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Darwinism defined the difference between fact and theory.doc

Darwinism defined the difference between fact and theory.doc

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I don't speak of the militant fundamentalists who label themselves with the oxymoron ''scientific

creationists,'' and try to sneak their Genesis literalism into high school classrooms under the guise of

scientific dissent. I'm used to their rhetoric, their dishonest mis- and half-quotations, their constant

repetition of ''useful'' arguments that even they must recognize as nonsense (disproved human

footprints on dinosaur trackways in Texas, risible misinterpretation of thermodynamics to argue that

life's complexity couldn't increase without a divine boost). Our strug- gle with these ideologues is

political, not intellectual. I speak instead of our allies among people committed to reason and

honorable argument.

Kristol, who is no fundamentalist, accuses evolutionary biologists of bringing their troubles with

creationists upon themselves by too zealous an insistence upon the truths of Darwin's world. He

writes: ''. . . the debate has become a dogmatic crusade on both sides, and our educators, school

administrators, and textbook publishers find themselves trapped in the middle.'' He places the

primary blame upon a supposedly anti-religious stance in biological textbooks: ''There is no doubt

that most of ur textbooks are still written as participants in the 'warfare' between sci- ence and

religion that is our heritage from the 19th century. And there is also little doubt that it is this

pseudoscientific dogmatism that has provoked the current religious reaction.''

Kristol needs a history lesson if he thinks that current creationism is a product of scientific

intransigence. Creationism, as a political movement against evolution, has been a continually powerful force since the days of the Scopes trial. Rather than using evolution to crusade against religion

in their texts, scientists have been lucky to get anything at all about evolution into books for high

school students ever since Scopes's trial in 1925. My own high school biology text, used in the

liberal constituency of New York City in 1956, didn't even mention the word evolution. The laws

that were used against Scopes and cowed textbook publishers into submission weren't overturned by

the Supreme Court until 1968 (Epperson v. Arkansas).

But what about Kristol's major charge -- anti-religious prejudice and one-dimensional dogmatism

about evolution in modern textbooks? Now we come to the heart of what makes me so sad about

Kristol's charges and others in a similar vein. I don't deny that some texts have simplified, even

distorted, in failing to cover the spectrum of modern debates; this, I fear, is a limitation of the genre

itself (and the reason why I, though more of a writer than most scientists, have never chosen to

compose a text). But what evidence can Kristol or anyone else provide to demonstrate that

evolutionists have been worse than scientists from other fields in glossing over legitimate debate

within their textbooks?

Consider the evidence. Two textbooks of evolution now dominate the field. One has as its senior

author Theodosius Dob zhansky, the greatest evolutionist of our century, and a lifelong Russian

Orthodox; nothing anti-religious could slip past his watchful eye. The second, by Douglas Futuyma,

is a fine book by a kind and generous man who could never be dogmatic about anything except

intolerance. (His book gives a fair hearing to my own heterodoxies, while dissenting from them.)

When we come to popular writing about evolution, I suppose that my own essays are as well read as

any. I don't think that Kristol could include me among Darwinian dogmatists, for most of my essays

focus upon my disagreements with the strict version of natural selection. I also doubt that Kristol

would judge me anti- religious, since I have campaigned long and hard against the same silly

dichotomy of science versus religion that he so rightly ridicules. I have written laudatory essays

about several scientists (Burnet, Cuvier, Buckland, and Gosse, among others) branded as

theological dogmatists during the nineteenth-century reaction; and, while I'm not a conventional

believer, I don't consider myself irreligious.

Kristol's major error lies in his persistent confusion of fact with theory. He accuses us -- without

giving a single concrete example, by the way -- of dogmatism about theory and sustains his charge

by citing our confidence in the fact of transmutation. ''It is reasonable to suppose that if evolution

were taught more cautiously, as a conglomerate idea consisting of conflicting hypothe- ses rather

than as an unchallengeable certainty, it would be far less controversial.''

Well, Mr. Kristol, evolution (as theory) is indeed ''a conglomerate idea consisting of conflicting

hypotheses,'' and I and my colleagues teach it as such. But evolution is also a fact of nature, and so

do we teach it as well, just as our geological colleagues describe the structure of silicate minerals,

and astronomers the elliptical orbits of planets.

