Due to the industrialization of agriculture, medicine, and landscape, humans have become the world’s greatest evolutionary force especially towards disease organisms, agricultural pests, commensals, and species hunted commercially. For example, nearly all Gram-positive infections were sensitive to penicillin in the 1940s but currently the majority of Gram-positive bacteria are penicillin-resistant and up to 50% are resistant to stronger drugs like methicillin. Infections are no longer treated by small antibiotic doses. Instead, huge concentrations or new drugs are required as a temporary solution. The cause of antibiotic resistance is often due to the inefficient use of antibiotics. This includes partial treatment of infections and insertion of antibiotics into animals and plants for an increase in valuable commercial traits.
In order to slow evolution of allele frequencies in populations, new methods are being tested. For example, overkill strategies use a combination of treatments to kill all infectious or invading pests. An overkill treatment is used for HIV; the drug cocktail includes a protease inhibitor and 2 different reverse transcriptase inhibitors. Another method to slow evolution is direct observation therapy. By ensuring the whole treatment regimen, drug doses are brought individually to patients who are observed while taking the drugs. The next step in reducing antibiotic resistance is coordinating these and other methods to create a widespread effect and a decrease in directional selection.
For more information on the causes of evolution due to humans and the methods of slowing evolution down see Palumbi, S. R. 2001. “Humans as the World’s Greatest Evolutionary Force.” Science. 293:1786-1790.
Population evolutionary psychology provides broad claims about human nature and culture for popular consumption. Just as natural selection has caused morphological adaptations, Pop EP has allowed for universal human nature adaptations such as face recognition, parental care, and mate attraction and retention. However, there are many faults within population EP. The largest fallacy is a lack of evidence from the conditions under which early human evolution occurred and therefore, a lack of evidence of the evolution of our ancestors’ psychological traits. For example, in order to discover why language evolved, one would need to identify the adaptive purposes it served among extinct hominins. But little evidence of these purposes exists. In addition, because features of the physical and social environments create a selective response on species’ motivational and cognitive processes, we would need to be able to precisely identify the adaptive problems and understand how preexisting traits were modified. However, we don’t have enough knowledge of our ancestors’ psychological traits to determine how selection affected the traits in order to form modern human minds.
Evidence that would support whether a trait has occurred or is occurring would be found using the comparative method. Nevertheless, the comparative method with our closest living relatives during the past six million years, the chimpanzee and the bonobo, would be futile with human traits. These relatives do not possess forms of the complex psychological human traits like language. If there was a way to compare the lifestyle of more closely related species with shared cognitive abilities, evidence could possibly be strong enough to support the claims within Pop EP. The time scale would take place over centuries to see the effects of adaptive problems and the psychological selection that occurs within the human mind.
For more information on the fallacies of pop evolutionary psychology, see Buller, D. J. 2009. “Four Fallacies of Pop Evolutionary Psychology.” Scientific American 300: 74-81.
The inclusive fitness theory, formalized by Hamilton as the inequality R>c/b, explains that cooperation is favored by natural selection if relatedness is greater than the cost to benefit ratio. R is the relatedness parameter and is expressed as the fraction of genes shared between the altruist and the recipient due to their common descent. This theory has stimulated measures of pedigree kinship and supplied hypothetical explanations for phenomena appearing in eusociality. However, the inclusive fitness theory was questioned due to the rarity of eusociality in evolution and the odd occurrences of it throughout the animal kingdom. This theory is a mathematical approach with many limitations such as not being capable of describing evolutionary dynamics or distributions of gene frequencies. Other limitations include that all interactions must be additive and pairwise, it can only deal with very specific population structures, and when in a limited environment where inclusive fitness theory works, it is identical to the condition derived by standard natural selection, providing no additional biological insight.
An alternative theory to the inclusive fitness theory is the fixed-threshold model projected for the development of the phenomenon in established insect societies. Variation, often genetic, exists in the response thresholds associated with different tasks. According to “The Evolution of Eusociality,” “When two or more colony members interact, those with the lowest thresholds are first to undertake a task at hand.” The activity inhibits their partners, who are then more likely to move on to other available tasks. This theory offers a different approach to explain eusociality but is limited by the specific insect society not found across the animal kingdom. The argument of which theory is right is worthwhile as it will cause new theories to be produced in the search for why eusociality occurs.
For more on eusociality and an alternative theory to eusocial evolution, see Martin, N., C. E. Tarnita, and E. O. Wilson. 2010. “The evolution of eusociality.” Nature 466: 1057-1062.
