2 A Tangled Bank Reflections on the Tree of Life and Human Health

Back

Rita R. Colwell

Writing almost 150 years ago, Charles Darwin coined the

name “tree of life” to describe the evolutionary patterns that

link all life on Earth. His work set a grand challenge for the

biological sciences—assembling the Tree of Life—that remains

incomplete today. In the intervening years, we have

come to understand better the significance of this challenge

for our own species. As human activity alters the planet, we

depend more and more on our knowledge of Earth’s other

inhabitants, from microorganisms to mega fauna and flora,

to anticipate our own fate. Aldo Leopold, the great naturalist

and writer, wrote, “To keep every cog and wheel is the

first precaution of intelligent tinkering” (1993:145–146).

However, the simple fact is that we do not yet know “what’s

out there,” and we are often unaware of what we have already

lost. The total number of species may number between 10

and 100 million, of which approximately 1.7 million are

known and only 50,000 described in any detail.

Today, we are in a better position to carry forward

Darwin’s program. Museums, universities, colleges, and research

institutions are invaluable repositories for data painstakingly

collected, conserved, and studied over the years. Add

a flood of new information from genome sequencing, geographical

information systems, sensors, and satellites, and we

have the raw material for realizing Darwin’s vision.

One of the great challenges we face in assembling the Tree

of Life is assembling the talent—bringing together the systematists,

molecular biologists, computer scientists, and mathematicians—

to design and deploy new computational tools for

phylogenetic analysis. Systematists are as scarce as hen’s teeth

these days. They may be our most endangered species.

The National Science Foundation (NSF) has a long history

of supporting the basic scientific research, across all

disciplines, that has placed us within reach of achieving this

objective. Now, the NSF has begun a new program to help

systematists and their colleagues articulate the genealogical

Tree of Life. We expect that this tree will do for biology what

the periodic table did for chemistry and physics—provide

an organizing framework. But advancing scientific understanding

is not the sole objective. New knowledge is important

for our continued prosperity and well being on the

planet. My aim is to explore some of the common ground

shared by the Tree of Life project and one important focus

of social concern—human health.

My title, “A Tangled Bank,” comes from Darwin’s The

Origin of Species, where he invites us to “contemplate a tangled

bank” and to reflect on the complexity, diversity, and order

found in this commonplace country landscape:

It is interesting to contemplate a tangled bank, clothed

with many plants of many kinds, with birds singing on

the bushes, with various insects flitting about, and

with worms crawling through the damp earth, and to

reflect that these elaborately constructed forms, so

different from each other, and dependent upon each

other in so complex a manner, have all been produced

by laws acting around us. (Darwin 1859)

18

A Tangled Bank 19

Darwin understood evolution as the source of complexity and

diversity, and his vision radically altered our perspective of

life on Earth, past and present. He developed much of his

theory in exotic places while sailing on the HMS Beagle. Just

more than a century later, another voyage, on the Apollo

spacecraft, gave us a first view of our blue Earth suspended

jewel-like in space. That image is now as familiar as Darwin’s

country landscape. Awe-inspiring and beautiful, planet Earth

appeared to us for the first time as a whole. But above all, we

saw it as finite and vulnerable.

Today, another 30 years down the road, we are better able

to chart the vast interdependencies that take us from country

bank to global systems. We are beginning to understand

that abrupt change and what we call “emerging” structures

characterize many natural phenomena—from earthquakes

to the extinction of some species. We know that the impact

of humans on natural systems is increasing, but we don’t yet

have the full picture of how environmental change—human

induced or otherwise—will cascade through natural systems.

There are two themes that intertwine in this chapter. The

first is the observation that the health of our species and the

health of the planet are inextricably linked. The second is that

a new vision of science in the 21st century, biocomplexity,

will speed us to a better understanding of those interconnections.

I use the term “biocomplexity” to describe the dynamic

web of relationships that arise when living things at all levels,

from molecules to genes to organisms to ecosystems,

interact with their environment.

Early on, we used the term “ecosystems approach” to

describe part of what we mean by “biocomplexity.” Now,

technologies allow us to delve into the structure of the very

molecules that compose cells—and simultaneously, to probe

the global system that encompasses the biosphere. Advances

in DNA sequencing, supercomputing, and computational

biology have literally revolutionized our view of the Tree of

Life. By comparing genetic sequences from different organisms,

we can now chart their genealogy and construct a universal

phylogenetic tree.