Rather than castigate Mr. Kristol any further, I want to discussthe larger issue that underlies both

this incident and the popular perception of evolution in general. If you will accept my premise that

evolution is as well established as any scientific fact (I shall give the reasons in a moment), then

why are we uniquely called upon to justify our chosen profession; and why are we alone subjected

to such unwarranted infamy? To this central question of this essay, I suggest the following answer.

We haven't received our due for two reasons: (1) a general misunderstanding of the different

methods used by all historical sciences (including evolution), for our modes of inference don't

match stereotypes of ''the scientific method''; and (2) a continuing but unjustified fear about the

implication both of evolution itself and of Darwin's theory for its mechanism. With these two issues

resolved, we can understand both the richness of science (in its pluralistic methods of inquiry) and

the absence of any conflict, through lack of common content, between proper science and true


Our confidence in the fact of evolution rests upon copious data that fall, roughly, into three great

classes. First, we have the direct evidence of small-scale changes in controlled laboratory

experiments of the past hundred years (on bacteria, on almost every measurable property of the fruit

fly Drosophila), or observed in nature (color changes in moth wings, development of metal

tolerance in plants growing near industrial waste heaps), or produced during a few thousand years

of human breeding and agriculture. Creationists can scarcely ignore this evidence, so they respond

by arguing that God permits limited modification within created types, but that you can never

change a cat into a dog (who ever said that you could, or that nature did?).

Second, we have direct evidence for large-scale changes, based upon sequences in the fossil record.

The nature of this evidence is often misunderstood by non-professionals who view evolution as a

simple ladder of progress, and therefore expect a linear array of ''missing links.'' But evolution is a

copiously branching bush, not a ladder. Since our fossil record is so imperfect, we can't hope to find

evidence for every tiny twiglet. (Sometimes, in rapidly evolving lineages of abundant organisms

restricted to a small area and entombed in sediments with an excellent fossil record, we do discover

an entire little bush -- but such examples are as rare as they are precious.) In the usual case, we may

recover the remains of side branch number 5 from the bush's early history, then bough number 40 a

bit later, then the full series of branches 156-161 in a well preserved sequence of younger rocks, and

finally surviving twigs 250 and 287.

In other words, we usually find sequences of structural intermediates, not linear arrays of ancestors

and descendants. Such sequences provide superb examples of temporally ordered evo- lutionary

trends. Consider the evidence for human evolution in Africa. What more could you ask from a

record of rare creatures living in terrestrial environments that provide poor opportunity for

fossilization? We have a temporal sequence displaying clear trends in a suite of features, including

threefold increase of brain size and corresponding decrease of jaws and teeth. (We are missing

direct evidence for an earlier transition to upright posture, but wide-ranging and unstudied

sediments of the right age have been found in East Africa, and we have an excellent chance to fill in

this part of our story.) What alternative can we suggest to evolution? Would God -- for some

inscrutable reason, or merely t test our faith -- create five species, one after the other

(Australopithecus afarensis, A. africanus, Homo habilis, H. erectus, and H. sapiens), to mimic a

continuous trend of evolutionary change?

Or, consider another example with evidence of structurally intermediate stages -- the transition from

reptiles to mammals. The lower jaw of mammals contains but a single bone, the dentary. Reptiles

build their lower jaws of several bones. In perhaps the most fascinating of those quirky changes in

function that mark pathways of evolution, the two bones articulating the upper and lower jaws of

reptiles migrate to the middle ear and become the malleus and incus (hammer and anvil) of


Creationists, ignorant of hard evi dence in the fossil record, scoff at this tale. How could jaw bones

become ear bones, they ask. What happened in between? An animal can't work with a jaw half

disarticulated during the stressful time of transition.

The fossil record provides a direct answer. In an excellent series of temporally ordered structural

intermediates, the reptilian dentary gets larger and larger, pushing back as the other bones of a

reptile's lower jaw decrease in size. We've even found a transitional form with an elegant solution to

the problem of remaking jaw bones into ear bones. This creature has a double articulation -- one

between the two bones that become the mammalian hammer and anvil (the old reptilian joint), and a

second between the squamosal and dentary bones (the modern mammalian condi- tion). With this

built-in redundancy, the emerging mammals could abandon one connection by moving two bones

into the ear, while retaining the second linkage, which becomes the sole articulation of modern


