Donkeys, Horses, Mules

and Evolution
The Phenotypic Effects of Chromosome Variation

Sean D. Pitman M.D.

© August 2003
Last update: February 2008
 Table of Contents

• Introduction
• The Same Information in Different Places
• Types of Chromosomal Alterations
o Non-Disjunction
o Robertsonian Fusion
o Tandem Fusion
o Translocations
o Pericentric Inversions
o Paracentric Inversions
o Drastic Rearrangements
• Discussion
• The Key Differences Between Humans and Apes

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Introduction

Much is made of DNA or protein sequence analysis as a way of determining

evolutionary ancestry. Branching phylogenetic trees are based on such sequence
analysis and are used to suggest various evolutionary relationships between different
creatures on the "Tree of Life." Even so called "pseudogenes" are often used to show
supposed evolutionary relationships. However, although sequence analysis is
interesting by itself and may in fact say a lot about common ancestry, such analysis
does not necessarily favor the theory of common descent in many cases. Certain
differences between the DNA sequences of various creatures can easily be explained
by the mindless naturalistic processes of random mutation and natural selection while
other differences cannot be so easily explained.
Not all differences are created equal. Some differences are neutral while others are
functional. In fact, most mutations are thought to be neutral with respect to
survival/reproductive advantage. Natural selection is not required to achieve neutral
genetic variations. Because of this, neutral variations arise relatively rapidly. Functional
variations, depending on the complexity of the functions in question, might take a lot
longer to evolve since there are a so many more non-functional, detrimental, or neutral
sequences that could evolve when compared to the relatively few beneficial functions
available to a given creature in a particular environment. So, a simple statement that
chimps and humans are 94% to 98% identical as far as DNA is concerned is deceptive
in that it says nothing about the type of differences involved (neutral or functional) or if
such differences are statistically possible to achieve in the amount of time allotted.
After presenting this argument, I am occasionally asked why I would lean toward
classifying horses and donkeys as the same "kind" or as having a common ancestor
while at the same time classifying humans and chimps as different "kinds" not having a
common ancestor (thought by most scientists to have lived some 5 to 8 million years
ago)?
This is not an easy question. While there may not be sufficient genetic evidence
yet to answer this question, an answer does appear to be on the horizon. Some
differences are obvious. For example, gross chromosomal differences are easily noted.
Humans and chimps differ not only in chromosome number, but also by nine pericentric
chromosomal inversions and one centric fusion. We also know that both humans and
chimps do have unique genetic sequences, but our knowledge has been rather limited
as far as exactly how the many differences affect the overall phenotypic function of the
two species. Because of this limited knowledge, it has been very difficult to say whether
or not such differences in genetic function can be achieved via random mutation and
natural selection given a few million years (since there certainly are limits to the level of
functional complexity that can be achieved by such "evolutionary" processes). However,
certain key functionally unique genetic differences are coming to light (see further
discussion below).
I am not a believer in design theory because of I have a problem with humans
sharing a common ancestor with chimps. This possibility really does not bother me at
all. What bothers me is that I know of various functions in different creatures that are
separated by large non-beneficial gaps in function. These non-beneficial gaps cannot
be crossed except by completely random mutations. These random mutations are
random because they cannot be guided by the forces of natural selection toward any
particular genetic sequence over any other particular genetic sequence - be it
beneficially functional or not. Such random drift simply takes too long to produce the
various independent functions that we do observe in living things. It is this problem that
has convinced me of the truth of design theory and of the implausibility of common
decent as an overriding explanation for the huge range in the form and function of living
things that we see in the natural world. A selection mechanism that is phenotypically
based cannot direct neutral or even detrimental genotypic changes toward a novel
potentially beneficial target or targets. This is my problem with the theory of evolution. I
do not have a problem with the idea of the common decent of anything, but I do have a
problem with the mechanisms that have been suggested as a driving force for such
changes.
So, if such evolutionary "boundaries" exist as I think they do, how can they be
delineated? Granted, it is very difficult to know exactly where and how to draw genetic
boundaries between various "kinds" or gene pools. It seems that such boundaries do
exist since there is a fair amount of evidence to support this hypothesis, but determining
exact boundaries seems to be a difficulty in many cases owing to a lack of sufficient
knowledge at this time to reach high levels of exactness and predictability in this regard.
However, there are clues as to which groups might have had an easier time
crossing the genetic distances that exist between them. For one thing, those "kinds"
that can breed and actually produce viable offspring are obviously very closely related
as far as their gene pools are concerned. Horses and donkeys can interbreed, while
humans and chimps cannot. For horses and donkeys, this ability to produce viable
offspring seems to be very good evidence of common ancestry. In other words, I
believe that horses and donkeys share the same genetic information and/or genetic loci
on their respective sets of chromosomes. All the information appears to be the same,
but the order of that information, as it is written on the chromosomal blueprints, is
different.

