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Researcher Seeks to Unravel the Mysteries of Mutant Genes









 
 

Researcher Seeks to Unravel the
Mysteries of Mutant Genes

Jason Morris, Ph.D., does genetic studies on Drosophila (a.k.a. the common fruit fly.)

Photo by Janet Sassi



“About three-quarters of human genes

that can cause disease when they are damaged

have a similar functioning gene,

or homologue, in the fly.”


 

By Janet Sassi

“Fried” and “Benedict” may bring to mind your weekend brunch menu.

Not so for Jason Morris, Ph.D., associate professor of biology.

Morris, one of three professors feted last month for his externally funded research, has a National Institutes of Health (NIH) grant to study two mutant fruit fly (Drosophila) genes through the flies’ lifecycles. Whoever thinks scientists have no sense of humor obviously hasn’t hung out with a fly researcher.

“In flies, the tradition is that you name your mutants based on what goes wrong in them, i.e., what is the phenotype,” said Morris, who works in the Department of Natural Sciences laboratories at the Lincoln Center campus. “Since these genes were all defective in making eggs, we named them after terrible things that happen to eggs. So we have ‘hard-boiled’ and ‘soft-boiled’ and ‘fried’ and ‘benedict’ and ‘poached.’

In fruit flies, Morris said, scientists only understand a small fraction of the genes essential for making eggs. He chose to study fried and benedict mutant flies, he said, because their eggs had unusual-looking chromosomes that suggested they had problems in the cell cycle.

“So it seemed like a fruitful (pardon the pun) area to study,” he said.

In a normal fruit fly, the life span is approximately one to two months. After hatching from eggs as larvae, the flies grow 200-fold in approximately five days. They then spend another five days as pupae, wrapped in cocoons, before they hatch into adulthood.

Because the ovary of an adult female fruit fly carries eggs at every stage of development, a scientist can open up one adult and see all the ways in which a gene is required for making eggs just by looking at the different defects in eggs at different stages in the mutant. Yet, scientists had never found benedict and fried mutants when they looked for genes that were defective in sterile females.

Morris discovered why: the genes actually interfere with adult development, so mutant fruit flies can never grow up. Instead, they languish in adolescence and then die.

Morris uncovered the role of benedict in making eggs when he engineered normal egg cells and benedict mutant egg cells to develop in the same ovary. While the normal eggs contained nice compact spheres of healthy DNA, the mutant eggs’ DNA was long and stringy, and the eggs were sickly and non-viable.

If no normal cells are present in a benedict mutant fly, said Morris, the mutant flies stop growing as larvae, three days after they are born, while the normal flies continue to grow very dramatically and become pupae on day five.

“The mutants actually arrest, but they don’t die,” Morris said. “They direct whatever energy they have toward survival behaviors rather than toward development. And that’s the really interesting problem. When resources are limited, what determines where you allocate them?”

In the case of the fruit flies, Morris said the mutants chose to grow their brains some and their salivary glands quite a bit, but they completely shunned the growth of their imaginal disks, which are pouches of cells used to make adult flys’ wings in the pupal stage.

“They seem to be allocating resources in a way that keeps only the larva growing, but they are not growing adult tissues,” said Morris, who said further experiments were needed to make a final determination.

While Morris confesses he finds fruit flies interesting in their own right, his NIH funding is specifically awarded to study genes for their potential applications for human health. While a fruit fly and a human being don’t look at all alike, on a genetic level, the two species share many links when it comes to disease.

About three-quarters of human genes that can cause disease when they are damaged have a similar functioning gene, or homologue, in the fly, Morris said. “So even though we are incredibly different, there is a closely related fly gene that carries out a similar function as our gene, and which is easier to study than a human gene.”

Morris said that there isn’t enough known about how the human body allocates resources when it is under some kind of stress, such as a lack of a certain nutrient or even starvation. He hopes his research on Drosophila may have some bearing.

Morris’ journey from dreaming of being a scientist to becoming one has been a “straight path.” The Long Island native was inspired to go into molecular biology when he attended a high school science camp at Cold Spring Harbor Laboratories. There, he altered the genes of simple bacteria, making them immune to antibiotics.

“You had to scrape me off the ceiling,” Morris said. “I couldn’t believe we’d changed the genes of this organism until the end of time, so that all of its progeny were going to be different. The power of it was so stunning that I knew I needed to be a geneticist.”

In addition to research, Morris applies his enormous enthusiasm toward inspiring undergraduates to pursue careers in science. He has mentored 19 Fordham students who have gone on to quality medical schools and to doctoral programs at some of the finest labs in the nation.

“Working with undergraduates is the most exciting part of what I do,” said Morris, who was this year’s recipient of Arts and Sciences Faculty Day’s undergraduate teaching award. “You can help them discover a passion they will savor for the rest of their lives, and that is incredibly rewarding.”

 


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