Third, and most persuasive in its ubiquity, we have the signs ofhistory preserved within every

organism, every ecosystem, and every pattern of biogeographic distribution, by those pervasive

quirks, oddities, and imperfections that record pathways of historical descent. These evidences are

indirect, since we are viewing modern results, not the processes that caused them, but what else can

we make of the pervasive pattern? Why does our body, from the bones of our back to the

musculature of our belly, display the vestiges of an arrangement better suited for quadrupedal life if

we aren't the descendants of four-footed creatures? Why do the plants and animals of the Galapagos

so closely resemble, but differ slightly from, the creatures of Ecuador, the nearest bit of land 600

miles to the east, especially when cool oceanic currents and volcanic substrate make the Galapagos

such a different environment from Ecuador (thus removing the potential argument that God makes

the best creatures for each place, and small differences only reflect a minimal disparity of

environments)? The similarities can only mean that Ecuadorian creatures colonized the Galapagos

and then diverged by a natural process of evolution.

This method of searching for oddities as vestiges of the past isn't peculiar to evolution, but a

common procedure of all historical science. How, for example, do we know that words have

histories, and haven't been decreed by some all-knowing committee in Mr. Orwell's bureau of Newspeak? Doesn't the bucolic etymology of so many words testify to a different life style among our

ancestors? In this article, I try to ''broadcast'' some ideas (a mode of sowing seed) in order to counter

the most ''egregious'' of creationist sophistries (the animal ex grege, or outside the flock), for which,

given the quid pro quo of business, this fine magazine pays me an ''emolument'' (the fee that millers

once received to grind corn).

I don't want to sound like a shrill dogmatist shouting ''rally round the flag boys,'' but biologists have

reached a consensus, based on these kinds of data, about the fact of evolution. When honest critics

like Irving Kristol misinterpret this agreement, they're either confusing our fruitful consonance

about the fact of evolution with our vibrant dissonance about mechanisms of change, or they've

misinterpreted part of our admittedly arcane technical literature.

One such misinterpretation has gained sufficient notoriety in the last year that we crave resolution

both for its own sake and as an illustration of the frustrating confusion that can arise when scientists

aren't clear and when commentators, as a result of hidden agendas, don't listen. Tom Bethell argued

in Harper's (February 1985) that a group of young taxonomists called pattern cladists have begun to

doubt the existence of evolution itself.

This would be truly astounding news, since cladistics is a powerful method dedicated to reforming

classification by using only the branching order of lineages on evolutionary trees (''propinquity of

descent'' in Darwin's lovely phrase), rather than vague notions of overall similarity in form or

function. (For example, in the cladistic system, a lungfish is more closely related to a horse than to a

salmon because the common ancestor of lungfish and horse is more recent in time than the link

point of the lungfish-horse lineage with the branch leading to modern bony fishes (including


Cladists use only the order of branching to construct their schemes of relationships; it bothers them

not a whit that lungfish and salmon look and work so much alike. Cladism, in other words, is the

purest of all genealogical systems for classification, since it works only with closeness of common

ancestry in time. How preciously ironic then, that this most rigidly evolutionary of all taxonomic

systems should become the subject of such extraordinary misunderstanding -- as devised by Bethell,

and perpetuated by Kristol when he writes: ''. . . many younger biologists (the so- called 'cladists')

are persuaded that the differences among species -- including those that seem to be closely related -are such as to make the very concept of evolution questionable.''

This error arose for the following reason. A small splinter group of cladists (not all of them, as

Kristol claims) -- ''transformed'' or ''pattern'' cladists by their own designation -- have adopted what

is to me an ill-conceived definition of scientific procedure. They've decided, by misreading Karl

Popper's philosophy, that patterns of branching can be established unambiguously as a fact of

nature, but that processes causing events of branching, since they can't be observed directly, can't be

known with certainty. Therefore, they say, we must talk only of pattern and rigidly exclude all

discussion of process (hence ''pattern cladistics'').

This is where Bethell got everything arse-backwards and began the whole confusion. A

philosophical choice to abjure all talk about process isn't the same thing as declaring that no reason

for patterns of branching exists. Pattern cladists don't doubt that evolution is the cause behind

branching; rather, they've decided that our science shouldn't be discussing causes at all.