A cartoon from the British satirical magazine, Punch,

published shortly after The Origin of Species, depicts the evolution

of a worm into a human—the human, in this case,

being Charles Darwin himself. The caption reads: “Man is but

a Worm.” The intent, of course, was to ridicule the notion

that a human could in any way be related to a lowly worm

(Punch 1882). Today, these odd juxtapositions are no longer

the subject of satire. In research published in February of

2002, S. Blair Hedges and colleagues from the United States

and Japan compared 100 genes shared among three organisms:

the human, the fruit fly, and the nematode worm (Blair

et al. 2002). The complete genomes of all three organisms

have been sequenced; so finding candidate genes was a

straightforward exercise in matching. The researchers determined

that the human genome is more closely related to the

fly than to the worm, clarifying a major branch on the Tree

of Life. But it doesn’t eliminate the worm from our ancestry.

In the area of genomics, many people are looking at divergent

organisms and beginning to realize connections

never before imagined. Steven Tanksley and his colleagues

at Cornell are exploring the genome of tomatoes to gain insight

into how wild strains have evolved into the delicious

fruits we find in supermarkets today. A single gene is responsible

for “plumping” in tomatoes. He discovered that this gene

is similar to a human oncogene—a cancer-causing gene. This

match suggests a common mechanism in the cellular processes

leading to large, edible fruit in plants and cancers in

humans (Frary et al. 2000). This illustrates an important

point. Getting the sequence is really only the first step. Functional

analysis is needed to confirm the inference of function

based on similar (homologous) sequences.

Our current genomic tool kit is a recent development.

Research initiated in the late 1920s led scientists to the

discovery that an extract from the bacterium that causes

pneumonia could change a closely related, but harmless,

bacterium into a virulent one in the test tube. A search

began for the “transforming factor” responsible for such

a change. Both protein and DNA were candidates, but

scientific opinion favored protein. The puzzle was solved

when Avery et al. (1944) determined that DNA was the

transforming factor. Another decade passed before Watson

and Crick (1953) described the structure of the DNA molecule

and set off a revolution in molecular biology that is

still unfolding.

The first genome of a self-replicating, free-living organism—

the tiny bacterium Haemophilus influenzae strain Rd—

was completed in 1995 (Fleischmann et al. 1995). The first

genome of a multicellular organism—the nematode worm

(Caenorhabditis elegans)—was published in 1998 (Caenorhabditis

elegans Sequencing Consortium 1998), followed by

the fruit fly (Drosophila melanogaster) genome in 2000 (Adams

et al. 2000). The sequencing of the human genome was completed

just last year (Venter et al. 2001). Today, we “stand

on the shoulders of many giants” who pioneered the revolution

in molecular biology and genomics. But all the disciplines

have contributed to our progress. From the tiny genome of

the first bacterium sequenced with 1.8 million base pairs to

the 3.12 billion that comprise the human genome was a leap

of enormous magnitude. Researchers from Celera Genomics,

who helped sequence the human genome, estimate that assembly

of the 3.12 billion base pairs of DNA required 500

million trillion sequence comparisons. Completing the human

genome project might have taken years to decades to

accomplish without the terascale power of our newest computers

and a battery of sophisticated computation tools.

We know that one of the most important tools in modern-

day science’s arsenal of genetic engineering is PCR—the

polymerase chain reaction. This technique was pioneered in

the 1980s in the private sector. But first came the discovery

of the heat-resistant DNA polymerase needed to untwine the

double strands of DNA. Brock and Freeze discovered the

source of this heat-resistant enzyme in 1968—a bacterium

20 The Importance of Knowing the Tree of Life

(Thermus aquaticus), found in a hot spring in Yellowstone

National Park (Brock and Freeze 1969).

These new tools have radically changed our perspective

of life on Earth and taught us to reorient ourselves on the

Tree of Life. DNA sequencing enables researchers to overcome

the limitations of culturing microorganisms in the lab

and vastly improves our ability to detect and describe microbial

species. The surprising feature is the diversity and

sheer multitude of microorganisms, which represent the

lion’s share of Earth’s biodiversity. Although microorganisms

constitute more than two-thirds of the biosphere, they

represent a huge unexplored frontier. Of bacterial species in

the ocean, fewer than 1% have been cultured. Just a milliliter

of seawater holds about one million cells of these unnamed

species and about 10 million viruses. On average, a gram of

soil may contain as many as a billion microorganisms.