The Same Information in Different Places

Looking a bit more into the genetics involved, horses have 32 pairs of
chromosomes while donkeys have only 31 pairs. When a male donkey and a female
horse mate, they produce a mule (a male horse with a female donkey produces a
different creature called a hinny). A mule has 31-paired chromosomes as well as an
extra chromosome from its horse mother that is not paired. Many think that this extra
non-paired chromosome is what makes the mule infertile. The suggested reason for
this is that during meiosis, the extra chromosome would not have a partner to match up
with. When the paired chromosomes are split apart into separate haploid gametes, the
split would be uneven, creating sterility. However, this is not an entirely satisfactory
explanation for several reasons. The most obvious reason that this hypothesis cannot
be such an automatic assumption is the fact that other matings of odd-paired
chromosomes do give rise to virile offspring. For example, hybrids of the wild horse (33
pairs) and the domesticated horse (32 pairs) are fertile, and yet they have an odd
chromosome out, just like mules do.
 Clearly then, something more than a difference in chromosome number is
contributing to the species-interbreeding barrier. If one thinks about it, it is not really all
that hard to imagine how the pairing of odd numbers of chromosomes could be realized
during meiosis so that fertility would not be lost. During meiosis all the chromosomes
double themselves. A cell undergoing gametogenesis in a diploid organism, such as
horses and donkeys, will become tetraploid during the first part of meiosis. At this point
genetic recombination occurs between the four copies of a given chromosome. After
this, the four copies are eventually split apart to occupy four different cells called
gametes. Each gamete, containing only one copy of a given chromosome, is termed
“haploid”. However, if there is an odd chromosome out when a cell starts
gametogenesis, this single chromosome with no sister chromosome can only double to
make two chromosomes during meiosis instead of the usual four chromosome copies.
Still, all is not lost. These two copies will also be sorted out into gametes. But, since
there are only half as many copies as "normal" diploid chromosomes, only half of the
gametes will get the extra chromosome. That means that 50% of the gametes will be
viable, having the complete set of genetic information needed to code for that particular
creature.
So, since hybrid fertility is clearly possible for those having odd chromosome
numbers, why are mules sterile? Horse-donkey hybrids (mules and hinnies), show a
"block" during testicular meiosis at the primary spermatocyte stage. This is caused by
incompatibility of synaptal pairing between paternal and maternal chromosomes -
resulting in a total arrest of spermatogenesis. But what exactly causes this block?
In order to understand this problem a bit more, it might be interesting to look into
how interbreeding creatures can have variations in chromosome numbers and yet have
the same information in those chromosomes. As it turns out, many interbreeding
creatures having different chromosome numbers have undergone chromosomal
translocations. What happens here is that a piece or "arm" of one chromosome
becomes detached from its normal position on one particular chromosome and
reattached to a different chromosome. There are several different types of
translocations and chromosomal fusions. Sometimes chromosomes can fuse with each
other to form much longer chromosomes or they can split at the centromere to form two
shorter chromosomes. One such rearrangement is known as a Robertsonian
rearrangement and is the result of the fusion of two centromeres into one or the splitting
of one centromere into two. A tandem fusion, on the other hand, is a fusion of two
chromosomes in which one end of a chromosome fuses with the end or the centromere
of another chromosome.
Comparisons between the chromosomal banding patterns of these rearranged
chromosomes show that the information is still the same, only rearranged a bit.
Moreover, it appears that certain types of rearrangements are quite group-specific for a
certain type of creature. One type of rearrangement that occurs in one type of animal
does not necessarily occur in another type of animal. The problem with this is that
during meiosis the various portions of translocated chromosomes must still match up
with their normal counterpart on different chromosomes during meiosis in order for
genetic recombination to proceed without lethal mistakes. Of course, one can only
imagine that some types of complicated chromosomal rearrangements would make
correct lineups impossible. Obviously then, if a matching lineup is impossible,
interbreeding impossible.
However, with some kinds of
chromosomal rearrangements, the various
segments are still able to pair up and crossover
even though there might be more than two
centromeres involved. For example, two
chromosomes might only match up half way
while the rest of each of these two
chromosomes, might match a third
chromosome (see visual illustration).6 This would make it possible for various
chromosome numbers to maintain the same information and still give rise to viable as
well as fertile offspring. And, various interbreeding creatures do in fact maintain a wide
range of possible chromosome numbers in their respective gene pools. Besides the
wild and domestic horse mentioned above, there are several other fairly well known
examples.
 Of particular interest are domestic dogs and wolves of the genus canis. They have
78 chromosomes while foxes have a varied number from 38-78 chromosomes. The
uniformity of chromosome number in canid dogs can be due to free interbreeding over a
wide range, whereas foxes live in small family groups and smaller territories so that new
arrangements will persist. If the "kind" is penned at the level of the family Canidae, then
the implications in terms of the number of animals required to produce the present
varieties are not as daunting as many fear. Indeed, numerous chromosome homologies
have been identified in animals today. The differences between many species can often
be explained with chromosomal rearrangements, as in the case of kangaroos, where
Robertsonian fusions can account for much of the variation that exists between the
different kangaroo species.