Andrade’s article was fascinating! She explained a theory behind cannibalism as a favored sexual selection trait in male redback spiders. Andrade provided two main points that support sexual cannibalism: increased paternity and decreased likelihood of female remating. Males that were cannibalized spent a median of 25 minutes in copulation while males that survived spent 11 minutes in copulation. As longer copulations resulted in the transfer of more sperm, the males that were cannibalized by nonvirgin females resulted in a twofold increase in their median paternity compared with the males that survived copulation. In addition, male mating with virgin females also increased their paternity by being eaten because cannibalism decreases the likelihood that the female will remate. Females that cannibalized the first male rejected the second male 67% of the time. Females that did not cannibalize the first male rejected the second male 4% of the time. My only issue with cannibalism being favored through sexual selection was the ability to continue mating throughout the male’s lifetime. Andrade explained that male redbacks who survived copulation appeared unlikely to mate more than once as traveling between female webs resulted in high mortality rates and the male redbacks’ intromittant organ always breaks off inside the female when used in copulation. Therefore, because male redbacks copulate only once, the increase in sperm and the decrease in likelihood of females remating would select for male redbacks who somersault during copulation and allow for cannibalism.
For more information on the male redback spiders and their complicity in sexual cannibalism, see Andrade, M. 1996. Sexual Selection for Male Sacrifice in the Australian Redback Spider. 271: 70-72.
The biological species concept (BSC) offers a definition for species that is applicable to most situations and widely accepted. BSC defines a species as members of populations that actually or potentially interbreed in nature, not according to similarity of appearance. This definition emphasizes cladogenetic processes; however, it is difficult to actually apply. BSC requires measuring the degree of reproductive isolation and it doesn’t apply to asexual lineages/organisms. The validity of BSC depends on the context of the work the scientists are conducting. As Darwin stated, “No one definition has as yet satisfied all naturalists; yet every naturalist knows vaguely what he means when he speaks of a species (1859).
After reading Harrison’s article, “Linking Evolutionary Pattern and Process”, I came to the conclusion that an absolute definition of species is unnecessary. For example evolutionary geneticists may believe that the transition to isolation/cohesion species encompasses the essence of the speciation process, while systematists may focus on the evolution of diagnosable and exclusive groups. Harrison explains that both of these views on speciation are legitimate. There is no single definition for such a complex term.
Harrison includes 7 different species concepts or definitions within his paper. The genealogical species concept is an exclusive group of organisms whose members are more closely related to each other than to any organisms outside the group. This definition left me more confused by the definition of species than prior to reading the paper. One must question where to draw the line on ‘closely related’. Must the genome be exactly the same? What if there are mutations in the organism? Another concept that left me unsettled was the phylogenetic species concept where species are an irreducible cluster of organisms, diagnosably distinct from other such clusters, and within which there is a parental pattern of ancestry and descent. This definition could be potentially arbitrary as it may depend on which particular DNA sequences that are used for the phylogeny. The generality of these 7 definitions creates an overall understanding that 1 definition is not appropriate. There are too many exceptions in nature to define species within a few words.
For more information on the definition of species, see Harrison, R. 1998. Linking evolutionary pattern and processes: the relevance of species concepts for the study of speciation. Endless Forms: Species and Speciation: 19-31.
Nicholas Barton and Peter Keightley, authors of “Understanding Quantitative Genetic Variation”, explain the current and potential use of identifying quantitative trait loci (QTL)—portions of DNA that cause trait variation. Typically, QTLs underlie continuous traits such as height or body weight. In addition, many QTLs are associated with a single trait as many genes usually determine a single phenotypic trait. QTLs are vital in the field of genetics. Knowing the number of QTLs that explain variations in the phenotypic trait determines the genetic architecture of a trait. However, various biases exist in the distribution of QTL effects. Barton and Keightley provide several factors that clarify why it is difficult to estimate the actual numbers and effects of loci that influence a quantitative trait.
These biases include missing closely linked QTL with opposite effects, having undetected QTL that reside below the lower limit, mistaking closely linked QTL with effects in the same direction for a single QTL of larger effect, and the ‘Beavis effect’—the inflation of the estimated effects when samples are not large enough. These factors provide a remarkable insight into our knowledge and lack of knowledge of genetic variation. They result in an overall underestimate of the numbers of QTL and an overestimate of their effects and need to be noted when analyzing QTLs.
For more information on QTL, see Barton, N. and P. Keightley. 2002. “Understanding Quantitative Genetic Variation” by Barton and Keightley, Nature Reviews: Genetics 3: 11-21.
I am interested in combining evolution and medicine. I would like to research toxic snail venoms in search for potential pharmaceutical drugs. Determining which neurotoxins in the venom affect certain receptors will allow the venom to act in isolation and produce a specific reaction on the body’s systems without side effects. I plan to research the relationships of cone snails to determine the helpfulness of their venom. My hypothesis is that the proteins in cone snail venom can be found and provide beneficial drugs in many of the 500 species of cone snails and not just the 1% that has been studied. To go about this process I will need to collect cone snails from different coral environments and extrapolate the venom. By comparing the relationships of these snails, the more related species should have more of the same peptides in their venom allowing for similar uses in medicine. The evolutionary principle of using morphological and biochemical traits to determine phylogenies will provide a foundation for determining the effects of certain cone species and the practicality of these species to humans.