Research is also revealing phenomenal diversity among

microorganisms, especially among prokaryotes. They inhabit

a wide range of what we consider extreme environments—

hydrothermal vents on the sea floor, the ice floes of polar

regions, and the deep, hot, stifling darkness of South African

gold mines. Researchers have discovered that these organisms

display novel properties and assume novel roles in

ecosystems and in Earth’s cycles. Many are being investigated

for these unique properties and the applications that harnessing

them can provide.

In these and other less extreme places, microorganisms

have been wildly successful. They adapt very rapidly and

evolve very quickly to thrive in novel environments. Among

other feats, they have evolved diverse symbiotic relationships

with other creatures. The familiar shape of the Tree of Life

might appear radically altered if we take into account the

intriguing variety of ways that prokaryotes exchange genetic

information with other organisms, including lateral gene

transfer.

Only a handful of microorganisms are human pathogens.

Others infect plants and both domestic and wild animals. But

what an impact on human life they have had—both past and

present. We know that infectious diseases are a leading cause

of death in the world today, including the Americas (WHO

2001). Bacteria play a prominent role, but a wide variety

of viruses, protozoa, fungi, and a group of worms, the helminthes,

and other parasites also cause infectious diseases.

Pathogens—particularly bacteria and viruses—display the

same ability to adapt and the same genetic flexibility as their

harmless cousins. The increasingly serious problem of drug

resistance in pathogens is a direct result of this evolutionary

flexibility. Pathogens respond to the excessive and unwarranted

use of antibiotics, for example, by developing antibiotic

resistance. In many cases, antibiotic genes are linked to

heavy metal resistance. Work in my own laboratory in the

late 1970s and early 1980s on bacteria in Chesapeake Bay

shows a link between genes that encode for metal resistance

and genes that encode for antibiotic resistance, notably on

plasmids. Other linkages may yet be described.

Knowing how microorganisms have evolved into pathogens

and how they differ from less harmful relatives can provide

the key in tracking the origin and spread of emerging

diseases and their vectors. In 2000 and 2001, several outbreaks

of polio were reported from Hispaniola. Phylogenetic

analysis showed conclusively that the poliovirus was not the

“wild” variety that is the target of eradication efforts worldwide.

Where had it come from? The Sabin oral vaccine, a live

but weakened poliovirus, is widely used in developing countries.

These viruses are shed in the feces of vaccinated individuals.

When individuals who have not been vaccinated

come into contact with these viruses, possibly in unsanitary

food or water, they will become infected. The puzzle in the

Hispaniola case is how the attenuated virus reverted to

a virulent strain. Genetic sequencing demonstrated that

the poliovirus combined with at least four closely related

enteroviruses. As the virus spread, one of these variants

developed virulence (Kew et al. 2002).

This example demonstrates that human institutions are

as much a part of the ecology of infectious disease as recombination

on the molecular level. An inadequate vaccination

program, combined with poor sanitary conditions, helped

to create the environment for the emergence of a new strain

of poliovirus.

The rapid increase in cases of dengue fever reported between

1955 and the present day provides another example

of a reemerging infectious disease. The World Health Organization

(WHO) estimates that as many as 50 million people

are infected each year, with an additional 2.5 billion people

at risk (WHO 1999). A major epidemic in Brazil caused more

than 300,000 cases of dengue in the first three months of

2002 alone. (WHO 2002) Dengue is not a new disease. Major

epidemics were recorded in the 18th century in Asia. What

caused this infectious disease to reemerge as a major public

health problem over the past 50 years? Genetic sequencing

has shown that dengue fever and its more deadly form, dengue

hemorrhagic fever, are caused by a group of four closely

related viruses that infect the mosquito Aedes aegypti (Loroсo-

Pino et al. 1999). Each variant of the dengue virus produces

immunity only to itself, so individuals may suffer as many as

four infections in a lifetime. Dengue hemorrhagic fever may

be caused by these multiple infections. Genetic sequencing

is indispensable in tracking the origin and spread of each

variant. Knowing which virus type is circulating may be

important in determining the potential risk for an outbreak

of dengue hemorrhagic fever.