Types of Chromosomal Alterations

Non-Disjunction:

When complex eukaryotes like humans replicate, specialized cells are created
("gametes", known as sperm and ovae) that have half as many chromosomes as the
rest the cells. Instead of having two of each chromosome, these gametes only have one
of each chromosome. Gametes from male and female partners fuse and recombine
their single chromosomes into pairs of chromosomes again where half of each pair
came from a sperm or male gamete and the other half from an ovum or female gamete.
On very rare occasions, when new chromosomes are being made, the new copies will
fail to separate (or "disjoin") from the original copy. When this happens, one gamete will
get an extra copy of the chromosome that failed to disjoin, and the other gamete will get
no copy. This is called a non-disjunction. In such a case if a sperm that retained two
copies of a given chromosome fused with an ovum that had one copy of that
chromosome the resulting cell would have three copies of that chromosome instead of
the normal two copies. Usually, the gain of an extra copy of a chromosome is fatal, and
the cell dies, but not always.
Another way to increase chromosome number is by duplicating all of the
chromosomes in a sort of whole genome non-disjunction resulting in polyploidy. This
seems to work alright for plants, but for animals, this is very rare. However, there are
many examples of tetraploid (4n) and hexaploid (6n) insects, triploid and tetraploid fish
(Catfish, Cyprinids and Carp), and even a hexaploid fish (a subspecies of the tetraploid
Carp). There are also several tetraploid species of claw-toed frogs, and even a
tetraploid rat (the red viscacha rat, or Tympanoctomys barrerae). In the case of this rat
species, the number of chromosomes (102) is much lower than one might expect by
looking at closely related rat species. Based on these relatives, one would expect the
tetraploid rat to have 112 chromosomes, which brings us to the other mechanisms for
changing chromosome number.