Now I happen to think that this philosophy is misguided; in unguarded moments I would even deem

it absurd. Science, after all, is fundamentally about process; learning why and how things happen is

the soul of our discipline. You can't abandon the search for cause in favor of a dry documentation of

pattern. You must take risks of uncertainty in order to probe the deeper questions, rather than

stopping with sterile ecurity. You see, now I've blown our cover. We scientists do have our

passionate debates -- and I've just poured forth an example. But as I wrote earlier, this is a debate

about the proper approach to causes, not an argument about whether causes exist, or even whether

the cause of branching is evolution or something else. No cladist denies that branching patterns

arise by evolution.

This incident also raises the troubling issue of how myths become beliefs through adulterated

repetition without proper documentation. Bethell began by misunderstanding pattern cladistics, but

at least he reports the movement as a small splinter, and tries to reproduce their arguments. Then

Kristol picks up the ball and recasts it as a single sentence of supposed fact -- and all cladists have

now become doubters of evolution by proclamation. Thus a movement, by fiat, is turned into its

opposite -- as the purest of all methods for establishing genealogical connections becomes a weapon

for denying the mechanism that all biologists accept as the cause of branching on life's tree:

evolution itself. Our genealogy hasn't been threatened, but my geniality has almost succumbed.

When I ask myself why the evidence for evolution, so clear to all historical scientists, fails to

impress intelligent nonscientists, I must believe that more than simple misinformation lies at the

root of our difficulty with a man like Irving Kristol. I believe that the main problem centers upon a

restrictive stereotype of scientific method accepted by most non-practitioners as the essential

definition of all scientific work.

We learn in high school about the scientific method -- a cut- and-dried procedure of simplification

to essential components, experiment in the controlled situation of a laboratory, prediction and

replication. But the sciences of history -- not just evolution but a suite of fundamental disciplines

ranging from geology, to cosmology, to linguistics -- can't operate by this stereotype. We are

charged with explaining events of extraordinary complexity that occur but once in all their details.

We try to understand the past, but don't pretend to predict the future. We can't see past processes

directly, but learn to infer their operation from preserved results.

Science is a pluralistic enterprise with a rich panoply of methods appropriate for different kinds of

problems. Past events of long duration don't lie outside the realm of science because we cannot

make them happen in a month within our laboratory. Direct vision isn't the only, or even the usual,

method of inference in science. We don't see electrons, or quarks, or chemical bonds, any more than

we see small dinosaurs evolve into birds, or India crash into Asia to raise the Himalayas.

William Whewell, the great English philosopher of science duringthe early nineteenth century,

argued that historical science can reach conclusions, as well confirmed as any derived from

experiment and replication in laboratories, by a method he called ''consilience'' (literally ''jumping

together'') of inductions. Since we can't see the past directly or manipulate its events, we must use

the different tactic of meeting history's richness head on. We must gather its won- drously varied

results and search for a coordinating cause that can make sense of disparate data otherwise isolated

and uncoordinated. We must see if a set of results so diverse that no one had ever considered their

potential coordination might jump together as the varied products of a single process. Thus plate

tectonics can explain magnetic stripes on the sea floor, the rise and later erosion of the

Appalachians, the earthquakes of Lisbon and San Francisco, the eruption of Mount St. Helens, the

presence of large flightless ground birds only on continents once united as Gondwanaland, and the

discovery of fossil coal in Antarctica.

Darwin, who understood the different rigor of historical scienceso well, complained bitterly about

those critics who denied scientific status to evolution because they couldn't see it directly or

reproduce its historical results in a laboratory. He wrote to Hooker in 1861: ''Change of species

cannot be directly proved . . . The doctrine must sink or swim according as it groups and explains

phenomena. It is really curious how few judge it in this way, which is clearly the right way.'' And

later, in 1868: ''This hypothesis may be tested . . . by trying whether it explains several large and

independent classes of facts; such as the geological succession of organic beings, their distribution

in past and present times, and their mutual affinities and homologies.''

If a misunderstanding of the different methods of historical inquiry has impeded the recognition of

evolution as a product of science at its best, then a residual fear for our own estate has continued to

foster resentment of the fact that our physical bodies have ancient roots in ape-like primates,

waddling reptiles, jawless fishes, worm-like invertebrates, and other creatures deemed even lower

or more ignoble. Our ancient hopes for human transcendence have yet to make their peace with

Darwin's world.

