Speciation and its Consequences

Ch. 18 - Sympatric Speciation and Darwin’s Finches

All allopatric speciation invokes an imporobable number of range splitting and rejoinings - this leads some to consider parapatric and sympatric speciation. Sympatric speciation is a good way to account for presence of large number of sister species in environment with many niches

1st Step: A stable polymorphism can exist in heterogeneous environments with two niches, even with adults forming a single randomly mating population

2nd Step: Evolution of reproductive isolation between populations in the two niches. May involve habitat selection, female choice, or a large number of other variables.

It’s unclear how likely sympatric speciation is to occur in nature. even well investigated models can be explained with allopatric speciation. It’s nearly impossible to reject one explanation in favor of the other as more likely.

Sympatric speciation is best investigated with polymorphic species that show current signs of splitting. However, these signs can be temporary - proceed with caution. Cactus finches appeared to be in the early stages of subdivision, but this was caused by a food shortage and intensive disruptive selection. Mating remained random, so the population could not subdivide further.

Why Sympatric Speciation Couldn’t Occur
1. niches were not different enough
2. extreme fluctuations in environment prevent prolonged divergence. need temporal stability of environment for further divergence.
3. random mating
4. mate choice was not genetically correlated with the individual’s niche
5. difference between male beak size was about 6%, which is not large enough to foster mating discrimination. 15% or so is required for coexistence

The likelihood of a subdivision like this going completely to speciation appears to be very low.

The most important factor so far appears to be temporal stability of a heterogeneous environment. Niches must be different enough to support sustained disruptive selection. This probably doesn’t occur often for vertebrates because they’re generally behaviorally flexible organisms. The between niche variation must be greater than the within niche variation.

How it might happen in vertebrates:
1. genetic drift might do what selection can’t. more things are possible with a smaller population.
2. There are some genetic systems that make it more possible to split under the right conditions: species with two morphs could work, if the morphs are gene-based and they mate assortively.

Speciation and Macroevolution

Speciation Rate:
Speciation can occur rapidly no matter what the driving force. Transition times are generally shorter whenever the process involves an unstable intermediate stage; the forming species must either cross that unstable stage quickly or dissolve (involves sympatric phase or crossing adaptive valley). Transition times for allopatric speciation can be longer since the groups are separated by geographic barriers and are prevented from interbreeding anyway. However, one should not conclude that all cases of rapid speciation occurred sympatrically. It is unsafe to infer biogeographic or genetic modes of speciation from rates of speciation. A good fossil record is rare, but by far the most reliable.
One fairly solid prediction from the authors: For a given divergence time, the amount of reproductive isolation between taxa with overlapping ranges should be greater than that of completely allopatric taxa.
Calculating speciation intervals seems shaky at best at this point. Most estimates vary by millions of years at least.
I find it quite interesting that some groups have apparently not experienced much noticeable morphologic changes for hundreds of millions of years.

Biogeography: Theory and experimental data predict that transition times for speciation events involving a sympatric phase will typically be shorter than for those that are purely allopatric. Reinforcement probably artificially lowers the apparent transition time, though.

Currently the best way to estimate biological speciation intervals is to correlate the divergence time between sister taxa with their degree of reproductive isolation.

Factors Affecting Speciation Rates:
“key innovations”: factors that increase the rate at which new species arise

1. Properties of organisms that facilitate speciation: things that speed up evolution of reproductive isolation; traits that promote sexual selection in animals, for instance. Also when organisms are involved in biological interactions with other species — adapting to other species which are evolving themselves can cause faster change
2. Properties of organisms that prevent extinction: If the group that possesses it does not die, the trait and perhaps some that accompany it will be spread.
3. Properties of organisms that open up new “adaptive zones”: Traits that allow rapid invasion of new habitats can trigger massive adaptive radiations. Preadaptations? Usually impossible to determine exactly what the trait was.
4. “Species-level traits” that affect speciation or extinction rates: Species selection instead of selection on individuals?

Traits that increase rates of extinction could also increase rates of speciation. The opposite could also be true. There is a great deal of speculation and inferences in this field of study…

Species Selection: might produce evolutionary trends not predictable from selection acting within species. Daughter species would acquire traits of ancestor species.
What? Is this like group selection? I thought this was disproved / out of style…? Rather confused.

Done with Speciation by Coyne and Orr!

