David R. Benson, Ph.D., Professor of Microbiology, retired on June 1 after more than 40 years at UConn. Dr. Benson’s distinguished career includes service as Head of the Molecular and Cell Biology Department from 2007-2012. During that time, he oversaw the expansion of the department personnel, doubled undergraduate course enrollment, built administrative protocols and brought national visibility to MCB, and increased graduate student recruitment. Dr. Benson’s guidance encouraged department members to participate in public and community outreach thereby highlighting awareness of the department.

Friend and colleague, Dr. Peter Gogarten describes Benson as “an encouraging mentor, advisor and co-advisor, an effective cheerleader for students, colleagues, and the department.” As colleagues mutually interested in the use of anciently duplicated genes in unraveling the early history of life, Gogarten says, “Our collaborations on the comparative genomics of Frankia strains, transposable elements, and the secretome of Frankia grown under different conditions launched several students onto successful scientific careers.”

Dr. Benson received his doctoral degree from Rutgers University in Microbiology and Biochemistry and did postdoctoral work at the University of Wisconsin, Madison in biochemistry before coming to UConn in 1980. Benson's research and teaching expertise are in the Microbial genomics, microbial biogeography and ecology, physiology and molecular biology of bacteria, symbiosis, psychrophile evolution, food microbiology, bio-security He is particularly interested in genomic and biochemical characteristics that align with the distribution of microorganisms in environments.

Dr. Benson served as a Jefferson Science Fellow to the U.S. Department of State from 2012-2017. As a Jefferson Fellow, he served as a Senior Science Advisor to the Biological Policy Staff in the Bureau of International Security and Non-proliferation. In addition, he is a Fellow of both the American Association for the Advancement of Science (AAAS) and the American Academy of Microbiology and was twice elected as the Chair and Councilor of the General Microbiology Division of the American Society for Microbiology and has served on the Editorial Board of the journal Applied and Environmental Microbiology. He has been elected to the Connecticut Academy of Arts and Sciences and served as visiting professor at the University of Waikato, New Zealand.

Dr. Michael Lynes, professor and current head of the Molecular and Cell Biology Department said, “I celebrate David’s career – for his achievements and the investments he made in other faculty and their success, his contributions to the scientific community in MCB, his teaching of content critical to our students, and for his role as a thoughtful and cheerful colleague.” Dr. Benson has been appointed by the UConn Board of Trustees as Professor Emeritus, Molecular and Cell Biology.

The following MCB employees have reached important milestones in their service to the state and the University. Though the celebration of these achievements will be delayed until all employees are back working in person on campus, it is important that we recognize and applaud their commitment and dedication to UConn and MCB. Thank you!

Celebrating 10 years - Colleen Spurling, Mark Longo

15 years - Craig Nelson, Elaine Mirkin, Victoria Robinson

20 years  -  Andrei Alexandrescu, Michael O’Neill

25 years - Carolyn Teschke

30 years - Michael Lynes, Johan Gogarten

35 years- Dana Masse

Researchers Explore Potential Treatment for Mitochondrial Diseases

UConn researchers are studying a group of compounds that could protect mitochondria in ways that might prevent devastating illnesses like muscular dystrophy and ALS.

Huntington’s. Parkinson’s. Muscular dystrophy. Lou Gehrig’s. These diseases share a common cause that devastatingly robs sufferers of their energy, muscle control, and in the case of Huntington’s, their sanity. But now, a group of researchers from UConn describes how a possible therapy might work.

What all those fearsome diseases have in common is dysfunctional mitochondria. Mitochondria are the body’s tiny power plants. These minuscule, rod-shaped structures inside our cells take in oxygen and nutrients and put out ATP, the body’s fuel (ATP is to cells what gasoline is to cars.) When mitochondria don’t work so well, the dysfunction can cause strange and awful symptoms that are particularly distressing in parts of the body that require lots of energy: particularly muscles, the brain, and nerve tissue.

Mitochondrial diseases tend to worsen with age. Scientists have guessed that mitochondria age as the rest of our body does. Damage acquired over time may contribute to mitochondrial diseases, but they aren’t entirely sure what’s happening or how to stop it.

“They’re insidious diseases because they rob your cells of their energy. They’re so hard to diagnose and the symptoms can be so diverse,” says Nathan Alder, a molecular biophysicist in the Department of Molecular and Cell Biology at UConn.

Alder and other researchers from UConn, the University of Texas, and Alexandria LaunchLabs are researching a group of compounds that seem to protect and even repair damage to mitochondria. The researchers describe the compounds, called SS peptides, and one potential way they may work to heal mitochondria in an upcoming issue of the Journal of Biological Chemistry.

SS peptides are made of amino acids, the building blocks of proteins, but each SS peptide is only four amino acids long. They all have the same basic plan: two amino acids with a positive charge alternating with two aromatic amino acids (“aromatic” is a chemistry term meaning they have a ring-like structure similar to benzene).

Previous research by Hazel Szeto at Cornell University, who first described SS peptides and served as co-author on this study, showed that SS peptides can enter into any cell in the body, and mitochondria suck them up like sponges. Alder and his colleagues wanted to figure out what the peptides were doing when they got in there. Using approaches ranging from computer modeling to studying mitochondria in the lab, they began to see the peptides’ effects. It looks like they can alter and potentially repair mitochondria by tuning the electric properties of their membranes.

Mitochondrial membranes are intricately creviced double-layers of fatty molecules called lipids that surround proteins sticking out of the membrane itself. The outer layer of the membrane “talks” to the rest of the cell, sensing conditions and passing ATP and other molecules back and forth. The labyrinthine inner layer of the membrane holds the ATP factories. One of the special lipids enriched in the inner membrane, cardiolipin, has a strong affinity for SS peptides.

Mitochondria tend to accumulate positively charged things like calcium ions—mitochondria actually serve as storage centers for cellular calcium. Yet calcium overload can cause damage to mitochondria’s cardiolipin-containing membranes over time, ripping into the membrane and causing permanent damage.

SS peptides can prevent that from happening, Alder and his colleagues found. The peptides are positively charged but in a gentler way than calcium; they snuggle up against the mitochondrial membrane and shield it from the smaller, more damaging calcium ions.

“This is probably not the only effect of SS peptides. But it’s an interesting one,” Alder says. The researchers want to understand more about how the peptides interact with the mitochondria and why they appear to have such broad-based efficacy against so many mitochondrial disorders. The team is currently using UConn’s nuclear magnetic resonance facilities to get detailed pictures of SS peptide structural features and how the peptides might alter or maintain the shape of the mitochondrial membranes. “We know they work. We want to know how they work. By understanding the mechanism of action, we can engineer more effective peptide analogs and possibly tailor them to treat specific mitochondrial afflictions,” Alder says.

Article in UConn Today