PG NewsPG delivery
Pittsburgh Post-Gazette Home Page
PG News: Nation and World, Region and State, Neighborhoods, Business, Sports, Health and Science, Magazine, Forum
Sports: Headlines, Steelers, Pirates, Penguins, Collegiate, Scholastic
Lifestyle: Columnists, Food, Homes, Restaurants, Gardening, Travel, SEEN, Consumer, Pets
Arts and Entertainment: Movies, TV, Music, Books, Crossword, Lottery
Photo Journal: Post-Gazette photos
AP Wire: News and sports from the Associated Press
Business: Business: Business and Technology News, Personal Business, Consumer, Interact, Stock Quotes, PG Benchmarks, PG on Wheels
Classifieds: Jobs, Real Estate, Automotive, Celebrations and other Post-Gazette Classifieds
Web Extras: Marketplace, Bridal, Headlines by Email, Postcards
Weather: AccuWeather Forecast, Conditions, National Weather, Almanac
Health & Science: Health, Science and Environment
Search: Search post-gazette.com by keyword or date
PG Store: Pittsburgh Post-Gazette merchandise
PG Delivery: Home Delivery, Back Copies, Mail Subscriptions

Headlines by E-mail

Headlines Region & State Neighborhoods Business
Sports Health & Science Magazine Forum

New species right out of the box

Sunday, February 21, 1999

By Byron Spice, Science Editor, Post-Gazette

One of the abiding mysteries of biological science is how life came to acquire so many different forms. Charles Darwin showed that species change over time, but the creation of novel features that mark a new species remains what has been called "the big black box of evolution."

 
Anthropologist Jeffrey Schwartz and his sudden-origins chart. (Bill Wade, Post-Gazette illustration) 

How did soft-bodied and hard-shelled animals spawn creatures with bony spines 400 million years ago? How did modern horses end up with hooves when their immediate ancestors had three toes? Where did birds get their beaks?

The answer, according to a provocative new theory, may be a set of regulatory genes that is shared by every animal, from unsegmented worms to humans. Called homeobox genes, they comprise a universal box of tools that shape development from the time an embryo is but a small collection of cells.

Molecular biologists, who discovered homeobox genes 15 years ago, have used fruit flies and other laboratory animals to show that features can be added or subtracted from an animal by changing the activation of one or more homeobox genes.

These regulatory genes could be a key mechanism in creating new species, suggests Jeffrey Schwartz, a physical anthropologist at the University of Pittsburgh.

 
    Related Articles:


Lab mice breeder catalogs genetic surprises

Academic or radical, Schwartz always thinks for himself

 
 

It's a theory bound to raise hackles among many scientists, but the implications could force a major rethinking of evolutionary principles. New species would need not be the result of gradual changes that accumulate over many generations, as suggested by conventional evolutionary theory.

Instead, new species could appear suddenly, as they do in fossil records.

Schwartz maintains this requires no great leaps of logic or science. Homeobox genes obey the same classical laws of inheritance as all other genes. So mutations could spread silently through a population over many generations, until animals suddenly begin producing mutated offspring. That would be the birth of a species.

This might explain why paleontologists have had such trouble finding fossils of the "transitional" species predicted by Darwinians - generation after generation of animals displaying subtle changes that slowly culminate in a fin becoming a hand or a composite eye becoming an eyeball in a socket. Rather, the fossil record shows, new species appear without warning.

"You don't see gradual evolution of feathers - you either have feathers or you don't," Schwartz says. The first fossil animals to display teeth flash entire mouthfuls, not just a single tooth.

Paleontologists continue to look for the missing links while creationists use these gaps in the fossil record as a major argument against the theory of evolution.

But Schwartz's theory suggests there are no gaps.

"It does help to explain why we don't pick up the expected intermediates in the [fossil] record," says Ian Tattersall, head of the anthropology department at the American Museum of Natural History. "This may not be the whole story ... but what I see is a potential solution to a set of problems that haven't been adequately addressed."

Dr. Thomas Gill, a pathologist and human geneticist who retired last year from the University of Pittsburgh School of Medicine, says Schwartz has provided a clear genetic mechanism for the origin of species that's simple as well. "Really useful scientific theories are usually simple."

Few people know much about it, but that should change soon. An article on Schwartz's theory will appear next month in The New Anatomist, a scientific journal. His book, "Sudden Origins: Fossils, Genes and the Emergence of Species," will be published in April by John Wiley & Sons. And he will present a public lecture April 24 at the American Museum of Natural History in New York City.

Schwartz, 50, has a long history of taking scientifically controversial positions and his new theory is no exception, says Tattersall, a longtime collaborator.

Paleontologists, for instance, still disagree over whether the gaps in the fossil record are real. And though generally acknowledging its plausibility, some biologists dismiss the theory as an updated version of "hopeful monsters," a discredited idea that a shuffling of chromosomes could lead to the sudden appearance of a species.