The causes of the current global pandemic are not well

understood. But the spread of Aedes aegypti is certainly a factor.

Aedes, a vector for yellow fever, was nearly eradicated

in the 1950s and 1960s. After a vaccine for yellow fever became

available, mosquito control efforts waned, and Aedes

has come back with a vengeance to repopulate and even expand

its former territory. The Asian tiger mosquito, Aedes

albopictus, is also a potential vector of epidemic dengue. In

the United States, it was first reported in 1995 in Texas, and

A Tangled Bank 21

has since become established in 26 states. It is simply not

known whether the tiger mosquito could initiate a major

dengue epidemic in the United States. Like Aedes aegypti, the

tiger mosquito can survive in urban environments. And like

Aedes aegypti, it is also a possible vector for yellow fever. Once

the vector is present, the pathogen may not be far behind.

Genetic sequencing is a critical new tool in the battle to

control infectious disease. Sequencing may help to determine

the origin of a pathogen, for example, whether it is endemic

or imported. And tracking the geographical or ecological

origins based on sequencing can also pinpoint natural reservoirs,

where health efforts can be focused. We may never

be able to eradicate pathogens that are widespread in the

environment, but knowledge of how they evolved, their

mechanisms of adaptation, and their ecology will help us

design effective prevention and control measures.

My own research has focused on the study of how factors

combine to cause cholera, a devastating presence in

much of the world, although largely controlled in the United

States. It is endemic in Bangladesh, for example, where I’ve

done much of my research. My scientific quest to understand

cholera began more than 30 years ago, in the 1970s, when

my colleagues and I realized that the ocean itself is a reservoir

for the bacterium Vibrio cholerae, the cause of cholera,

by identifying the organism in water samples from the Chesapeake

Bay. Copepods, the minute relatives of shrimp that live

in salt or brackish waters, are the hosts for the cholera bacterium,

which they carry in their gut as they travel with currents

and tides. We now know that environmental, seasonal,

and climate factors influence copepod populations, and indirectly

cholera. In Bangladesh, we discovered that cholera

outbreaks occur shortly after sea-surface temperature and

height peak. This usually occurs twice a year, in spring and

fall, when populations of copepods peak in abundance. Ultimately,

we can connect outbreaks of cholera to major climate

fluctuations. In the El Niсo year of 1991, a major outbreak of

cholera began in Peru and spread across South America. Linking

cholera with El Niсo/Southern Oscillation events provides

us with an early warning system to forecast when major

cholera outbreaks are likely to occur (Colwell 2002).

Understanding cholera requires us to explore the problem

on different scales. We study the relationship between

the bacterium Vibrio cholerae, which causes the disease, and

its copepod host. We look at the ecological factors that affect

copepod reproduction and survival. We observe the

local and oceanic climatic factors related to currents and

sea-surface temperature. On a microscopic level, we look at

molecular factors related to the toxin genes in V. cholerae to

understand the function of genes and how they evolved and

adapted in relation to copepods. This in turn may provide

new insight into how these pathogens cause disease in humans.

Add the economic and social factors of poverty, poor

sanitation, and unsafe drinking water, and we begin to see

how this microorganism sets off the vast societal traumas of

cholera pandemics (Lipp et al. 2002). We cannot eradicate

the cholera bacterium. Understanding V. cholerae on the

molecular level, tracing the ecology of the disease, forecasting

major outbreaks, and controlling them are our only options

(Colwell 2002). Other infectious diseases—relayed by

vectors, water, food, air, or otherwise—also interact with

climate. The El Niсo/Southern Oscillation climate pattern has

been linked to outbreaks of malaria, dengue fever, encephalitis,

and diarrheal disease as well as cholera. Environmental

change of all kinds may affect agents of infectious disease.

Changes in climate could nudge pathogens and vectors to

new regions. Agents of tropical disease could drift toward the

polar regions, creating “emerging diseases” at new locales.

Because the evolutionary “speed limit” of many pathogens is

remarkably high, pathogens might adapt to new ecological

circumstances with remarkable ease.

When we look for connections between the Tree of Life

and human health, infectious diseases may be the first case

that comes to mind. But the nexus among evolution, ecology,

genomics, and human health guides us farther afield.

