Student Research at Duke

So, like I said earlier, I spent the entire first week getting acquainted with the lab setting. We handled the mice, we toured the different labs, we shadowed various researchers and asked questions, but we didn’t really get started on our project until this past week. (I say we because, lucky for me, I am working with another undergrad, Chase, who is at Duke for the summer in the Mechanisms of Behavior program. And I can honestly say that it is really nice to have someone to work with during those long hours spent in Mouse Room 5.) Anyway, one thing I have found out about research is that it doesn’t work around your schedule. For example, we are testing our mice during both the light and dark cycle in case there is a problem with their circadian rhythms. The light cycle has been modified for us so that we aren’t there past midnight, but it isn’t perfect. The lights go off at three o’clock every day and we give them an hour to adjust to the “night,” the result being that we don’t begin dark testing until four each day. Then there is the fact that we need to test them for three consecutive days as they habituate to the activity boxes, which brings us in to work at nine o’clock on a Saturday morning. At the same time, we do get a lot of down time in between trials and it is during these breaks that I’m able to not only catch up on reading Molecular Biology of the Cell (an incredibly heavy 1616 page book lent to me by Dr. West describing in detail everything I could ever want to know about transcription factors and much, much more!) but I also have time to think about what my ultimate goal is for this summer.

So what question am I trying to answer? Specifically, I want to find out if there is any significant difference between the behavior of the CaRF knockout mice and that of normal mice. But what does that really mean? Well, it means that there is a protein called CaRF that has been found to bind specifically to the DNA sequence of Brain-derived neurotrophic factor. (BDNF is an activity-dependent protein that has many important functions, perhaps the most important of which is promoting brain cell survival). By binding to the BDNF gene, CaRF helps to “turn on” the expression of BDNF. However, if that were the end of the story, we would have noticed a much more drastic change in the knockout mice; in fact, there probably would have been a very high mortality rate if CaRF were the only protein able to promote BDNF transcription. What this implies is that not only is CaRF one of multiple transcription factors, but that in the absence of CaRF, another transcription factor completely takes over its role. This functional substitution is an example of redundancy, a concept crucial to the evolution and survival of species. It can be seen all throughout all forms of life where nature has delegated the same job to two separate systems so that in the event of a failure, homeostatic balance is preserved. Perhaps this is why, although we are hoping to find a significant difference in our mice, it would not be so devastating to find concrete evidence of normality after weeks of testing (although I’m still keeping my fingers crossed for something a bit more exciting!)

This entry was posted on Monday, June 18th, 2007 at 11:19 pm and is filed under My Project, Experience in the Lab. You can follow any responses to this entry through the RSS 2.0 feed. Responses are currently closed, but you can trackback from your own site.