Monday, November 28, 2011

Promiscuity and the Rate of Molecular Evolution at Primate Immunity Genes

The article I chose to summarize and analyze focuses on the correlation between pathogen-interacting genes and promiscuity in primates entitled “Promiscuity and the Rate of Molecular Evolution at Primate Immunity Genes” (4). The idea for this study was largely generated by a previous study, which found a positive correlation between basal leukocyte counts and mating systems in primates (2). This conclusion prompted the formation of this study’s hypothesis; that perhaps promiscuity could correlate with the evolution of primate immune systems. The scientists heading this project used maximum likelihood to determine protein evolution rates of terminal branches of primates and concluded that immunity genes do evolve faster in more promiscuous primate species, but only those which interact very closely with pathogens.

Many documented relationships between immunity and reproduction exist. One such example describes immune gene expression in Drosophila (female immune gene expression undergoes significant chances post-mating) (1). Another example is present in Zuk’s work, which suggests that sexual selection may be partially dependent on the interference between a particular male’s ejaculate and the female’s immune function (5). Other studies detail the nature of STDs, finding that they differ in their character when compared to most infectious diseases. These differences include the focal point at which the disease is effective. STDs most often target fitness with respect to reproductive ability, not in mortality. This suggests that perhaps STDs impose selective pressures on their host that differ from other breeds of infectious disease (2).

These previous articles helped the scientists who conducted this study form their questions. The authors of “Promiscuity and the Rate of Molecular Evolution at Primate Immunity Genes” (Gabriela Wlasiuk and Michael W. Nachman) decided to expand on this topic, with an increased focus on, specifically, the study question of Nunn (3). The authors decided that if basal leukocyte count actually correlates with disease risk, then by natural selection, other factors of the immune system may also be affected. The authors formed their predictions based on these findings and with respect to primates, as the studies with supportive evidence were performed with primates, and primates exhibit a wide variety of mating systems and, thus, promiscuity. Along with promiscuity, the effect of group size, density, habitat and diet on the rate of molecular evolution of immunity genes was recorded.

This study collected previously published data on 15 immune defense genes in primates and sought to find a relationship between particularly promiscuous species and positive selection in these genes. One factor that was not initially accounted for, but later realized, was the difference in pathogen-important genes and non-pathogen important genes. The sociological variables investigated (diet, density, group size, and habitat) resulted in information already recorded in separate studies, showing that these factors influence the incidence of disease in different ways. The influence of diet on disease is relative to the area in which food is found. Food in trees will be less likely to carry disease than food found on the ground because fecal matter (found on the ground) is often disease ridden. Also, primates who consume foliage have been found to be at a higher risk for disease than those who consume hardier foods. This is because foliage eating animals must consume a higher volume of food to reach the same level of nutrition as those who eat fruit or meat; with a larger amount eaten comes an increased chance of infection.

Overall, the authors chose to use group size and mating system as core variables in this study. They denoted large group sizes as LG and small group sizes as SG. They categorized mating system as either unimale (UM) or multimale (MM). With the rearrangement of phylogenetic trees (with respect to protein similarities; using parsimony, maximum likelihood, and distance) and dN/dS ratios, the study took off. The authors used dN/dS ratios as the dependent variable, and all other sociological factors as independent variables. They performed a single analysis of each independent variable separately with respect to the dependent variable, but for future analyses only used group size and female promiscuity as independent variables. Variance in dN/dS ratios across species of MM vs. UM mating systems were compared using z-tests and t-tests, means and variances were compared in LG vs. SG, and multiple regression models were created. Additionally, proportions of branches with >1 dN/dS (positive selection) were compared between UM and MM, LG and SG.

These analyses yielded fascinating results! It was found that when pathogen interacting immunity genes were separated from non-pathogen interacting immunity genes, significant data existed. Group size also showed a significant difference in dN/dS ratios, suggesting that group size and female promiscuity may influence the rate of evolution of immunity genes. However, what I find most interesting is that mating system was only found to be a significant factor in pathogen important genes, not in those genes which do not interact with pathogens. Since a dN/dS ratio greater than one is the definition of positive selection, the occurrence of that value was compared across MM vs UM and LG vs SG. When this occurrence was summed across groups, a significant difference was found between the number of MM groups that had dN/dS greater than one and UM groups that had dN/dS greater than one. Statistically speaking, MM groups had a significantly higher amount. The incidence of dN/dS ratios that were greater than one were also compared across SG vs. LG and no statistical difference was found between the two sets. This data promotes the argument that sexual promiscuity among primates may results in positive selection in immunity genes!

