Student Blogs

Epigenetics. When I first heard the word, I was reminded of biology class in my freshman year of high school. Although my class was unable to fully explore epigenetics, my main takeaway was that our DNA is affected by our lifestyles and environments. What we eat, the pollution we breathe in, where we live -- that all affects our DNA in some way.  

However, through my CIRM program experience, I have uncovered a whole new side to epigenetics. Instead of focusing on factors outside the human body, I am now studying chemical changes that affect DNA from inside the human body. 

This summer, I have been working in the Nuñez lab, which studies epigenetics. For my project, I am studying Methyl-Cpg-Binding-Domain Protein 3, also known as MBD3. This protein is part of the MBD nuclear protein family (proteins found within the nucleus). MBD3 is the smallest protein in the family, making it an attractive choice for epigenetic editing. 

When it comes to engineering new technologies to modify the genome, the primary issue is size. Cells are small, so whatever is being used to edit DNA needs to be even smaller. Our goal is to modify the epigenome with MBD3, so we are forming five DNA fragments that contain varying MBD3 regions. We want to determine where exactly in the MBD3 region does transcriptional repression occur.  

Before this summer, I was nervous about working in a wet lab for the first time. But with the support of the Nuñez lab, I have learned so much in terms of new material and techniques. From DNA methylation (adding a methyl group  to DNA in the form of a “tag”) to the centrifuge (a machine that utilizes centrifugal force to separate different parts of a liquid), this experience has continued to increase my love for science. Furthermore, I have discovered that science is not linear. When conducting experiments, I may not always get the result that I want. But, I know that I have to keep trying. 

I have always loved science, specifically biology, but I have never been given an opportunity to delve deep into it before CIRM. The program includes weekly lectures that touch upon new scientific breakthroughs, daily lives of various individuals in medicine and science, and more. CHORI SSRP and CIRM have allowed me to venture beyond the boundaries of what I previously thought was possible with science. 

For any other high school students who are nervous for their first laboratory research experience, I have some advice to offer. First, don’t be afraid to ask questions. Everyone around you wants to support you! Second, label everything. Always make sure to label all of your tubes, plates, etc. so you know what you’re working with. Third, never stop writing notes, either in your lab notebook or somewhere else. For some of the experiments you will do, such as PCR amplification, you will most likely need to do them again in the future. My lab notebook contains all the procedures for the experiments I have conducted and I constantly refer back to those pages. Fourth, read, read, read! Look up scientific papers that go into detail about what topic you’re studying. Fifth, take some time to soak it all in. This is a special opportunity, but it may be overwhelming at times. You should take a moment to relax and to realize how lucky you are to work in a professional lab!

Being part of the CHORI SSRP and CIRM program has allowed me to explore the wonderful world of cells. I am excited to see where this research takes me!

As an alumni applying to the SSRP, I wanted to experience something new this summer and to challenge myself. Last year, the programming was online and I learned the ways of research all through my computer. This year, I was fortunately able to experience what it is like to be in an actual lab!

My research project is centered around neural stem cells. Before this, I had no idea what stem cells were. After attending a workshop, I was fascinated to find that stem cells have the ability to either renew themselves or become specialized cells that have specific functions. This unique ability is a promising area of research because of the potential of stem cells to replace damaged cells in order to treat many diseases that we don’t have cures for today.

In the adult central nervous system, neural stem cells are found in different locations (or niches) in the brain. My project is part of a bigger research project which seeks to figure out how cell-to-cell communication in aging neurogenic niches affects neural stem cell fate decisions. As we age, there’s a decrease in neurogenesis which is the production of neurons. This leads to a decline in cognitive abilities such as learning and memory, as well as weakened repair of damaged tissue. Two causes for reduced neural stem cell neurogenesis with age are the decrease of the neural stem cell pool from cells increasing their asymmetric divisions, and the transition of neural stem cells into an inactive state. To see how neural stem cells’ function and behavior change as the niche ages, I will recreate the subventricular zone niche in vitro. Results of this project will aid in the research of the niche's control of neurogenesis in the adult brain, and why cells go dormant and how to induce proliferation. Overall, this has the potential to help in the development of therapies for neurodegenerative diseases in the future.

As we all know, the mitochondria are powerhouses of the cell, providing energy in the form of ATP. But what happens when the instructions, or DNA, in the powerhouse are disrupted, and subsequently, proteins are not able to function correctly? Mutations in mitochondrial DNA (mtDNA) can cause mitochondrial disease and each year about 1 in 4,000 children in the United States are born with a mitochondrial disease caused by mtDNA mutations. Not only can mtDNA mutations cause mitochondrial disease, but they are also linked to cancer, cardiovascular diseases, and neurodegenerative disorders. Mitochondrial DNA (mtDNA) research is a relatively new field of study, and for the first time in 1963 researchers Marget and Sylvan Nass discovered DNA fibers outside of the nucleus and in mitochondria. 

At the Lewis Lab at the University of California Berkeley, we are working with the nematode Caenrohabditis elegans in order to unlock the mysteries of mitochondrial DNA. Specifically we are looking at C. elegans with a deletion in the mtss-1 gene, that codes for the mtss-1 protein. This protein is involved in keeping single stranded DNA separated and preparing the DNA for adding the new complementary strand during replication, and is preserved in humans as the SSBP1 gene and protein. C. elegans are a great model organism for this mutation accumulation experiment because it is able to reproduce in about 3 days enabling us to rapidly observe the different generations. 

For our project, we are specifically comparing C. elegans with a perturbed mtss-1 gene in order to determine if more random mutations arise in the mutant C. elegans compared to non-mutated, also known as wild type C. elegans. We will observe both groups over 10 generations, and transfer C. elegans onto new seeded plates in order to keep all lines in parallel, and allow for spontaneous mutations to accumulate with minimal natural selection. After 10 generations, we will perform PCR on both the control and mutant worms, observe the deletions during gel electrophoresis, and send the information for sequencing to determine the specific deletions. In addition, we will also be comparing the C. elegans brood size or number of offspring they produce in both the control and mutant worms, as well as image the C. elegans to observe if the location of mitochondria, and shape of mitochondria changed in the mutant types. 

Understanding the mitochondrial DNA mutations that arise in C. elegans is extremely important because it will help us understand how mitochondrial diseases arise in humans with the same deletions. With further research on mtDNA mutations, we can develop a refined list of targets for the development of mitochondrial disease therapeutics, and drugs that target the protein product of the mtss-1 gene and its human homolog SSBP1.