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2003

VICE PRESIDENT'S LETTER

CLARK FORK RIVER BASIN MAP

RIVER RESCUERS
UM'S NEW RIVERINE SCIENCE CENTER

POISONED HEARTS
ARSENIC EFFECTS ON CARDIOVASCULAR HEALTH

WATER WIZARDRY
BIO STATION'S NEW FLOOD PLAIN MODEL

RIVERS THAT TIME FORGOT
AN UNDISTURBED RUSSIAN WILDERNESS

SODIUM SOLUTIONS
COALBED METHANE IN EASTERN MONTANA

HEAVY METAL
SCIENTISTS STUDY IMPACT OF METALS ON MICROBES

COTTONWOOD CONUNDRUM
MONTANA'S DISAPPEARING RIVER TREES

WATER WARDENS
UM'S WATERSHED HEALTH CLINIC

TALLYING TADPOLES
STUDYING MONTANA AMPHIBIANS

FISH FINDERS
DNA IN WATER REVEALS LOCATION OF FISH

WET AND WILD
A PRIMER ON MONTANA AQUATIC LIFE

WATER THAT WAS
THE SECRETS OF GLACIAL LAKE MISSOULA

QUICK LOOKS

NEWS TO USE
THE WEIRD LIFE CYCLE OF SWIMMER'S ITCH

BACKTALK
GIARDIA: A WATER DRINKER'S GUT-WRENCHING SURPRISE

About Vision 2003

Of fish & human fertility

Professor Fred Allendorf
Professor Fred Allendorf

It seems UM researchers think racing might be the key that unlocks the
mystery of male infertility ... sperm racing, that is.

Professor Fred Allendorf, along with Neil Gemmell of the University of Canterbury in New Zealand, is taking a closer look at mutations on the cellular level that may lead to male infertility in fish, after recent research that suggests a certain type of mutation may be responsible for the same malady in human males. The work is being funded by a grant from the Royal Society of New Zealand.

The suspected mutations occur in the mitochondria — small structures in each cell that supply energy and are inherited from the mother. Since sperm are powered by a group of mitochondria at the base of the flagellum, any mutation in the mitochondria could result in a reduction of power output, and therefore, reduce sperm mobility and male fertility.

"The original observations for this research were concerned with male infertility in humans," Allendorf says. "But because of the type of mutation, because it isn't eliminated through natural selection, it could have serious effects for populations of any species."

The mutation isn't eliminated through natural selection because the variation does not affect female reproduction. For example, if a female has the mitochondrial mutation, she still can reproduce and pass the mutation along to male and female offspring. The mutation does not affect those female offspring, who will later reproduce and pass the mutation along again. But it is suspected that the mutation will cause the male offspring to have low sperm mobility, and therefore, be less fertile. In time, this cycle will produce greater numbers of subfertile or infertile males.

"The implications of this mutation could be very important," Allendorf says. "If small populations of any species have a high proportion of males who aren't fertile, they could be very susceptible to extinction."

Allendorf studies the relationships between sperm motility, egg fertilization and the genetic information in the mitochondria of the sperm through sperm races. "We mix equal amounts of sperm from two male fish with different genes for the DNA in the mitochondria," he says. "We then put eggs from a female fish in the water and put the sperm on top. It really is a race because only one sperm gets to fertilize each egg. We're testing to see how fast the sperm swim, to see if there are deformities— we're basically measuring sperm performance of males with different genes."

It is especially important that fish have sperm that are strong swimmers since many species, such as trout and salmon, spawn in fast-moving water.

"We're studying infertility in fish," Allendorf says, "but, because it's all related, whatever we find out will be relevant for humans."

 

Cary Shimek, Managing Editor
Judy Fredenberg, Office of the Vice President for Research and Development
The University of Montana-Missoula
32 Campus Drive | Missoula, MT 59812
phone 406-243-2522 | fax 406-243-4520
Copyright 2007 The University of Montana

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