When we view our planet through the eyes of complexity,

we see motifs that recur with striking constancy. We can often

use motifs found in harmless organisms to better understand

the mechanisms in their close cousins that cause disease.

One case in point is recent research on aphids, the

tiny plant pests that cause major agricultural damage. A tiny

bacterium, Buchnera, lives inside the aphid’s cells. It provides

essential nutrients to the aphid hosts, and the hosts

reciprocate. Over the years, aphids and Buchnera have evolved

together, so that today, different species of aphids are associated

with different species of the bacterium. Baumann and

colleagues have traced this cospeciation more than 150–250

million years (Bauman et al. 1997).

The role of these endosymbionts in the adaptation of

the aphids to host plants is under investigation as part of

the NSF biocomplexity initiative. One of the questions

of interest concerns the extent of convergence in the evolution

of symbiotic bacteria found within a range of insect

groups. Buchnera was the first endosymbiont genome to be

sequenced. Sequence analysis has shown that Buchnera is

missing many of the genes required for “independent life”—

including the ones that turn off production of the nutrients

necessary for the host’s survival. Recently, Ochman and

Moran (2001) have contrasted the Buchnera genome with

a hypothetical ancestor of the enteric bacterium Escherichia

coli, thought to be a relative of Buchnera. The comparison

shows massive gene reduction in Buchnera, a phenomenon also

found in many pathogens. Gene loss in both symbionts and

pathogens may be key to understanding how human pathogens

cause disease. By studying symbionts such as Buchnera

that live in harmony with their hosts, it may be possible to

unravel the adaptive mechanisms that pathogens living inside

human cells use to evade the body’s defenses. New strategies

for combating infections could follow.

Organisms can also shape the physical environment. An

example is work by Jillian Labrenz and colleagues (2000)

22 The Importance of Knowing the Tree of Life

looking at a complex environment: an abandoned and flooded

mine. Biofilms here live on the floors of the flooded tunnels.

The goal of the work is to understand geomicrobiological processes

from the atomic scale up to the aquifer level. Acid drainage

from such mines is a severe environmental problem. At

one mine being studied, workers accidentally left a shovel

in the discharge; the next day half the shovel was eaten away

by the acid waste.

We search for ways to remediate the damage in areas like

these. Some of the microorganisms in the biofilms play a

surprising role (Labrenz et al. 2000). For one, they can clean

the zinc-rich waters to a standard better than that of drinking

water. At the same time, bacteria in the biofilms are depositing

minerals on the tunnel floors. Aggregates of tiny zinc

sulfide crystals just 2–5 nm in diameter are formed in very

high concentrations by the activity of microorganisms. The

work sheds light on an environmental problem, while giving

insights into basic science with economic benefit: we are

learning how mineral ores of commercial value are formed.

Researchers are studying this system on a number of scales—

from the early evolution of life on Earth to the nanoscale

forces operating inside the microorganisms and in their immediate

environment.

Because microorganisms play a central role in the cycling

of carbon, nutrients, and other matter, they have large impacts

on other life—including humans. Recent research has

shed new light on these complex interdependencies in the

oceans. The molecule rhodopsin is a photopigment that

binds retinal. Activated by sunlight, retinal proteins have been

found to serve the energy needs of microorganisms, as well

as steer them to light. In people, a different form of the molecule

provides the light receptors for vision. Until recently,

rhodopsin was thought to occur only in a small number of

species, namely, the halobacteria, which thrive in environments

10 times saltier than seawater. Despite the name, they

are actually members of the Archaea, one of the three major

branches of life and among the oldest forms of life on Earth.

Obed Bйjа, Edward DeLong, and colleagues at the

Monterey Bay Aquarium Research Institute have now shown

that bacteria containing a close variant of this energy-generating,

light-absorbing pigment are widespread in the world’s

oceans (Bйjа et al. 2000). This is the first such molecule to

be associated with bacteria. The researchers also discovered

that genetic variants of these bacteria contain different

photopigments in different ocean habitats. The protein pigments

appear to be tuned to absorb light of different wavelengths

that match the quality of light available (Bйjа et al.