Gould and Lewontin described adaptationism as, “An attempt to explain the existence and the particular forms of any phenotypic trait as the result of natural selection.” In other words adaptationism is the belief that natural selection is the only important method of evolution while spandrels are phenotypic characteristics that did not originate by the direct action of natural selection and that were later co-opted for a current use. Gould and Lewontin provide an analogy of spandrelism with the concept of spandrels in Renaissance architecture. These tapered spaces between arches supported a dome and were an architectural by-product. The spandrels were not designed for the artistic purposes for which they were often employed. Overall, Gould and Lewontin believed that the practice of assuming an organism’s current use of a trait is the reason for its evolution is a ‘sloppy’ form of evolutionary thinking.
According to Pigliucci and Kaplan, the concept of spandrelism has changed over the past 20 years in that much discussion and general acknowledgment of the role of constraints, tradeoffs and costs in evolution has taken place. In general, selection (panglossianism) and constraints (spandrelism) are seen as the two deterministic participants in phenotypic evolution either working together or opposing one another. In addition, the effects of the far from constant environments has been investigated with a “wider range of theoretical tools”, showing that the external environment results in as much limitation to adaptive evolution as genetic or epigenetic constraints. Furthermore, empirical advances are allowing biologists to assess the actual balance between non-adaptive forces and selection in natural populations.
I did not fully understand how the experiments for the empirical advances occurred.
For more information on the advances since the Spandrels, see Pigliucci, M. and Kaplan, J. 2010. “The fall and rise of Dr. Pangloss: adaptationism and the Spandrels paper 20 years later.”
Richard Dawkins, author of The Ancestor’s Tale, agrees with Tomoko Ohta’s nearly neutral theory of molecular evolution where one can predict a relationship between population size and the rate of molecular evolution. Small animals with short generation times tend to have large populations. While large animals with large generation times tend to have small populations. Even though the majority of mutation occurs between generations, and would therefore be larger in a short life cycle, the large populations tend to dilute or remove the mutations before they can become fixed. Furthermore, organisms with smaller populations and longer generation times have mutations that are more likely to become fixed allowing for equal mutation rates between organisms with different lengths of life cycles.
I agree with the nearly neutral theory for the most part. In the paper, Dawkins uses the comparison of mutation rates between elephants and fruit flies. Fruit flies have short life cycles with a large population while elephants have long life cycles and a relatively small population size. To prove the nearly neutral theory both species must have the same mutation rate. This can be explained by understanding that smaller populations have a greater chance of fixing a mutation than large populations. I am hesitant when it comes to some organisms such as rodents, who have exceptional rates of mutations. This was mentioned in Dawkins article and avoided by carefully choosing the clock genes. Does this mean that microorganisms fit into this theory as well? How can the mutation rates of elephants have the same rate as Staphylococcus aureus? The evidence is there it’s just hard to wrap one’s mind around!
For more information on mutation rates, see Dawkins, R. “The Ancestors Tale: A Pilgrimage to the Dawn of Evolution.” Houghton Mifflin. Boston, 2004.
Evo-devo is a field of biology comparing the developmental processes of different organisms to discover the evolutionary relationship between them and to further understand how the developmental processes evolved within the organisms.
An evolutionary biologist can discover vital patterns from using an evo-devo conceptual framework. Understanding that the same master genes are found in fundamental body plans and parts across the animal kingdom will allow connections to be made within species. Determining the purpose of one gene in a species could allow a biologist to comprehend the gene in another species. For example, the BMP4 gene can signal cells to begin producing bone in birds, the more BMP4 protein produced, the thicker the beak of the bird. BMP4 acts in the same way with the jaw of fish. Most likely, this gene plays a role in the evolution of many other species dependent on the development of jaw changes such as lizards, rabbits, and mice.
The major finding of the Davis, et al, 2007 paper was that Polyodon, a basal actinopterygian, and tetrapods both show an inverted collinear expression of HoxD genes in the distal region of the appendage not found in teleosts. This similarity is a developmental hallmark of the autopod and is shown in tetrapods to be controlled by a ‘digit enhancer’ region. Therefore, the novelty in the appendages of lobe-finned and ray-finned fish has arisen by both changes in regulation, as in tetrapods, and by loss of portions of an ancient and conserved pattern of Hox expression in teleosts.
In the article “From a Few Genes, Life’s Myriad Shapes”, the author explains the theory that major events in evolution may be set in motion due to the right ecological situation where “such bold, new forms” will be beneficial. Does this process evolve through natural selection similar to mutations? Does increasing the protein from a few genes happen randomly and does it continue to appear if it is advantageous to the environment? What causes these genes to get turned on?
For more on a general picture of evo-devo, see Yoon, C. K. 2007. “From a Few Genes, Life’s Myriad Shapes.” The New York Times.
For more on the expression and function of genes implicated in the origin of the autopod in a basal actinopterygian, Polyodon spathula, see Davis, C. et al. 2007. “An autopodial-like pattern of Hox expression in the fins of a basal actinopterygian fish.” Nature 447: 473-476.