But what challenge can the facts of nature pose to our own decisions about the moral value of our

lives? We are what we are, but we interpret the meaning of our heritage as we choose. Science can

no more answer the questions of how we ought to live than religion can decree the age of the earth.

Honorable and discerning scientists (most of us, I trust) have always understood that the limits to

what science can answer also describe the power of its methods in their proper domain. Darwin

himself exclaimed that science couldn't touch the problem of evil and similar moral conun- drums:

''A dog might as well speculate on the mind of Newton. Let each man hope and believe what he


There is no warfare between science and religion, never was except as a historical vestige of

shifting taxonomic boundaries among disciplines. Theologians haven't been troubled by the fact of

evolution, unless they try to extend their own domain beyond its proper border (hubris and

territorial expansionism aren't the sins of scientists alone, despite Mr. Kristol's fears). The Reverend

Henry Ward Beecher, our greatest orator during Darwin's century, evoked the most quintessential of

American metaphors in dismissing the entire subject of conflict between science and religion with a

single epithet: ''Design by wholesale is grander

than design by retail'' --or, general laws rather than creation of each item by fiat will satisfy our

notion of divinity.

Similarly, most scientists show no hostility to religion. Why should we, since our subject doesn't

intersect the concerns of theology? I strongly dispute Kristol's claim that ''the current teaching of

evolution in our public schools does indeed have an ideological bias against religious belief.''

Unless at least half my colleagues are inconsistent dunces, there can be -- on the most raw and

direct empirical grounds -- no conflict between science and religion. I know hundreds of scientists

who share a conviction about the fact of evolution, and teach it in much the same way. Among these

people I note an entire spectrum of religious attitudes -- from devout daily prayer and worship to

resolute atheism. Either there's no correlation between religious belief and confidence in evolution - or else half these peple are fools.

The common goal of science and religion is our shared struggle for wisdom in all its various guises.

I know no better illustration of this great unity than a final story about Charles Darwin. This scourge

of fundamentalism had a conventional church burial -- in Westminster Abbey no less. J. Frederick

Bridge, Abbey organist and Oxford don, composed a funeral anthem expecially for the occasion. It

may not rank high in the history of music, but it is, as my chorus director opined, a ''sweet piece.''

(I've made what may be the only extant recording of this work, marred only by the voice of yours

truly within the bass section.) Bridge selected for his text the finest biblical description of the

common aim that will forever motivate both the directors of his building and the inhabitants of the

temple of science -- wisdom. ''Her ways are ways of pleasantness and all her paths are peace''

(Proverbs 3:17).

I am only sorry that Dr. Bridge didn't set the very next metaphor about wisdom (Proverbs 3:18), for

it describes, with the proper topology of evolution itself, the greatest dream of those who followed

the God of Abraham, Isaac, and Jacob: ''She is a tree of life to them that lay hold upon her.''

COPYRIGHT 1987 Discover

COPYRIGHT 2004 Gale Group

To See or Not to See: Evolution of Eye Degeneration in Mexican Blind Cavefish1

Jeffery, William R


In 1872 Charles Darwin wrote, "As it is difficult to imagine that eyes, though useless, could in any

way be injurious to animals living in darkness, I attribute their loss solely to disuse." This statement

launched more than a hundred years of speculation and debate on the evolutionary mechanisms

responsible for the loss of eyes in cave animals (Culver, 1982). Today this problem is still

unresolved, but prevailing opinions usually support one of two hypotheses.

The neutral mutation hypothesis suggests that eye degeneration is caused by random mutations in

eye forming genes, which gradually accumulate in the absence of selective pressure. In contrast, the

adaptation hypothesis suggests that natural selection causes the loss of eyes due to advantages in

losing eyesight. As exclaimed in Darwin's famous quotation, the actual benefits of blindness are

uncertain. Thus, different versions of the adaptation hypothesis have attributed the loss of eyesight

to energy conservation, citing the high cost of making an eye, or to enhancement of other sensory

organs that are highly beneficial to survival in the cave environment. Through the years, however,

little or no experimental verification has been leveled in support of any version of either hypothesis.

To understand the evolution of eye degeneration, it is necessary to determine the molecular and

cellular mechanisms of the degenerative process, and whether the same or different genes and

mechanisms are involved in loss of vision.

