Lamprey genome may lead to cures for human diseases

Print More

By CELESTE BOTT
Capital News Service
LANSING – Genetic mapping of sea lamprey may lead to ways to control the invader and improve human health, new research suggests.
A team of scientists has assembled the sea lamprey genome, providing insight into how to control the invasive species that has terrorized the Great Lakes basin since the late 1800s.
That same research could help cure a rare disease in human newborns and further the study of degenerative brain disease.

Photo credit: Michigan State University

Photo credit: Michigan State University


Researchers said that decoding the lamprey’s DNA has revealed genetic factors that enable it to survive and thrive in the Great Lakes.

In addition to the invasive species, two types of lamprey are native to the Great Lakes – silver lamprey and American brook lamprey.
“The American brook isn’t harmful to fish, but the silver is parasitic,” said Marc Gaden, communications director of the Great Lakes Fishery Commission in Ann Arbor. “As far as we know, there’s no genetic difference – one simply has the bloodsucking mouth and one doesn’t.
“But can you modify the genes so that the lamprey never transforms from nonlethal larvae?”
There’s no definitive answer, but 59 researchers, led by Michigan State University’s Weiming Li, may find out now that they’ve mapped the sea lamprey genome.
Sea lamprey – unlike the silver and American brook species – come from the Atlantic Ocean, accidentally introduced to the Great Lakes through shipping canals.
Like the native silver lamprey, sea lamprey are parasitic, with sharp teeth and a sucking disc mouth that allows them to feed on the blood of host fish. Also like the silver lamprey, they are harmless in their early stages of development.
Sea lamprey spend the first four years of their life as larvae in the soft bottom and banks of lakes or streams, according to the New York Department of Environmental Conservation.
During its life as a parasite, each sea lamprey can kill more than 40 pounds of fish. Aggressive sea lampreys prey on all species of large Great Lakes fish, including lake trout, salmon, rainbow trout, whitefish, chubs, burbot, walleye, catfish and even sturgeon.
As they mature, they change into the harmful predator threatening the Great Lakes today, said Yu-Wen Chung-Davidson, a senior research associate on Li’s team.
Scientists hope the genome project will prove useful in preventing that transformation from harmless to harmful.
“If you have all of the genome, then you can figure out the factors that control reproduction and growth – you can control their life cycles,” Chung-Davidson said. “If you can block the transformation to the harmful stage, then you can block the process.”
Research on the horizon may also include a cure for biliary atresia, a rare disease in which human newborns are born without a bile duct, which eventually causes liver failure.
“Sea lamprey that transform from larvae to parasites lose their gall bladder and bile ducts,” Chung-Davidson said. “They develop an alternative mechanism in which their intestine starts producing bile salts instead, making healthy digestion possible.
“It’s a long shot,” she acknowledged. “But our genetic understanding of this in the lamprey might help. Maybe we can help find a cure for the biliary atresia.”
Scientists at the Marine Biological Laboratory in Massachusetts, who are contributing to the project, have discovered that lampreys – unlike humans – don’t have myelin, an insulating sheath around neurons that allows faster conduction of nerve impulses.
However, the same myelin-associated molecules that inhibit damaged nerves from regenerating in humans were found in the sea lamprey genome.
Jennifer Morgan, one of the marine lab researchers, said that discovery could open the door for better understanding of human spinal cord injury and neurological diseases such as Alzheimer’s and Parkinson’s.
“There is an interesting conundrum,” Morgan said. “What are these myelin-associated genes doing in an animal that doesn’t have myelin, and yet is good at regeneration? It opens up a new and interesting set of questions.
“Addressing them could bring insight to why humans lost the capacity for neural regeneration long ago, and how it might be restored,” she said.
Morgan also said that the structure of lamprey nerves allowed for easier disease research.
“In addition to finding genes linked to human neurodegenerative disorders, we found that they also have large nerve cells, so you can see and study them in a basic microscope,” she said. “That helps our research. We can go in and microinject different experimental drugs.
“Lamprey also express myelin-related inhibitors that work to block the process of regeneration in mammals,” Morgan said. “Vertebrates that can regenerate – like the lamprey – grow a bridge across the injury site that provides a path for nerves to follow. In humans, the nervous system responds by forming more of a barrier than a bridge, destroying tissue and leaving a scar.”
Morgan and her fellow researchers severed the spinal cord of sea lamprey and observed its recovery over time, discovering that the lamprey could swim perfectly in 10-12 weeks.
“Here is a vertebrate that can undergo the worst spinal cord injury possible, but while a person will likely be in a wheelchair permanently, the lamprey moves fine in a couple of months,” she said.
As the project’s scientists continue with new research opportunities, the Great Lakes Fishery Commission, which helped pay for Li’s work with the genome, continues to control the invasive lamprey with pesticide.
“But we need better, cheaper and more effective ways to do so,” Gaden said. “Understanding the genome will help unlock weaknesses and manipulate the population.”

Comments are closed.