Scientist Profile – Professor Juan Fuxman Bass
The Fuxman Bass Lab studies how viruses and their human hosts can regulate each other’s genes
Juan Fuxman Bass, Ph.D. – Associate Professor of Biology
The Fuxman Bass Lab aims to uncover new insights into gene regulation by studying how viruses impact the activation of genes in their human host—and how the host, in turn, impacts genetic expression in the virus. The research could lead to a better understanding and treatment of many diseases including cancer.
Professor Juan Fuxman Bass (Biological Design Center) talked about his research and how fascinatingly strategic viruses can be in terms of gene regulation. He also shared a source of particular fatherly pride as well as his joy of experimental cooking.
How would you describe your research and the goals of your lab?
My lab studies how genes are regulated, or how they are turned on and off under different conditions. One way to think about it is that each gene has multiple switches, and different switches can turn on different lights (genes), and what we want to know is which switches turn on which lights.
My team focuses on these molecular switches, called transcription factors, investigating what they regulate and how. “Transcription factors” are proteins that control the rate of genetic information from DNA to messenger RNA, and humans encode for approximately 1,600 of them. Some of these factors are expressed in specific cell types and tissues, some in specific developmental stages. Some factors are only active under specific conditions like when there’s oxidative stress or an infection. Some factors are active only when certain cells are interacting or communicating with other cells, sending signals to the nucleus about the intracellular and extracellular environment to determine what precise response is needed.
More specifically, my lab studies how genes are regulated in the human immune system, how genes are regulated in cancer or dysregulated in cancer, and how mutations affect the regulation of those genes. We have some projects in development concerning gene regulation in early embryo cell fate specification. We also have projects focusing on viral regulation, in particular what happens when you have a viral genome together with a host genome in infected cells, each with their own sets of regulators (or “switches”) because one thing that can happen is that a switch from the virus can turn on a gene from the human host, and vice versa. We study how the viruses benefit from that process to self-replicate as well as to evade the host’s immune system.
Can you describe a specific project in this line of research?
One of our projects involves finding the regions that control the expression of different viral genes across viruses that infect humans, then identifying the regulators for those regions. For instance, some viruses like the herpes virus can remain latent for long periods after infecting the host cells. At some point, however, these viruses must decide, “Well, I need to get out of here, I need to infect other cells or infect other hosts.” So how do they know when to do that? Making a timely and well-informed decision is vital for the virus, because if they express genes at the wrong time they may not be able to replicate effectively. Expressing viral genes at the wrong time may even signal to the host that the cell is infected, thus triggering the immune system to kill the cells and the virus along with it.
In other words, viruses must be very strategic. Part of how they make their decision involves sensing their cellular environment, but the challenge for them is that viruses have very small genomes, so they can’t encode for a large variety of sensors. It turns out, one fascinating way they can leverage their environment is to recruit human factors that sense specific cellular states. The viruses then exploit those recruited human sensors to inform their decisions on whether and when to express their own genes.
What we want to know is which viral genes sense which signals, and how does that relate to a latent virus’ reactivation? For example, if the host gets some type of infection that is somehow advantageous to the virus (e.g. because it weakens the host’s immune defenses) you may get reactivation. Other potential factors include hormones, vitamins, certain drugs, all of which can potentially affect regulators and modulate viral gene expression.
Did you always want to be a scientist?
Even as a child I was very interested in science. I can remember reading physics books when I was nine years old. Around that age I also took an interest in paleontology and astronomy. There was a time in school when I was primarily pursuing mathematics, but I switched to biology in part because the results of the research seemed more tangible.
What do you like about working at Boston University?
It’s such a collegial environment. Colleagues are happy when you do well. I appreciate being able to work with people that I’m happy to see every day. We also have very talented and motivated students.
What is a fact about you that surprises people?
People are often surprised to learn that I have a daughter who is old enough to be in her fourth year of medical school. It might be slightly less surprising lately, now that I have some gray hair in my beard, but I had my only daughter when I was just 20 years old—at the time I was still an undergraduate. She studies medicine at the University of Buenos Aires in Argentina (where I’m originally from) which means she has another three or four years to go since in Argentina you begin medical school as an undergraduate.
What are your hobbies outside of the lab?
I like hiking and painting—I wish I was able to paint more often. I also like cooking, and I don’t follow recipes. Sometimes I’m in the mood to eat something I can’t find at any restaurant, and at those times it can be fun to create a fusion-style dish. I recently made a dish that combined empanadas, a traditionally Latin dish, with a French-style stew called Bœuf Bourguignon, and I think it came out very well!
Interview conducted and edited by Jim Cooney.