"There are many other equally compelling, or perhaps more compelling, explanations [of speciation] that can be made," insists Chung-I Wu, chairman of the evolution and ecology department at the University of Chicago.

But others suspect Schwartz may be on to something. "These sorts of [homeobox] mutations could have quite strong effects," agrees Dr. Andrew Lumsden of Guy's Hospital, head of developmental neurobiology at King's College in London. Their role in speciation deserves careful study, he says.

Schwartz's theory suggests a way out of a dead end where geneticists now find themselves, says Judith Masters, a geneticist and assistant director of the Natal Museum in Pietermartizburg, South Africa. The "nuts and bolts" approach of comparing the structural genes of animals has not produced satisfying answers about how species differ and how new species come about, she maintains.

"How could we share 95 or 99 percent of our genes with a chimpanzee," she wonders, yet still be such different animals? "There must be something else going on."


Darwin left a mystery

Schwartz insists he didn't set out to pick any fights. "I was just going to write a book about how wonderful homeobox genes are and why we ought to pay attention."

But in sorting out the facts for himself, he went back to read Darwin's "On the Origin of Species" and other evolutionary literature of the past two centuries. As he read on, "all these things started to click."

Despite the title of his 140-year-old tome, Darwin never addressed where species come from. The British naturalist established that species change over time, adapt to different environments and suffer extinctions, a view at odds with Biblical accounts of creation. His theory of natural selection, oversimplified as "survival of the fittest," suggested how species might adapt or become extinct.

But Darwin, writing before genes were known to exist, had only an inkling of how species might diverge from each other. Whatever the mechanism, Darwin believed speciation would occur gradually.

It was a conviction, many of his contemporaries pointed out, that did not square with the fossil record, beginning a long-running debate that Schwartz's theory renews.

While Darwin was developing his theory of evolution, Gregor Mendel, an Austrian abbot, was tending the peas in his garden. A would-be mathematician, he was able to deduce laws of inheritance based on cross-breeding experiments. A plant's traits, such as height or seed color, are the result of "factors" inherited from both parents, he found.

Some factors are dominant. For instance, when green-seeded peas are crossed with yellow-seeded, the offspring have green seeds. The green-seed factor is dominant and occurs if inherited from either parent. Yellow seeds, a "recessive" trait, may still pop up occasionally, but only if a plant inherits the trait from both parents.

Mendel published his findings in 1865, just a few years after Darwin's theory, but the implications were not appreciated until the 20th century, when scientists discovered genes and realized they were the "factors" Mendel described.

Controversy raged over whether genetics or natural selection controlled evolution until the 1930s, when a British statistician, Ronald Fisher, developed the synthetic theory of evolution, or Neo-Darwinism. Both Darwin and Mendel were correct, Fisher and his colleagues agreed. Genes cause variation, but natural selection controls the speed and direction of evolution.

The consensus was that new species would develop gradually. In 1940, however, a German-American developmental geneticist, Richard Goldschmidt, proposed that "macromutations" - rearrangements of the chromosomes - could abruptly create new species. But what were the chances, critics asked, that one of these "hopeful monsters" could find another monster of the opposite sex with which to mate? Goldschmidt had no answer.

Still, scientists had to contend with a fossil record favoring abrupt, not gradual, change in species. Attempts have been made to reconcile fossils with theory, but many have found it easier simply to pick a position and stick with it.

"You see what you want to see," Tattersall says, though he personally sees trouble in the human fossil record. Two million years ago, hominids were small and had odd proportions. "Then suddenly we see hominids that are much larger and are proportioned much like our own selves." What happened?


Surprising discovery

Schwartz suspects that scientists at Indiana University and the University of Basel in Switzerland may have stumbled upon the answer 15 years ago. They were using fruit flies to study homeotic genes, which were thought to be master controls that told other genes what to do. Unlike structural genes, such as those that determine the color of a person's eyes, or the height of pea plant, these genes would regulate the development of an embryo. Homeotic genes would tell which end of the organism was the front, which the back, which cells should become brain cells, which cells should form sphincters.

The researchers designed a molecular probe that would locate a specific piece of DNA on one of the fly's homeotic genes. To their surprise, the probe attached itself to more than a dozen homeotic genes. As other biologists began using this probe for what became known as the "homeobox," they found these same homeobox genes in every species they investigated.

It appears humans have about 39 homeobox genes that are clustered along four chromosomes in the cell's nucleus, says Lumsden, the British developmental scientist. These genes are thought to activate in sequence during development. But researchers also are finding the homeobox DNA sequence scattered through many other genes; more than 100 human genes contain the homeobox sequence, he adds, and more are being discovered.

The homeobox genes, Schwartz said, are the same from one species to another. The number of copies may differ - humans have many more copies than fruit flies - but the genes themselves do the same job from animal to animal. The same homeobox gene that, in a human, leads to the development of a human head, will direct the development of a fruit fly-like head when spliced into a fruit fly. In a sense, they are like computers that can do different jobs simply by being reprogrammed.

