Craig E. Nelson
Questions like the following have been received from time
to time, so we thought it might be helpful to post the comments
and references offered by ENSI Co-Director Craig E. Nelson in
response, in case others might wonder....
Query from an ENSI user...
One question was directed my way - and I am not sure of the
answer. Perhaps you could help me.
As we all know one mechanism of speciation would be chromosome
mutations such as translocations etc. resulting in reproductive
Where I am not clear: How does the first chromosome
alteration get passed along to future generations?
Let us presume a female has the alteration and is now producing
different gametes than the rest of the population. How does
she pass along this change to progeny if her ova cannot be fertilized
by the unchanged spermatozoa which still occur in the rest of
Thanking you in advance if you can provide an answer...
Great question. You have hit on the core difficulty with this
model for speciation.
First note that her eggs can be fertilized by any male. The
barrier isn't in fertilization. Rather, the change will mess
up meiosis in the offspring.
PLANTS: Second note that chromosomal change speciation is most frequent
in plants that can self-fertilize. And remember that in plants
the flowers develop from somatic tissues--there is no germ line.
So a change in one cell can give rise to an entire branch on
which all of the flowers have the change, heterogzygously, so
many of the ova and pollen have the new mutation and when those
meet--bingo--you have the new form homozygous.
ANIMALS: The classic example in animals is Australian desert grasshoppers.
These have population booms and busts with local rains and have
many local populations that differ chromosomally. For speciation
to work easily, the female needs to be in a very small population.
Ideally, she is fertilized and then is (almost) the only survivor
in a patch of vegetation. When the rains come, she lays her eggs
and lots of offspring emerge. If the mutation occurred early
in the germ line, about half of her eggs will carry it (it can
be rarer if she has enough offspring mating). In a small population,
her sons will have a good chance of mating with her daughters.
IF they can produce some viable gametes (i.e. if the problems
at meiotic metaphase in some cells allow a partitioning with
some gametes getting normal chromosomes and some getting the
new form), THEN some of the matings will produce some individuals
that are homozygous for the new chromosomes and do not have meiotic
problems. This then sets up selection for mating preferentially
with your own chromosomal type (mutant or other).
I hope that the number of fairly severe assumptions in that
model make it clear why this form of speciation is not the
commonest form in animals.
You can find more details and some alternative models by typing
"chromosomal speciation" into Google. Here's
an example of what you can find:
1. Chromosome speciation: Humans, Drosophila,
and mosquitoes (by Francisco Ayala et al, PNAS, 2005) (click on title here for abstract at PNAS – then click on “Full Text (PDF)" to right of the abstract for free copy to download). The following is the abstract:
"Chromosome rearrangements (such as inversions, fusions,
and fissions) may play significant roles in the speciation between
parapatric (contiguous) or partly sympatric (geographically overlapping)
populations. According to the "hybrid-dysfunction"
model, speciation occurs because hybrids with heterozygous chromosome
rearrangements produce dysfunctional gametes and thus have low
reproductive fitness. Natural selection will, therefore, promote
mutations that reduce the probability of intercrossing between
populations carrying different rearrangements and thus promote
their reproductive isolation. This model encounters a disabling
difficulty: namely, how to account for the spread in a population
of a chromosome rearrangement after it first arises as a mutation
in a single individual. The "suppressed-recombination"
model of speciation points out that chromosome rearrangements
act as a genetic filter between populations. Mutations associated
with the rearranged chromosomes cannot flow from one to another
population, whereas genetic exchange will freely occur between
colinear chromosomes. Mutations adaptive to local conditions
will, therefore, accumulate differentially in the protected chromosome
regions so that parapatric or partially sympatric populations
will genetically differentiate, eventually evolving into different
species. The speciation model of suppressed recombination has
recently been tested by gene and DNA sequence comparisons between
humans and chimpanzees, between Drosophila species, and
between species related to Anopheles gambiae, the vector
of malignant malaria in Africa. "
2. CHROMOSOMAL SPECIATION:Cascading Chromosomal Speciation… (by William P. Hall, Dept. of EPO Biology, U. of Colorado, Boulder, CO, 1979)
Chromosomal Differentiation and Cascading Speciation
NOTE THAT THERE REMAIN SUBSTANTIAL CONFLICTING IDEAS ON
Chromosomes, Conflict, and Epigenetics: Chromosomal
(by Judith Brown, et al, Genomics and Human Genetics, Annual Review, 2010). [Access to full text: $20. Here's the Abstract:]
Since Darwin first noted that the process of speciation was indeed
the "mystery of mysteries," scientists have tried to
develop testable models for the development of reproductive incompatibilities-the
first step in the formation of a new species. Early theorists
proposed that chromosome rearrangements were implicated in the
process of reproductive isolation; however, the chromosomal speciation
model has recently been questioned. In addition, recent data
from hybrid model systems indicates that simple epistatic interactions,
the DobzhanskyMuller incompatibilities, are more complex.
In fact, incompatibilities are quite broad, including interactions
among heterochromatin, small RNAs, and distinct, epigenetically
defined genomic regions such as the centromere. In this review,
we will examine both classical and current models of chromosomal
speciation and describe the "evolving" theory of genetic
conflict, epigenetics, and chromosomal speciation.
Chromosomal speciation of humans and chimpanzees revisited: studies of DNA divergence within inverted region, (by JM SZamalek, et al, in Cytogenetic and Genome Research, 2007). [Access to full text: $35. Here's the Abstract:]
The human and chimpanzee karyotypes are distinguishable in terms
of nine pericentric inversions. According to the recombination
suppression model of speciation, these inversions could have
promoted the process of parapatric speciation between hominoid
populations ancestral to chimpanzees and humans. Were recombination
suppression to have occurred in inversion heterozygotes, gene
flow would have been reduced, resulting in the accumulation of
genetic incompatibilities leading to reproductive isolation and
eventual speciation. In an attempt to detect the molecular signature
of such events, the sequence divergence of non-coding DNA was
compared between humans and chimpanzees. Precise knowledge of
the locations of the inversion breakpoints permitted accurate
discrimination between inverted and non-inverted regions. Contrary
to the predictions of the recombination suppression model, sequence
divergence was found to be lower in inverted chromosomal regions
as compared to non-inverted regions, albeit with borderline statistical
significance. Thus, no signature of recombination suppression
resulting from inversion heterozygosity appears to be detectable
by analysis of extant human and chimpanzee non-coding DNA. The
precise delineation of the inversion breakpoints may nevertheless
still prove helpful in identifying potential speciation-relevant
genes within the inverted regions.
Emeritus Professor of Biology
Indiana University, Bloomington, IN
with live URLs for some of my articles]