2001). These bacteria are present in significant numbers and

over a wide geographic range, and may occupy as much as

10% of the ocean’s surface. Such abundance may point to a

significant new source of energy in the oceans. It is also a

startling reminder of what we have yet to discover. We begin

to map biocomplexity by tracing the links from the function

of a protein to the distribution and variation of bacterial

populations to biogeochemical cycles. Human health is ultimately

linked to the complex dynamics of these vast biogeochemical

cycles. Understanding how they function is vital

in order to anticipate how disruptions might alter them.

I’ve taken my examples from the world of microorganisms

partly because I’m a microbiologist—but also because

this is an emerging frontier. Microorganisms may well be our

“canaries in the mineshaft,” warning us of subtle environmental

changes, from the local to the global. Carl Woese, whose

work has done so much to expand our vision of microbial

diversity, goes further: “[M]icrobes are the essential, stable

underpinnings of the biosphere—without bacteria, other life

would not continue to exist” (Woese 1999:263).

This past March, the U.S. Geological Survey published

an assessment that sampled 139 waterways across the U.S.

for 95 chemicals (Koplin et al. 2002). They found a wide

array of substances present in trace amounts in 80% of the

waterways sampled. The chemicals ranged from caffeine, to

steroids, to antibiotics and other pharmaceuticals. All are

bioactive substances—chemicals that interact with organisms

at the molecular level. Yet we have very little understanding

of how these substances may be affecting microbial communities.

Are they altering the structure of microbial ecosystems

in soils and water? What are the selective pressures on organisms

exposed to these substances? If the composition of

microbial communities is seriously altered, or if the abundance

or diversity of microorganisms is diminished, what are

the implications for the availability of nutrients in ecosystems

and for agricultural productivity?

Other organisms may be providing some answers. Research

reported recently by Tyrone Hayes and colleagues

from the University of California–Berkeley found that atrazine,

the nation’s top-selling weed killer, turns tadpoles into

hermaphrodites with both male and female sexual characteristics.

The herbicide also lowers levels of the male hormone

testosterone in sexually mature male frogs by a factor of 10,

to levels lower than those in normal female frogs. Hayes is

now studying how the abnormalities affect the frogs’ ability

to produce offspring. Although Hayes used the African

clawed frog in his research, he and his colleagues found native

leopard frogs with the same abnormalities in atrazinecontaminated

ponds in the U.S. Midwest (Hayes et al. 2002).

Help in dealing with contaminants in the environment

may come from the plant kingdom. Sunflowers have been

planted in fields near the Chernobyl nuclear power plant, in

what is now Belarus, in an experimental effort to clean the

heavily contaminated soils that linger long after the catastrophic

accident. One study in 1996 found that the roots

of sunflowers floated on a heavily contaminated pond near

Chernobyl rapidly adsorbed heavy metals, such as cesium,

associated with nuclear contamination (Reuther 1998). The

NSF, the U.S. Environmental Protection Agency, and the

Office of Naval Research have teamed up to fund new research

on plants that can remove organic toxins and heavy

metals from contaminated soils. Lena Ma of the University

of Florida and colleagues discovered Chinese brake ferns

A Tangled Bank 23

thriving in soils contaminated with arsenic at the site of an

abandoned lumber mill (Ma et al. 2001). Arsenic was once

widely used as a pesticide in treated wood. Ma found arsenic

levels greater than 7,500 parts per million in these samples.

Plants fed on a diet of arsenic accumulate more than 2% of

total mass in arsenic. Ma is now examining the mechanisms

of arsenic uptake, translocation, distribution and detoxification.

Other researchers are surveying a wide array of microorganisms

for their potential to remove heavy metals and

other contaminants from soil and water.

Understanding how organisms respond to change requires

that we know what organisms inhabit our world and

how they interact. The Tree of Life provides the baseline

against which we measure change. In this context, the

planned National Ecological Observation Network (NEON;

National Science Foundation) will be invaluable. When completed,

NEON will be an array of sites across the country

furnished with the latest sensor technologies and linked by

high-capacity computer lines. The entire system would track

environmental change from the microbiological to global

scales. Today, we simply do not have the capability to answer

ecological questions on a regional to continental scale,

whether involving invasive species that threaten agriculture,

the spread of disease or bioterrorist agents. Tools such as

NEON—which will in time reach international dimensions—

will give us a much richer understanding of how organisms

react to environmental change.

