Published April 29, 2016
Evan Myers, a candidate in the physiology doctoral program, has been recognized by the American Physiological Society for his research in the area of blindness caused by dysregulated pH homeostasis in the cornea.
He received a Robert Gunn Student Award for his poster presentation at the 2016 Experimental Biology (EB2016) conference in San Diego. Myers is first author on the study.
Working in the lab of Mark D. Parker, PhD, assistant professor of physiology and biophysics, Myers was part of a team that discovered a new function of the membrane transport protein Slc4a11 that led it to propose a novel mechanism by which mutations in this gene can cause a type of blindness known as congenital hereditary endothelial dystrophy (CHED).
“In simple terms, CHED is associated with defective water movement in the cornea, and Evan has discovered a new molecular action for Slc4a11 that could explain why the water movement is disturbed in individuals with this disease,” says Parker, who holds a secondary appointment in ophthalmology.
Almost every Slc4 protein transports bicarbonate with the purpose of neutralizing acid as the body constantly struggles with dietary and metabolic acids to maintain a tightly regulated pH balance.
“The interesting thing Evan found is that the Slc4a11 protein doesn’t transport bicarbonate. Instead, when exposed to an alkaline environment, it transports protons, or pure acid,” Parker says.
One cause of blindness is endothelial dystrophy — a clouding of the cornea caused by excessive amounts of fluid accumulation.
“There is a transparent array of collagen fibrils in the corneal stroma at the front of the eye. Normally that protein acts almost like a sponge, drawing water from the fluid inside the eye,” Parker says.
Accumulation of that fluid in the stroma would disturb the regular array of collagen fibrils and cause them to scatter light. Thus, the stroma would become opaque and loss of vision would result.
“A layer of cells called endothelia at the back of the corneal stroma are constantly pumping water from the stroma to keep it properly hydrated and clear,” Parker says. “In individuals with CHED, and in mice with Slc4a11 mutations, these cells are inactive or absent.”
Slc4a11 is expressed in corneal endothelial cells. These cells express numerous pH-sensitive and acid-base transporting membrane proteins that contribute to the removal of fluid from the stroma.
“We hypothesize that when Slc4a11 senses an alkaline-disturbance in the vicinity of these transporters, it will open in response to the alkalinity and release protons to balance pH and keep the transporters that support fluid movement operational,” Parker says.
Myers says working with Parker has been a tremendous help to him because of the extensive one-on-one training he has received.
“We usually meet at the end of each week to discuss new data, future data and scientific papers relevant to our work,” he says. “I think it is this routine of hands-on science early in the week followed by lengthy discussions at the end that has helped me grow.”
Parker says Myers has demonstrated exceptional academic ability throughout his undergraduate and graduate training and continues to excel as a researcher in the fields of cellular and molecular physiology.
“Evan has demonstrated a passionate interest in the molecular mechanisms of homeostasis and an impressive technical ability that has enabled him to gather high quality data from day one,” he says.
Parker says the size of his lab at UB is a significant benefit to graduate students such as Myers.
“We have several talented undergraduate students in the lab, but Evan is the main focus,” he says.
To be considered for the award, Myers had to submit a poster abstract along with his curriculum vitae and a letter of recommendation four months before the EB2016 meeting.
He then received notice about a month prior to the conference that he had been selected as a finalist and was invited to present at a special poster session with 11 other finalists.
“I prepared myself by practicing with faculty and students around the lab,” he says. “Their input really helped me when it came time to present at the conference.”
The award is named in honor of Robert Gunn, MD, professor and former chair of the Physiology Department at Emory University Medical School, who died in 2005.
Parker notes that his lab’s current studies were influenced by Gunn’s pioneering work in studying anion and proton transport by the founding member of the Slc4 family, Slc4a1, in red blood cells.
Slc4a11 was the last of the family to be discovered, and in fact, Parker was part of the team of researchers that discovered it in 2001 in the laboratory of Michael Tanner, PhD, at the University of Bristol in England.
“Robert Gunn was working on the very first one to be discovered, and we are working on the very last one,” he says.
Parker is senior author on the study. Lab manager Aniko Marshall is also an author.