The argument found in the discussion that I personally offer most support to is that which takes STDs into account. One possible explanation for this data speaks to the evolutionary arms race proposal. This idea states that, since individuals are more promiscuous, fast-evolving pathogen-interacting immune genes are selected for, rather than slow-evolving pathogen-interacting immune genes. Individuals in this scenario who have slow-evolving immune genes would theoretically end up with STDs, which directly affects one’s ability to reproduce, thus that individual would be removed from the gene pool. This selection for fast-evolving genes would eventually result in a correlation between fast-evolving immunity genes and high levels of promiscuity. This idea also transmits to the finding in smaller groups, that there is a significant correlation between pathogen-important immunity genes and promiscuity. This finding was limited to SG, but LG were found to have a significant increase in the dN/dS ratio with an increase in promiscuity across all immunity genes, not pathogen-important immunity genes specifically. The fact that in SG, pathogen-important immunity genes experienced a significant increase in dN/dS with increased promiscuity shows that the pathogen evolution and the pathogen-interacting immunity genes must also compete with each other in a co-evolutionary arms race. If immunity genes, which are specific to pathogen protection, did not evolve as quickly as the pathogens themselves, eventually the species would fail. By natural selection acting on slow evolving immunity genes, pathogens and pathogen-specific immune genes may grow to evolve in very similar speed.

Published scientific literature varies widely in reliability, soundness, and thoroughness of background research. I find that this article was very interesting and well conducted. I do not find any gaps in knowledge, and was able to apply what I have learned in BI 445 to understand difficult concepts. The way the study was carried out makes sense and seems water-tight, with different methods of statistical analysis employed in order to catch errors in computation or the incidence of false significance. The topic is of personal interest, and the relationship between pathogen specific immunity genes and promiscuity in females is a correlation I would have never thought of, but is logical. The article was well written and valid, I do not have issue with its research tactics and find the results of interest and inherently logical.

Literature Cited

1. Lawniczak MKN and Begun DJ. A genome-wide analysis of courting and mating responses in Drosophila meanogaster females. Genome 2004;47:900-910.

2. Lockhart AB, Thrall PH, Antonovics J. Sexually transmitted diseases in animals: ecological and evolutionary implications. Biological reviews of the Cambridge Philosophical Society 1996;71:415-471.

3. Nunn CL. A comparative study of leukocyte counts and disease risk in primates. Evolution 2002a;56:177-190.

4. Wlasuik G and Nachman M. Promiscuity and the rate of molecular evolution at primate immunity genes. Evolution 2010;64(8): 2204-2220.

5. Zuk M, Stoehr AM. Immune defense and host life history. American Naturalist 2002;160:s9-s22.

5 comments:

  1. This is a very interesting article, nice job.

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  2. Very interesting...I'd be interested though to see which "immunity genes" are involved here. In general, some immunity related genes, especially HLA's, are fast evolving in general and this could just be normal interspecific immunological variation. Also it would interesting to see if this correlation could be explained by other social behaviors. I'm not a zoologist by any means, but it would make sense to me that a promiscuous species would be in contact with other members in general, not just in the sexual sense and thus that could also drive evolution of immunity. Unfortunately, it would be nearly impossible to experimentally test this in a primate model, and other faster breeding organism models wouldn't be sufficiently complex in their immunology to be attributable to human/primate function. There's also the issue of a genetic correlation being made with promiscuity...such a behavioral trait is probably as much environmental as genetic (if not more so) and I find it hard to believe that the two would ever find themselves correlated. An interesting hypothesis though.

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  3. This study's conclusion that high promiscuity is correlated to fast-evolving pathogen-interacting immune genes is very interesting. However, I wonder if the researchers considered whether or not these groups carry SIV. The trasnmission of SIV could possibly lead to fast-evolution of pathogen-interacting immune genes as well. Even though this may be a confounding variable that the researchers may not have consider, the spread and resistance of SIV would have similar but more profound results as other STDs in promiscous groups. Perphaps a study could be conducted that compares immune evolution in primate groups that have SIV in there distant lineage and primate groups that have more recently acquired the virus.

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  4. I found this article very interesting. The correlation between promiscuity and immunity is a topic I would never have thought to question and research. It would be interesting for more research to be done on this gene and see if there was any other correlation to primate social behavior. On a side note a friend of mine works with Chimps Inc. and has done research into the promiscuity of Chimpanzees. Some research explains that female Chimps (in the wild) are promiscuous and engage in polyandry so that their will be paternal confusion. This reduces the chance of infanticide by dominate males.

    Great Article!

    -written by Karina Belica

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  5. The correlation between promiscuity and the evolution of primates immune system completely makes sense. Since the promiscuous primates are exposed to more pathogens then their immune system probably has higher selection pressure compared to a primate that is less promiscuous. This could definitely lead to an arms race between the pathogens and the immune system.

    This article makes me wonder if this correlation will continue or if the arms race will lead to extreme virulence and the hosts immune system will no longer be able to handle the onslaught.

    Another question I have is if this correlation is between promiscuity or just close interactions with multiple primates.

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