Robertsonian Fusion:

Robertsonian fusion changes the

chromosome number, but not the arm number.
When chromosomes line up during meiosis I, a
metacentric chromosome lines up with two
acrocentric chromosomes (see illustration). For example, the house mouse Mus
Musculis has 40 chromosomes, and a population of mice form the Italian Alps was
found to have only 22 chromosomes. This population differs slightly from the normal
house mouse in morphology as well and is classified as a different species named Mus
poschiavanus. Other populations have been discovered with chromosome numbers
varying between 22 and 40. For example, over 40 Robertsonian "races" of Mus
musculus domesticus have been found in Europe and North Africa.1 The number of
chromosome arms are the same and banding studies reveal the genes to be
homologous. Obviously, in terms of their relationship, these different species are all one
group.
Another example of a Robertsonian polymorphism is the house musk shrew that
lives in the central region of West Malaysia and has a variation in chromosome numbers
from 36 to 40. Also, in Southern India and Sri Lanka musk shrews can be found with
having between 30 and 32 chromosomes due to Robertsonian-type changes.2
A new Robertsonian translocation has been found in cattle. A bull from
Marchigiana breed (central Italy) was found to be a heterozygous carrier of a centric
fusion translocation involving chromosomes 13 and 19 according to RBA-banding and
cattle standard nomenclatures. CBC-banding revealed the dicentric nature of this new
translocation, underlining the recent origin of this fusion. In fact, both the bull's parents
and relatives had normal karyotypes. In vitro fertilization tests were also performed in
the bull carrying the new translocation, in two bulls with normal karyotypes (control) and
in four other bulls carrying four different translocations.3
The significance of centric fusions (Robertsonian translocations) in domestic
animals, with special reference to sheep, is also interesting. A study was done that
considered 856 ewes with either a normal chromosome number 2n = 54 or carrying one
or more of the three different translocations (centric fusions) t1, t2 and t3 in various
heterozygous and homozygous arrangements. Rams, which were used in the matings,
were homozygous for one of the translocation chromosomes (2n = 52), double
heterozygotes (2n = 52), triple heterozygotes (2n = 51), or were carriers of four
translocation chromosomes (2n = 50) and five translocation chromosomes (2n = 49). A
remarkably even distribution of segregation products was recorded in the progeny of all
combinations of translocation ewes plus translocation rams in those groups in which
sufficient animals were available for statistical analysis. Forty-eight chromosomally
different groups of animals were mated. Further, the overall fertility of the translocation
sheep (measured by conception rate to first service via the lambing percentage and
number of ewes that did not breed a lamb) was not significantly different from the New
Zealand national sheep breeding data where this study was done. In some groups the
poorer reproductive performance could be explained by the age structure of the flock
and inbreeding depression, which probably affected the performance of some animals.
Sheep with progressively decreasing chromosome numbers, due to centric fusion, 2n =
50, 2n = 49 and 2n = 48, were reported. The 2n = 48 category represents a triple
homozygous ewe and a triple homozygous ram and is the first report of the viable
evolution of such domestic animals. Less than 1% of phenotypically abnormal lambs
were recorded in a total of 1,995 progeny born over 10 years. It is now considered that
there is little or no evidence to suggest that centric fusions in a variety of combinations
affect the total productive fitness of domestic sheep. It is suggested that future research
should be more actively directed to understanding their genetic significance.4
A detailed investigation of testicular meiosis in a mule, a hinny and a Przewalski
horse/domestic horse hybrid were made. Abnormalities of pairing were observed in the
mule and hinny in most germ cells at the pachytene stage of meiotic prophase, and
spermatogenesis was almost totally arrested. A few mature spermatozoa were
recovered from the ejaculate and epididymal flushings of the hinny. The Przewalski
horse/domestic horse hybrid was fertile and showed normal spermatogenesis.
Chromosome banding studies showed a close homology between the karyotypes of the
Prezwalski horse (Equus przewalskii, 2n = 66) and the domestic horse (E. caballus, 2n
= 64), and it is evident that a single Robertsonian translocation occurred that
transformed four acrocentric chromosomes of E. przewalskii into two metacentric
chromosomes in E. caballus. The investigations showed that a trivalent is formed at
meiosis in the hybrid (2n = 65), segregation which gives two classes of genetically
balanced spermatozoa. Both of these are capable of producing normal offspring if they
fertilize the eggs of a domestic mare.5

Tandem Fusion:

