For additional examples and explanations of chromosomal changes, click on:
RETURN TO CHROMOSOMAL SPECIATION INDEX

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 isolation.

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 the population?

Thanking you in advance if you can provide an answer...
tom

Hi Tom,

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 THIS TOPIC

Chromosomes, Conflict, and Epigenetics: Chromosomal Speciation Revisited
(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.

--
Craig E. Nelson
Emeritus Professor of Biology
Indiana University, Bloomington, IN
[CV with live URLs for some of my articles]