Eventually, such observatories must be extended to the

oceans as well, perhaps with links to the ocean observatories

now in the planning stages. The deep sea floor covers

nearly 70% of Earth’s surface. It may be the most extensive

ecosystem on the planet, yet we have only begun to explore

its secrets. It may harbor the source of new drugs, or it may

be a reservoir for as yet unknown human pathogens. We can

only be certain that it will produce surprises. We are all familiar

with the submarine vents discovered two decades ago

in the deep ocean, marked by the exquisite mineralized chimneys

called “black smokers” that form around the hydrothermal

vents on the seafloor and tower over dense communities

of life. Creatures there live without photosynthesis—relying

on microorganisms for sustenance. They exemplify the diversity

that we have only recently begun to explore—even

in the most extreme environments. These hot springs in the

deep sea could have been the wellspring for life on our planet.

The deep sea is a reminder that we stand on the very

threshold of a new age of scientific exploration, one that will

give us a more profound understanding of our planet and

allow us to improve the quality of people’s lives worldwide.

Yet some of the changes we humans bring about are not for

the better. The ozone hole that now appears over Antarctica

every year is a reminder that the cumulative effect of billions

of individual human actions can have far-reaching, although

unintentional, consequences. We understand now that

changes in global climate cannot be understood without

taking into account the effect that humans have on the environment—

the way our individual and institutional actions

interact with the atmosphere, the oceans, and the land.

The greatest question of our times may be how we can

avoid the pitfalls and still grasp the opportunities that science

and technology hold. When we limit our view of human

health to problems of disease, diagnosis, and cure, we miss

a significant perspective. A larger vision recognizes the evolutionary

processes through which we arrived on the scene

and the ecological balances that sustain us. We see the vulnerability

of the planet and our co-inhabitants on it as our

vulnerability. The study of biocomplexity science and its

essential backbone, the Tree of Life, provide us with a way

through and beyond these conundrums. Understanding the

relationships among organisms and between organisms and

the environment is our surest path to a healthier, more secure

future.

Literature Cited

Adams, M. D., S. E. Celniker, R. A. Holt, C. A. Evans, J. D.

Gocayne, G. A. Amanatides, S. E. Scherer, P. W. Li, R. A.

Hoskins, R. F. Galle, et al. 2000. The genome sequence of

Drosophila melanogaster. Science 287:2185–2195.

Avery, O. T., C. M. MacLeod, and M. McCarty. 1944. Studies

on the chemical nature of the substance inducing transformation

of pneumococcal types: induction of transformation

by a desoxyribonucleic acid faction isolated from Pneumococcus

type III. J. Exp. Med. 79(2):137–158.

Baumann, P., N. A. Moran, and L. Baumann. 1997. The

evolution and genetics of aphid endosymbionts. Bioscience

47(1):12–20.

Bйjа, O., L. Aravind, E. V. Koonin, M. T. Suzuki, A. Hadd, L. P.

Nguyen, S. B. Jovanovich, C. M. Gates, R. A. Feldman, J. L.

Spudich, E. N. Spudich, and E. F. DeLong. 2000. Bacterial

rhodopsin: evidence for a new type of phototrophy in the

sea. Science 289:1902–1906.

Bйjа, O., E. N. Spudich, J. L. Spudich, M. Leclerc, and E. F.

DeLong. 2001. Proteorhodopsin phototrophy in the ocean.

Nature 411:786–789.

Blair, J. E., K. Ikeo, T. Gojobori, and S. B. Hedges. 2002. The

evolutionary position of nematodes. BMC Evol. Biol. 2:7.

Brock, T. D., and H. Freeze. 1969. Thermus aquaticus gen. n.

and sp. n., a non-sporulating extreme thermophile. J.

Bacteriol. 98:289.

Caenorhabditis elegans Sequencing Consortium. 1998. Genome

sequence of the nematode C. elegans: a platform for

investigating biology. Science 282(5396):2012.

Colwell, R. R. 2002. A voyage of discovery: cholera, climate and

complexity. Environ. Microbiol. 4(2):67–69.

Darwin, C. 1859. On the origin of species by means of natural

selection, or the preservation of favoured races in the

struggle for life. John Murray, London.

Fleischmann, R. D., M. D. Adams, O. White, R. A. Clayton,

E. F. Kirkness, A. R. Kerlavage, C. J. Bult, J. F. Tomb, B. A.

Dougherty, J. M. Merrick, et al. 1995. Whole-genome

random sequencing and assembly of Haemophilus influenzae

Rd. Science 269(5223):496–512.