We study the mechanisms of visual degeneration in the Mexican Tetra, Astyanax mexicanus, a

single species consisting of a surface-dwelling form (surface fish) (Fig. IA) and many cave dwelling

(cavefish) forms inhabiting different caves (Fig. IB-E) (Jeffery, 2001). The Mexican tetra is easy to

raise in the laboratory and exhibits many of the attributes that have made zebrafish a popular model

system in developmental biology. These features include external fertilization, frequent and

abundant spawning, transparent embryos, a 4-6 month generation time, and the opportunity for

molecular, developmental, and genetic analysis. The surface and cave forms of A. mexicanus are

interfertile, and successful mating is also possible between different cavefish populations (Sadoglu,

1957; Wilkens, 1971). Because of these attributes Astyanax cavefish represent one of the few cave

animals in which laboratory experiments can be conducted on the mechanisms of eye degeneration

and these mechanisms can be compared in the same species from different caves. Here we review

current progress on the evolution and development of Astyanax cavefish and discuss how these

studies have contributed to understanding the evolutionary basis of eye degeneration.


To evaluate differences or similarities in the mechanisms of eye degeneration, it is first necessary to

understand the evolutionary history of cavefish populations. Did all cavefish populations originate

from a common ancestor and lose their eyes only once or did they evolve many times and lose their

eyes independently? Different approaches have been used to determine the evolutionary

relationships of cavefish, including allozyme analysis, biogeography, and phylogenetic

reconstruction using molecular sequences. We will briefly consider the results obtained from the

first two approaches and then describe the phylogenetic studies in more detail.

Figure 2 shows a map of the Sierra de El Abra region in northeastern Mexico illustrating the

locations of known caves harboring Astyanax cavefish populations. The major cavefish region

consists of the Sierra de El Abra, thé Sierra de Guatemala, the Micos region (Fig. 2), and the valleys

lying between these limestone ridges in the states of Tamaulipas and San Luis Potosi, Mexico

(Wilkens and Burns, 1972; Mitchell et al., 1977). An outlying cavefish population has also been

discovered in the state of Guererro in south central Mexico (Espinasa et al., 2001).

In an electrophoretic study showing minimal divergence in 17 allozyme loci, Avise and Selander

(1972) concluded that the Sierra de El Abra cavefish had a common origin. However, a limited

number of cavefish populations (Pachon, Los Sabinos, and Chica; Fig. 2) were sampled in this

study. In contrast, Mitchell et al. (1977), who surveyed 29 different cavefish populations in the

Sierra de El Abra, Sierra de Guatemala, and Micos region, proposed several different origins of

Astyanax cavefish. Mitchell et al. (1977) also estimated the divergence between surface fish and

cavefish to have occurred about 10,000 to 100,000 years ago in the Sierra de El Abra region. The

possibility of multiple cavefish origins is strongly supported by the recently discovered Guerrero

cavefish from a cave located several hundred miles southwest of the main cavefish region (Espinasa

et al, 2001).

The first phylogenetic studies of cavefish populations were done using DNA polymorphisms

amplified by arbitrary primers (RAPDs) (Espinasa and Borowsky, 2001). This analysis supported a

single origin of Sierra de El Abra cavefish and an independent origin of Subterraneo cavefish in the

Micos region (Fig. 2). The limited number of RAPD markers scored in this study, however, left

some uncertainty about the true relationships among the Sierra de El Abra cavefish. Thus far, it has

proved difficult to obtain sufficiently variable sequence information from nuclear genes to construct

robust phylogenetic trees, presumably due to the recent divergence of surface fish and cavefish.

Thus, Dowling et al. (2002) were prompted to use NAD1 dehyrdogenase-2 (ND-2), a rapidly

evolving mitochondrial gene, to infer cavefish relationships (Fig. 3).

Before discussing the resulting ND-2 mitochondrial DNA (mtDNA) phylogeny, it is necessary to

comment on the currently unresolved taxonomy of A. mexicanus and related forms. Some

taxonomists recognize two separate Astyanax species in Mexico: A. mexicanus in northern Mexico

and Astyanax aeneus in southern Mexico (Obregon-Barbosa et al., 1994). Others be lieve that all

Mexican and Central American Astyanax are a single species, Astyanax fasciatus (see Wilkens,

1988). Here, we defer to the first classification, designating the northern Mexican form as A.

mexicanus, the southern Mexican form as A. aeneus, and the Central American form as A.

fasciatus. Our justification is that these taxa are strongly supported by the mtDNA phylogeny (Fig.