Tandem fusion changes arm number and chromosome number. Tandem fusions
have been found in some antelope species where a sex chromosome is fused with an
autosome. Although rare, one can assume that the organisms probably had a common
forerunner. The antelope displaying this fusion range in size from the eland (the largest
of all the antelopes) to smaller species such as the sitatunge and the bushbuck.
However, they all share common features, such as similar shapes of the horns and
stripes on the body which may be prominent as in the case of the Bongo or less
prominent as in the case of the eland. Species with this type of fusion are: the eland,
bongo, lesser and greater kudu, bushbuck, sitatunge and nilgai (Indian antelope) where
the y-chromosome is fused to an autosome. Tandem fusions are also found in
Malaysian swamp buffalo and Asian river buffalo. Another very interesting example of
this type of fusion is also found in the Asian deer. In the species Muntiacus muntjac, the
females have only 6 chromosomes and the males have 7 chromosomes (this is the
smallest chromosome number in mammals). However, in a different "species" of the
group, Muntiacus reevesi, both the males and the females have 46 chromosomes.
However, banding studies show that the same genetic material is present in both
species, the chromosomes in M. muntjac are just fused together to form very long
chromosomes. Once again no new information is added, it is just reshuffled, thus
providing differential expressions and increased variety.

Translocations:

A translocation is what happens when two

chromosomes that are not part of a pair get stuck
together as if they were a pair, and exchange
segments. If the segments that get exchanged are
large enough most of both chromosomes can move onto one single chromosome. In
this figure, the blue and red figures are cartoons of two different chromosomes. The
indentions in their centers represent the "centromeres" where the cell attaches filaments
that drag the chromosomes around. When these chromosomes cross-over, the result is
two chromosomes of very different sizes. One larger chromosome, contains almost all
of the genetic material of the two chromosomes, while the other smaller chromosome
contains almost none. In this example, the material from one chromosome has been
moved or "translocated" onto another chromosome. In dramatic cases where one
chromosome is significantly smaller after the translocation than the other chromosome
the smaller chromosome may be lost resulting in a reduced chromosome count.
Translocations can also lead to reduced fertility. In humans a well-known example
of a translocation of part of chromosome 21 results in Down Syndrome. Humans with
such translocations generally experience many problems as well as reduced fertility
depending upon when the translocation occurred and how much genetic information
was involved. However, in some insects and plants that have meiotic drive, healthy,
viable, and even fertile offspring can be produced via such translocations.6

Pericentric Inversions:

These provide changes in arm number but not chromosome number.

The number of arms depends on the position of the centromere. If it is
located at the end, then there is one arm and if in the middle there are two
arms. The inversion can change acrocentric chromosomes to metacentric
chromosomes. The rodents Neotoma and Peromyscus differ by this inversion.

Paracentric Inversions:

In this type of inversion the centromere is not included. This inversion

is relatively uncommon, but has been proposed for some bats, hares and
apes.2

Drastic Rearrangements:
 Under certain circumstances of severe environmental stress, drastic
rearrangements can produce greater varieties, which could enhance survival. These
changes can be rapid when new adaptive zones are entered (canalization model). Such
rearrangements have been proposed for the Spalax mole rat.2

Discussion

So, the potential problems with chromosomal rearrangements are obvious. There
can be multiple translocations involving the same chromosome as well as chromosomal
inversions and a number of other interesting cuttings and splicings of chromosomes.
These can result in a difficult or even impossible situation where chromosomes in such
involved hybrids simply cannot match up properly during meiosis. This lack of matching
capability results in sterility. For example, if a piece of donkey chromosome is inverted
relative to its counterpart in horses, then gene-by-gene pairing cannot occur without
elaborate looping and twisting. The chance of a successful cell division is very much
reduced. So, the mule cannot make egg or sperm cells. Thus, the mule is sterile.
However, a mule can still be born healthy because such growth of non-meiotic cells
occurs via a different process called mitosis. Mitosis does not have to match things up;
it only has to make copies. So, inversions and translocations do not prevent the mule
from growing up to be an adult.7
Rearrangements can and do account for differences in insectivores, bats,
primates, marine mammals, rodents, rabbits and hares, ungulates etc. The potential for
change certainly exists. Nevertheless, there are certain barriers that cannot be
transgressed. Such changes, as occur with reshuffling of genetic information, do not
add to that information. The information itself is still the same. True, there are a few
documented cases where mutations do actually result in unique or novel functions that
are beneficial to the host, such as the galactosidase evolution experiments performed
by B.G. Hall, the nylonase evolution experiments performed by Kinoshita, et. al. and of
course the all to familiar everyday examples of antibiotic resistance by bacteria.
Surprisingly though, these very examples of evolution in action are the ones that make
the boundaries of evolutionary processes most clearly delineated.