Selection vs. Drift

This chapter’s question: Does natural selection or genetic drift play a larger role in the origin of species?

A lovely table directly from the book summarizes definitions nicely (p. 384):

Selection
1. Direct: direct natural selection for reproductive isolation. Direct selection characterizes models of sympatric speciation and reinforcement.  — Definitely not ubiquitous, especially in allopatric speciation.
2. Indirect: Reproductive isolation arises as a pleiotrophic side effect of natural or sexual selection.  –Probably more common than direct.
   • Primary: Selection acts on a character and the same character ultimately causes reproductive isolation
   • Secondary: Selection acts on a character and the genes involved pleiotrophically affect another character that ultimately causes reproductive isolation.
   • Tertiary: Selection acts on a character and the linked genes that hitchhike along with those under selection ultimately cause reproductive isolation.

Genetic Drift
1. Neutral: reproductive isolation results from genes whose divergence was strictly or nearly neutral. Further explanation later in chapter: all alleles are equally fit and selection acts only in those rare instances when alleles that differ by two mutational steps segregate together in a population. Males and females that differ by 0 or 1 steps can interbreed, but those that differ by 2+ steps cannot.  – Probably not common
   
2. Peak shift: Reproductive isolation involves a period of maladaptive evolution, during which genetic drift must overcome selection. This class of model often involves founder-effects

Conclusions:  Selection plays a much larger role in speciation than does drift.  Firm evidence for genetic drift speciation is very rare and direct laboratory tests provide little or no support for founder-effect speciation.  This makes sense for me.  The modern theory of evolution *is* called evolution by natural selection, after all.  It seems that natural selection would be much stronger and more common than genetic drift.

Reinforcement

Reinforcement: enhancement of prezygotic isolation in sympatry by natural selection - Two taxa diverge in allopatry; upon secondary geographic contact, hybridization occurs at some rate, yielding unfit hybrids. Because production of hybrids is maladaptive, individuals who only mate with their own taxa enjoy a fitness advantage.

Evidence: Reveals that sympatry can enhance prezygotic isolation, but does not indicate how often sympatry matters.

Prezygotic isolation is often stronger in sympatry than allopatry.

A publication bias exists since studies that support the existence of reinforcement are more exciting than those that do not.  However, the bias does not counteract the probable existence of reinforcement; the evidence is still convincing.

Alternative theories exist and some of them are probable.  A good way to tell if what you’re looking at is really reinforcement:  Reinforcement should typically result in a larger change in females in sympatry than in males, since females suffer larger fitness costs from mating with the wrong male.  Eggs and / or pregnancy is much more expensive than sperm.  This is a reasonably robust signature of reinforcement.

Recombinational Speciation

Recombinational Speciation: hybridization between 2 species gives rise to a new lineage that is both fertile and true breeding, but is reproductively isolated from both parental species.

Forms novel genotype that is homozygous for several chromosome arrangements that differentiate the parental species

Certain rare hybrid genotypes can be fitter than parentals, though most hybrids are less fit / at some kind of disadvantage.

Can be produced in lab with many generations of artificial selection.

It is also possible in nature. The well-documented cases are flowers, but it also seems possible in animals. More study is needed to confirm the animal cases, however. Amazon mollies are hybrids, aren’t they?

Hybrids between parentals are almost* completely sterile, but surviving F₂ and later generations gradually increase in fertility. The hybrid species can actually be stabilized in a few generations. The new species are usually ecologically isolated from the parentals.

*If all hybrids between the species were completely sterile, then recombinational speciation would not be possible.

Polyploidy

Polyploid Classification:
Autopolyploids: result from an increase in ploidy level within a species (AAAA)
Allopolyploids: Result from hybridization between species

• Genomic allopolyploids: carry entire chromosome sets from 2 or more species. Chromosomes from different species do not pair during meiosis. (AABB)
• Segmental allopolyploids: some chromosomes do not pair, others do. Often unstable and continue to evolve. (A1A1A2A2)
• Autoallopolyploids: involve both autopolyploidy and allopolyploidy (AAAABBBB)

Pathways to polyploidy: More than just these 3, but this is a good start.