The mtDNA phylogeny infers at least two separate origins of cavefish, one before the divergence of

the present day A. mexicanus and A. aeneus, and the other after the bifurcation of these taxa (Fig.

3). Accordingly, two distinct mtDNA lineages are recognized: the A lineage, including A.

mexicanus and A. aeneus surface fish and Pachon and Subterraneo cavefish, and the B lineage,

including Tinaja, Los Sabinos, and Curva cavefish (Dowling et al., 2002). The A lineage exhibits

one of more than 20 different Type A ND-2 haplotypes, which vary from each other in only a few

nucleotide positions and are mostly represented in surface fish. The B lineage exhibits one or two of

only a few Type B ND-2 haplotypes, which differ in 7 or more nucleotide sites from the Type A

haplotypes and are present in cavefish but not in any nearby surface fish populations. Sampling

from Texas to Costa Rica failed to find any surface fish populations with Type B haplotypes

(Dowling et al., 2002), suggesting that the surface fish stock that established the B lineage cavefish

may be extinct.

Although the mtDNA tree has strong bootstrap support, our interpretation of these data must be

treated with caution. First, the tree is based on only a single gene. However, a recent phylogenetic

analysis has confirmed the topology of this tree using a different mitochondrial gene, cytochrome b

(Strecker et al, 2003). second, mtDNA trees could be influenced by hybridization, which is known

to have occurred between some of the cavefish populations and nearby surface fish (Mitchell et al,

1977; Romero, 1983; Langecker et al., 1991). Third, a recent phylogeny using microsatellite loci is

more consistent with a common origin of the Sierra de El Abra cavefish (Strecker et al., 2003),

suggesting replacement of mitochondrial DNA may have occurred by hybridization in Pachon

cavefish. It is clear from the mtDNA data, however, that A and B lineage cavefish are genetically

isolated populations.

In summary, separate origins with accompanying episodes of eye degeneration may have occurred

in the Guerrero, Sierra de Guatemala (Molino), Micos (Subterraneo), and Lineage A and B Sierra

de El Abra cavefish populations. Below we will compare the developmental mechanisms of eye

degeneration in some of these cavefish.


To determine the mechanisms of eye regression, we focused on the nature and timing of

degenerative processes in the embryonic eye primordia. In every cavefish population we have

studied, the eye primordium appears to be smaller than its surface fish counterpart. However, the

cavefish eye seems to develop normally up to about the hatching stage, forming a lens and optic

cup. Subsequently, development gradually arrests, the retina becomes disordered, and the

degenerating eye disappears into the orbit (Cahn, 1958; Langecker et al., 1993). The cavefish lens

does not differentiate arrays of aligned crystallin fibers and the retina, although at first layered

normally, eventually shows disorganization and complete or partial loss of photoreceptor cells. In

many developing systems, an alternative to cell differentiation is apoptosis: programmed cell death

(White, 1996). Therefore, we first investigated whether apoptosis occurred during cavefish eye


If cell death is restricted to a single eye tissue, or begins in one tissue and later spreads to others,

then the tissue that dies first is a strong candidate to initiate the degeneration process. Apoptosis

was compared in surface fish and in Pachon cavefish embryos using the TUNEL assay (Jeffery and

Martasian, 1998), which detects DNA fragmentation. Surface fish embryos showed little or no

programmed cell death in the developing eye (Fig. 4A), except in the isthmus that temporarily

forms between the budding lens and the surface ectoderm, as has been previously described in the

mammalian eye (Silver and Hughes, 1968). Cavefish showed the same apoptotic event in a small

number of isthmus cells as the lens vesicle pinched off from the surface ectoderm. About a day after

the cavefish lens vesicle was formed, however, an additional and more extensive episode of

apoptosis was detected in its central core (Fig. 4B), the region where lens fiber cells would normally

differentiate from lens epithelial cells. No apoptosis was detected at this time in the surface fish lens

(Fig. 4A), and no other cavefish eye tissue died at this stage of development. A few days later, the

retina began to undergo apoptosis. Retinal cell death is restricted to the outer nuclear layer and the

region adjacent to the ciliary marginal zone (CMZ) (A.G.S., unpublished), where most new retinal

cells are produced in the teleost retina (Johns and Easter, 1977; Harris and Perron, 1998). Thus, the

lens is the first tissue to undergo cell death during eye degeneration in Pachon cavefish.