24 The Importance of Knowing the Tree of Life

Frary, A., T. C. Nesbitt, A. Frary, S. Grandillo, E. van der

Knaap, B. Cong, J. Liu, J. Meller, R. Elber, K. B. Alpert, and

S. D. Tanksley. 2000. A quantitative trait locus key to the

evolution of tomato fruit size. Science 289:85–88.

Hayes, T. B., A. Collins, M. Lee, M. Mendoza, N. Noriega, A. A.

Stuart, and A. Vonk. 2002. Hermaphroditic, demasculinized

frogs after exposure to the herbicide atrazine at low

ecologically relevant doses. Proc. Natl. Acad. Sci. USA

99:5476–5480.

Kew, O., V. Morris-Glasgow, M. Landaverde, C. Burns, J. Shaw,

Z. Garib, J. Andrй, E. Blackman, C. J. Freeman, J. Jorba,

et al. 2002. Outbreak of poliomyelitis in Hispaniola

associated with circulating type 1 vaccine-derived poliovirus.

Science 296(5566):356.

Koplin, D. W., E. T. Furlong, M. T. Meyer, E. M. Thurman,

S. D. Zaugg, L. B. Barber, and H. T. Buxton. 2002. Pharmaceuticals,

hormones, and other organic wastewater contaminants

in U. S. streams, 1999–2000: a national

reconnaissance. Environ. Sci. Technol. 36(6):1202–1211.

Labrenz, M., G. K. Druschel, T. Thomsen-Ebert, B. Gilbert, S. A.

Welch, K. M. Kemner, G. A. Logan, R. E. Summons, G. De

Stasio, P. L. Bond, B. Lai, S. D. Kelly, and J. F. Banfield.

2000. Formation of sphalerite (ZnS) deposits in natural

biofilms of sulfate-reducing bacteria. Science

290(5497):1744.

Leopold, A. 1993. Round river. Oxford University Press, New

York.

Lipp, E. K., A. Huq, and R. R. Colwell. 2002. Effects of global

climate on infectious disease: the cholera model. Clin.

Microbiol. Rev. 15:757–770.

Loroсo-Pino M. A., C. B. Cropp, J. A. Farfбn, A. V. Vorndam,

E. M. Rodrнguez-Angulo, E. P. Rosados-Paedes, L. F. Flores-

Flores, B. J. Beaty, and D. J. Gubler. 1999. Common

occurrence of concurrent infections by multiple dengue

virus serotypes. Am. J. Trop. Med. 61(5):725–730.

Ma, L. Q., K. M. Komar, C. Tu, W. Zhand, Y. Cai, and E. D.

Kennelley. 2001. A fern that hyperaccumulates arsenic.

Nature 409:579.

NSF. Available: http://www.nsf.gov/bio/bio_bdg03/neon03.htm

and http://ibrcs.aibs.org/neon/index.aspl. Last accessed 25

December 2003.

Ochman, H., and N. A. Moran. 2001. Genes lost and genes

found: evolution of bacterial pathogenesis and symbiosis.

Science 292(5519):1096.

Punch’s Almanack, 1882.

Reuther, C. 1998. Growing cleaner: phytoremediation goes

commercial, but many questions remain. Academy of

Natural Sciences, Philadelphia. Available: http://

www.acnatsci.org/research/kye/phyto.html. Last accessed

25 December 2003.

Venter, J. C., M. D. Adams, E. W. Myers, P. W. Li, R. J. Mural,

G. G. Sutton, H. O. Smith, M. Yandell, C. A. Evans, R. A.

Holt, et al. 2001. The sequence of the human genome.

Science 291:1304–1351.

Watson, J. D., and F. H. C. Crick. 1953. A structure for

deoxyribose nucleic acid. Nature 171:737–738.

WHO. 1999. Strengthening implementation of the global

strategy for dengue fever/dengue haemorrhagic fever. Report

of the informal consultation, 18–20 October. World Health

Organization, Geneva.

WHO. 2001. The world health report 2001. World Health

Organization, Geneva.

WHO. 2002. Communicable disease surveillance and response,

disease outbreaks reported. May 8 notice. World Health

Organization, Geneva.

Woese, C. 1999. No title. ASM News. 65(5):263.