for further study involving their role(s) in DNA damage response.
What did you base your hypothesis off of and why do you think your results were inconsistent with the hypothesis?