The Key Human-Ape Differences

It is becoming more and more clear that the key functional differences between

living things, like humans and apes, are not so much found in protein-coding genes, but

in the non-coding regions of DNA once thought to be functionless "junk-DNA" -

evolutionary remnants of past mistakes that are shared between various creatures.

This notion is starting to be shed with more and more discoveries that show that many

of these same regions are not just functional, they carry the vast majority of the genetic

information. The "genes" that were once thought to be so important for genetic

function are turning out to be equivalent to the most low-level basic building blocks

within the genome, like bricks and motor. Surprisingly, it is the non-coding regions of
DNA control what is done with these building blocks - that determine what kind of

"house" to build so to speak. The following article is very interesting in this regard:

"Seventy-five percent of known human miRNAs [microRNAs] cloned in this study

were conserved in vertebrates and mammals, 14% were conserved in invertebrates,

10% were primate specific and 1% are human specific. The new miRNAs have a

different conservation distribution: more than half of the human miRNAs were

conserved only in primates, about 30% in mammals and 9% in nonmammalian

vertebrates or invertebrates; 8% were specific to humans. We saw a similar distribution

for the chimpanzee miRNAs.

 The different miRNA repertoire, as well as differences in expression levels of

conserved miRNAs, may contribute to gene expression differences observed in human

and chimpanzee brain . Although the physiological relevance of miRNAs expressed

at low levels remains to be shown, it is tempting to speculate that a pool of such

miRNAs may contribute to the diversity of developmental programs and cellular

processes . . . For example, miRNAs recently have been implicated in synaptic

development and in memory formation. As the species specific miRNAs described here

are expressed in the brain, which is the most complex tissue in the human body, with an

estimated 10,000 different cell types, these miRNAs could have a role in establishing or

maintaining cellular diversity and could thereby contribute to the differences in human

and chimpanzee brain ... function." 8

References:

1. Hauffe HC, Searle JB, Chromosomal heterozygosity and fertility in house mice
(Mus musculus domesticus) from Northern Italy. Department of Zoology, University
of Oxford, Oxford OX1 3PS, United Kingdom.
2. Sharma et al. 1969;. Aswathanarayana and Prakash 1976; Yosida 1982, Ishikawa
et al. 1989, Young, 1970, 1971, 1974; Sam et al., 1979
(http://www.amazingdiscoveries.org/postdeluge-p2.html)
3. Molteni L, De Giovanni-Macchi A, Succi G, Cremonesi F, Stacchezzini S, Di Meo
GP, Iannuzzi L. A new centric fusion translocation in cattle: rob (13;19). Hereditas
1998;129(2):177-80 Institute of Animal Husbandry, Faculty of Agricultural Science,
Milan, Italy. (http://bison.zbs.bialowieza.pl/isacc/suncus/srihtm.htm)
4. Bruere AN, Ellis PM., Cytogenetics and reproduction of sheep with multiple centric
fusions (Robertsonian translocations). J Reprod Fertil 1979 Nov;57(2):363-75.
(http://bison.zbs.bialowieza.pl/isacc/suncus/srihtm.htm)
5. Chandley AC, Short RV, Allen WR., Cytogenetic studies of three equine hybrids. J
Reprod Fertil Suppl 1975 Oct;(23):356-70.
(http://bison.zbs.bialowieza.pl/isacc/suncus/srihtm.htm)
6. http://www.madsci.org/posts/archives/may2001/989331026.Ev.r.html
 7. http://www.don-lindsay-archive.org/creation/mule.html
8. Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova, Ronald
Bontrop4, Edwin Cuppen & Ronald H A Plasterk, "Diversity of microRNAs in human
and chimpanzee brain", Nature Genetics, Vol 38 | Number 12 | December 2006 pp.
1375-1377. ( Link )

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