Does the embryonic lens also die in other cavefish populations? Using the TUNEL assay, we

showed that the Los Sabinos cavefish lens also dies before any other tissue in the degenerating eye

(Fig. 4C). The results suggest that lens apoptosis may be responsible for triggering eye degeneration

in both A and B lineage cavefish.

The cessation of retinal growth in cavefish could be caused by the failure of the dying lens to

produce a growth-promoting factor or it could be due to an independent event in the retina. A

reasonable candidate for an independent retinal event would be interference with cell proliferation.

Surface fish have an active CMZ. Proliferating cells can be detected by incorporation of labeled

nucleotides into DNA, the presence of the DNA polymerase cofactor PCNA, and the expression the

homeobox genes RxI and Vsx2 (Fig. 4D, G), throughout the period of eye growth (Strickler et al,

2002; A.O.S., unpublished results). all of these cell proliferation markers were expressed in the

Pachon cavefish CMZ (Fig. 4E, H), although the retina does not markedly increase in size during

this period (Strickler et al., 2002). Presumably, new cells are removed from the retina soon after

they are formed by the apoptotic events that begin a few days after the initiation of lens cell death.

We next asked whether the surprisingly wasteful process in which retinal cells appear to cycle

quickly between birth and death also occurs in other cavefish populations? As shown in Figure F, I,

RxI and Vsx2 are also expressed in the CMZ of Los Sabinos cavefish, despite a comparable lack of

net growth. Thus, we conclude that arrest of cell proliferation is not the major cause of eye

degeneration in A and B lineage cavefish populations.

The results described above focus our attention back to the lens. Does the lens organize the whole

eye and could its removal by apoptosis result in the arrest of eye formation? The central role of the

lens in eye formation has recently been appreciated (Beebe and Coats, 2000; Thut et al., 2001), due

largely to developmental studies with cavefish (Yamamoto and Jeffery, 2000). We developed a lens

transplantation assay to determine the role of the lens in surface fish eye development and in

cavefish eye degeneration (Yamamoto and Jeffery, 2000, 2002).

The embryonic lens was removed from a donor embryo shortly after it pinched off from the surface

ectoderm, about a day before the first detection of largescale apoptosis in the cavefish lens, and it

was transplanted into the optic cup of a host embryo. Lens transplantation was done unilaterally,

with the unoperated eye of the host serving as a control. The first transplantation experiments were

carried out reciprocally between surface fish and Pachon cavefish: a surface fish lens was

transplanted into a cavefish optic cup and vice versa (Yamamoto and Jeffery, 2000). These

experiments also addressed the autonomy of programmed cell death in the cavefish lens: is cell

death determined by the lens itself or is it induced by another tissue, for instance the retina? When a

cavefish lens was transplanted into a surface fish optic cup it died on schedule, just as if it had not

been removed from the donor embryo. Likewise, when a surface fish lens was transplanted into a

cavefish optic cup it continued to grow and differentiated as it would have in the surface fish host.

Together, these results indicate that the Pachon cavefish lens is autonomously fated for apoptosis, at

least by the time of the transplantation (Yamamoto and Jeffery, 2000).

The autonomy of surface fish lens development in the cavefish host is the key part of the

transplantation experiment. After obtaining a surface fish lens, the Pachon cavefish eye reversed its

fate and began to grow and develop (Yamamoto and Jeffery, 2000). Eventually, the cornea and iris

appeared, which are normally missing in cavefish, and the retina enlarged and became more

organized. Further growth resulted in the presence of a highly developed eye containing all of the

expected eye tissues, including the cornea, iris, and photoreceptor cells, in the adult Pachon cavefish

host (Fig. 5B). When the donor lens was labeled with GFP no labeled cells appeared in the restored

tissues of the host (Yamamoto and Jeffery, 2000). Thus, the rescued eye tissues arise from the host

and not the donor. The cornea and iris are derived in part from optic neural crest cells, indicating

that cavefish neural crest cells are present and located in the proper positions to be induced by the

lens. In contrast to the eye with a transplanted lens, the unoperated eye of the cavefish host

degenerated and disappeared into the orbit according to its usual schedule (Fig. 5A). Likewise, after

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