1. Somatic doubling: Mitotic products in a diploid cell fail to segregate to opposite poles
2. Meiotic nonreduction: cell wall fails to form late in meiosis, yielding diploid gametes.
3. Polyspermy: 2 sperm fertilize a single egg -> (intermediate) triploid

Incidence: Polyploidy occur(s/ed) in ferns, moss, algae, virtually all groups of vascular plants, yeast, ancient vertebrates (why verts have 4x more chromosomes than inverts), ancient fish. Polyploidy is the norm in ferns, common in angiosperms, but rare in gymnosperms. Frequency varies across groups.

Frequency of auto vs. allopolyploidy: arise in nature at rates equivalent to genetic mutation. Allopolyploids considered more common in past literature. However, autopolyploids are probably more common than once thought; they’re just hard to identify. Allopolyploids still probably more common.

Ecology and persistence: polyploids are thrown into immediate competition with their diploid ancestors. Most probably go extinct quickly. Assortive mating and ecological differences required for a stable population of polyploids.

Why is polyploidy rarer in animals than in plants?
Nobody really knows, but there are some hypotheses. Author favors own hypothesis: transition from diploidy to tetraploidy disrupts dosage compensation of X chromosome(s). Hypothesis hinges on possession of smaller sex chromosome for heterogametic sex. – Consequences of commitment to chromosomal sex determination. However, author states that so little data exists that nobody should be surprised if all current hypotheses turn out to be wrong.

Genetics of Intrinsic Postzygotic Isolation

Haldane’s rule, paraphrased: The heterogametic sex is more likely to be absent, rare, or sterile in the offspring of two species; the homogametic is less likely to be affected by these things. This rule holds in most animals possessing sex chromosomes. Obviously this wouldn’t hold true for sex determined by temperature during incubation and such.

Explanations of Haldane’s Rule
1. Dominance Theory: Hinges on alleles that act recessively in hybrids. Hybrid inviability may affect the heterogametic sex just like X-linked disorders. If your one copy of a chromosome / gene is bad, then there’s nothing to override the negative effects.
2. Faster Male Theory: Incompatibilities afflicting heterogametic hybrids are more common than those afflicting homogametic hybrids. Thus, hybrid male sterils are more common than hybrid female sterils. Spermatogenesis inherently sensitive? Faster evolution due to sexual selection on males? Males sterile more often even when females are heterogametic. Does not explain hybrid inviability, only sterility.
3. Faster-X Theory: if X-linked genes have a disproportionately large effect on hybrid fitness.
4. Meiotic Drive: Selfish genetic elements; alleles distort mendelian ratios to their own advantage, often by inactivating sperm that carry a homologous chromosome (X sperm might inactivate Y sperm). Imposes a fertility cost on the bearers and other genes by distorting the sex ratio.

Dominance and Faster Male cause Haldane’s Rule. The other 2 forces may also play a role, but evidence is ambiguous.

Hybrid male sterility involves more genes than hybrid female sterility or hybrid inviability.
It is difficult to determine which / how many genes were involved in the initial evolution of hybrid incompatibility, simply because the species have continued to involve over time.
“Genes causing inviability typically affect both sexes, while genes causing sterility typically affect one sex only. Second, maternal effects on viability are common, while those on fertility are rare. Third, male sterility typically involves postmeiotic problems. — Intrinsic postzygotic isolation typically involves “ordinary” genes that have normal functions within species.” (Not novel genetic factors)

Postzygotic Isolation

I’ve found that I remember what I read better if I use this blog for note taking and then observations on what I’ve read. I’ll most likely use this approach for the remainder of this course unless there are objections. My thoughts on the reading will be in italics.

Notes!
Classification of postzygotic reproductive isolating barriers:

2 Types:
1. Extrinsic
   1. Ecological inviability: hybrids enoy normal development but suffer decreased viability, as they cannot find a suitable ecological niche. (Suspected increased fitness in intermediate environments, if they exist)
   2. Behavioral sterility: hybrids enjoy normal gametogenesis but suffer lowered effective fertility because they cannot obtain mates. Hybrids may present an intermediate courtship behavior or other phenotype that renders them unattractive to individuals of the opposite sex.

So a hybrid is not suitable for a specific niche and cannot find mates, even though it is otherwise functional.

2. Intrinsic
   1. Hybrid inviability: Hybrids suffer developmental defects causing full or partial inviability.
   2. Hybrid sterility:
      1. Physiological sterility: hybrids suffer developmental defects in their reproductive system causing full or partial sterility.
      2. Behavioral sterility: hybrids suffer a neurological or physical defect that renders them fully or partially incapable of courtship.