Kenneth Weiss, a professor of anthropology and biology at Penn State University, studies how homeobox genes create teeth. Fish, chicken and mice all have the same homeobox genes necessary for teeth, though they create traits as different as a beak and a mouse's overbite, depending on the timing of their activation, he says. In the earliest known vertebrates, these same genes were present, resulting in either a hard armor-plating over the body or teeth.

The more he learned about homeobox genes, the more impressed Schwartz became.

"It is mind-boggling," Schwartz writes in his paper for The New Anatomist, "to entertain the possibility that, for all intents and purposes, the difference between a fruit fly and a human might have as much (or even more) to do with turning on and off of homeobox genes that both animals share" as it does with differences in structural genes.

A mutation that affects the timing of those homeobox genes, he reasons, could result in dramatic changes in an animal's form.

Goldschmidt might have been closer to the truth with his "hopeful monsters" than anyone thought. The major weakness in that theory - the long odds that a creature with scrambled chromosomes could find a suitable mate - would not apply in this case, Schwartz says, because homeobox genes obey Mendelian principles.

A homeobox mutation that arose sporadically could spread through a population as a recessive gene trait. The mutation would not be noticed for generations, not until the mutation had spread widely. At some point, so many carriers of the trait would exist that they would begin to mate and eventually produce offspring that had two copies of the recessive gene. That animal would express the new trait.

Some of these new traits might be harmful, even fatal to an animal. But if the trait didn't kill, that animal would keep it and, over time, may find it offered some evolutionary advantage.

From a genetic point of view, the new trait would take generations to develop. But the expression would be sudden.

As the number of carriers within the population grew ever larger, the chances that many affected individuals would be spawned and mate with each other would also grow.

There's no reason to believe this speciation process doesn't continue and couldn't involve humans. No one can be sure what recessive genes lurk in the human genetic code, Schwartz notes, or what sort of hominid might result.


'Pretty wild hypothesis'

Biologists generally believe the origin of species scenario could happen, but disagree as to whether it's probable.

"I suppose it is possible, but at the moment it seems a pretty wild hypothesis," says William McGinnis, a homeobox researcher and chairman of biology at the University of California at San Diego. Mutations in the homeobox genes and their regulatory elements can result in drastically different forms within a species, he allows. But often these animals die or are very sick. More modest changes, he says, would result in transitional forms, not new species.

Homeobox genes might actually be the least likely mechanism for speciation, suggests the University of Chicago's Wu, because they are so slow to mutate.

This might seem an odd argument coming from Wu, who led a team that last year was the first to discover a homeobox gene, called Odysseus, that causes speciation in fruit flies. But his team's report in the journal Science suggested a different mechanism for creating new species than has Schwartz. And Wu insists the significance of Odysseus is not that it's a homeobox gene, but that it is the rare homeobox gene that rapidly mutates.

"Maybe what we're looking for [in a mechanism of speciation] is not the homeobox gene, but a fast-evolving gene," Wu says.

But Lumsden and Penn State's Weiss suggest that you don't need a mutation of the homeobox gene itself to result in a change in timing or activation of the gene.

Each gene is accompanied by short sequences of chemicals called enhancer sequences to which proteins that carry signals to the genes must attach. These enhancer sequences could easily be mutated. The effect, Weiss says, would be similar to changing a screw from a Philips head to a hex head. This could reprogram the gene without mutating it.

Weiss says he and other biologists have used homeobox genes to cause dramatic change in lab animals, but cautions that no one can say if such changes occur in nature. "I think we have to be very careful in overinterpreting this very appealing concept."

As far as the fossil record is concerned, paleontologists aren't sure a new theory is necessary.

Philip Gingerich, a professor of anthropology, biological and geological sciences at the University of Michigan, says the so-called gaps in the fossil records aren't that hard to explain. In grasslands and rain forests, dead animals are more likely to rot or be eaten than preserved. Even in swamps and river valleys, flooding that might trap fossils-to-be are episodic. Along the Mississippi River, for instance, big floods occur only every 100 years and, even then, any of a dozen different conditions necessary for fossilization might be absent.

K. Christopher Beard, assistant curator of vertebrate paleontology at the Carnegie Museum of Natural History, says the sudden appearance of new species in the fossil record in one locality may simply reflect immigration from another area.

Schwartz's theory is intriguing, Beard allows, but some of the most promising areas where missing links might be found have not been accessible to paleontologists. Only recently, for instance, have Western scientists had access to China, where Beard believes most modern mammals evolved. And parts of Africa, perhaps the most significant area of the world for primate evolution, remain off limits because of political turmoil.

Masters, the South African geneticist, says she finds Schwartz's theory exciting because it tries to provide a systemic explanation for new species. Given the similarities in structural genes between disparate species, she contends, some additional explanation for the origin of species is needed.



bottom navigation bar Terms of Use  Privacy Policy