   The hybrid is incapable of reproduction or is too developmentally flawed to live. Mules, for example - sterile, though viable.

Evolution of Extrinsic versus Intrinsic
1. Extrinsic
   1. Extrinsic isolation may be a byproduct of adaptive radiation
   2. “additive gene interaction” - Dominant and recessive homozygotes both fit, but the heterozygous type is unfit due to intermediate phenotype / behavior.
2. Intrinsic - Genetic Modes of Intrinsic Postzygotic Isolation: A Very Long Section
   Causes of Hybrid Difficulties
   1. Different ploidy levels: Polyploidy is more important in plant speciation than animal. Look in Ch. 9 for more about this.
   2. Different chromosomal arrangements: Structural changes in chromosomes might directly cause reproductive isolation. This can even cause semisterility within species.
      The greater the reproductive isolation ultimately caused by a rearrangement, the more it is selected against when it appears. New arrangements are selected against until they reach intermediate frequencies. More likely to succeed if population size is small so that genetic drift can overcome natural selection. Common in plants, probably not in animals.
   3. Different alleles that do not function together in hybrids: Between-locus incompatibilities (Gene at locus A from one species does not interact properly with gene at locus B from another species) often leads to hybrid sterility and inviability. Ancestor aabb diverged into aaBb and Aabb, then aaBB and AAbb. A and B are deleterious when together in a hybrid (AaBb), but are adapted to the alleles they normally occur with. Hybrid incompatibilities only occur at loci that have both experienced substitution.
   4. Cytoplasmic endosymbionts / cytoplasmic incompatibility: Wolbachia, a bacterial endosymbiont, is maternally transmitted. 15-20% of insects carry Wolbachia. Infected male x uninfected female = offspring that die as embryos. Reciprocal cross shows no lethality. Infected females can reproduce with any male, and uninfected females can only reproduce with uninfected males. Thus the bacteria is spread throughout the population. If two types of endosymbiont are present, the two infected types are usually incompatible; thus a population may not be overtaken by a single type. Natural selection at the level of parasites causes hybrid inviability at the level of hosts.
      Can cause speciation, but is relatively uncommon.

   Well, that’s interesting… I’d never heard of this sort of thing before.

   I’d like to finish this book this week. I have about 160 pages left (assuming the remaining chapters are all relevant), and I’m getting a bit tired of this subject for now. It’s time to move on.

Behavioral and Nonecological Isolation

Behavioral Isolation: may be more of a species identification mechanism?
Mechanical Isolation: square peg, round hole. It just doesn’t work.
Gametic Isolation: sperm competition / inactivation in heterospecific genital tract, and / or incompatible binding proteins on gamete surfaces. — I wondered how that worked.

Ecological Isolation

Habitat Isolation: often a direct byproduct of adaptation to the environment. Seems based on relatively few genes. “Habitat” can include host preference in addition to soil type preference and other habitats.
Pollinator Isolation: gene flow between flowering plants is reduced if the species use different pollinators. Strong dependence on a particular pollinator can limit flowers to the range of that pollinator. It’s produced largely by differences in flower color and nectar volume. Perhaps a small number of genes with large effects?
Temporal Isolation: gene flow is impeded due to different breeding times between species. “Some species of periodical cicada breed simultaneously only every two centuries” — Woah! That’s pretty interesting.
Diverse biological bases of temporal isolation: different responses to same environmental cue, different responses to different cues, or pleiotrophic byproduct of habitat differences (flowering time dependent on soil moisture). Temporal isolation can be completely non-genetic (offyear breeders can be produced by environmental or developmental accidents), and is the only isolating barrier that can cause sympatric speciation. Current studies suggest, however, that temporal isolation is not that important in animals. This raises more questions in my mind about the plausibility of sympatric speciation. Some do suggest that temporal isolation is more important in plants. Perhaps it simply happens post-speciation?

On a somewhat related note, reading this book made explaining speciation to the Intro Zoo (ZOO 1114) students I tutor a lot easier. Speciation is a difficult concept to grasp for many of them.
However, I do not think I will take much of an interest in this area in the future. The book is informative, but reading it makes me quite sleepy… The authors do suggest that (if one is interested) there is a fairly pressing need for more study.

Science would be a lot easier with a time machine or two.