Archive for October, 2010
There are many mechanisms that underlie exactly how and why sexual selection takes place- one is the ‘handicap’ /’costly honest signal‘ theory according to which a trait that is actually disadvantageous or a handicap for the host evolves to signal exactly that fact- that despite this handicap I am able to function well and must therefore be of better genetic quality; the most common example being the evolution of peacocks tail which is a handicap and makes the male peacock carrying a big tail more vulnerable for predation, but also is attractive to females and preferred by them. Another theory is that of ‘runaway selection’ i.e . a trait may evolve in a direction due to some genetic drift and the preference for it may also evolve in tandem such that there is a slight leaning or preference towards that trait. Now, in a competition, those, typically males, who have that trait will be selected by the females and their progeny will have an advantage as they are more likely to display that trait and be favored by subsequent generations; thus an arbitrary trait may get fixed by this runaway selection where all members of the species want to be part of the new fashion/club in town. I know I am drawing very loose analogy, but just to give an idea. Nakedness or loss of hairs in humans is predicted to have followed this pattern.
Of course sexual selection also differs on whether it is largely intrasexual, driven by competition (selection pressure) between males for eg having big antlers to defeat and subjugate another male; or is driven by mate preferences and has intersexual selection dynamics- like the peacocks tail.
What the authors of this paper hypothesized was that sexual selection is behind the evolution of altruism or selfless concern with non-kin and that this being the case and this sexual selection dynamics being driven by inetrsexual dynamics, there are bound to be genetic underpinnings to both the trait altruism as measured in males/females and the mate preferences for altruistic trait in both females as well as males. The reason they didn’t anticipate any differences in male sand females was that parental investment, as per them, is roughly equal in case of humans and so both males and females exert equally strong sexual selection pressure son each others traits and ‘choose’ their mates equally.
However, in this study they looked only at females and their genetic basis for altruistic traits as well as mate preference for altruism. The altruistic traits and mate preferential weer measured using self-report instruments. the genetic components underlying these were estimated using classical twin studies paradigm where correlation between mono-zygotic twins and di-zygotic twins are compared to estimate the genetic contribution. They also calculated the phenotypic correlation between mate preference for altruism and altruistic trait in individuals and tried to calculate how much of this correlation again was genetic in nature or in other words was a result of mating between those who had the trait and those who preferred the trait. . They hypothesized that in the ancestral environmental this type of mating for trait altruism would have taken place and thus these would be genetically correlated.
This is exactly what they found; they found that both altruistic personality and mate preference for altruism had genetic components and that they both co-varied and that covariance again had genetic component. the pare itself is full text open access and is written very well, so go ahead and read it yourself. this is an important paper that has come timely when the whole kin-selection paradigm for evolution of eusociallity is being challenged by E o Wilson and team and provides a fresh and alternative perspective of why altruism may have evolved.
Here is a tit-bit from the discussion:
We believe that the sexual selection hypothesis for the evolution of human altruistic traits should now be considered alongside other more established theory (Bshary & Bergmu¨ller, 2008; Lehmann & Keller, 2006), particularly as there is the possibility that multiple mechanisms might underlie a complex behaviour such as altruism. Empirical testing of contrasting theories might even be possible. For example, reciprocal altruism (Trivers, 1971) does not strictly predict the genetic correlation between MPAT and ‘altruistic personality’ found here as ongoing reciprocation towards others would not necessarily result in such a selective process. Indirect reciprocity (Leimar & Hammerstein, 2001) concerns reputation directed towards all other group members while the sexual selection hypothesis focuses solely on altruistic displays that can be evaluated by potential mates (Phillips et al., 2008). A study that examined ‘costly signalling’ of altruistic behaviour through personal donation to a children’s charity found a significant effect on male behaviour when witnessed by a female observer while no such effect was found when male participants were observed by same sex others (Iredale et al., 2008), a finding that could be seen to be at odds with indirect reciprocity. Additional studies could further elucidate the effects of altruistic reputation when directed towards same sex others as opposed to potential mates, thus testing the relative claims of indirect reciprocity against the sexual selection hypothesis.
Tim Phillips1, Eamonn Ferguson2, & Fruhling Rijsdijk (2010). A link between altruism and sexual selection: Genetic influence on altruistic behaviour and mate preference towards it British Journal of Psychology DOI: 10.1348/000712610X493494
I have written previously about CNV’s and how de novo CNV’s have been recently shown to correlate with disorders like autism and schizophrenia. I have also been militantly proposing that autism and psychosis are diametrically opposed disorders and have been gladdened to find that recent CNV data support that hypothesis. I reported how 16p11.2 duplications were associated with schizophrenia while micro-deletions at same site associated with autism. I also reported how a larger study which looked at multiple CNVs found the same reciprocal effects on CNV sites for autism and schizophrenia, thus bolstering the hypothesis that these are diametrically opposed.
By now you might be wondering what all this has to do with ADHD? Well, for one, early this year I started expanding my model and started conceptualizing ADHD as opposed to Autism in childhood and ADHD thus as belonging to psychotic spectrum; I mused that perhaps the same genetic vulnerability that leads to ADHD in childhood could lead to the manifestation of psychosis in teenage/adulthood. Its worthwhile noting that both ADHD and Psychosis are highly correlated with creativity.
So I could not stop my exuberance at finding that CNVs at another site 16p13.11 has been implicated in ADHD and the duplications are present in both ADHD and Schizophrenia. Also, as per the same study , ADHD children carry a large number of de novo CNV’s – a pattern similar ro Autism/schizophrenia. Some, for example the Neuroskeptic, have taken the same loci of CNVs to mean that these CNVs just confer a general risk of maladaptation, but I think they are missing the forest for the trees. The pattern points to the diametrical model and how CNvs are one mechanism in which tug-of-wars are played (whether evolutionary variation or parent-offspring or between paternal and maternal genomes).
Let me explain what I mean by tug-of-wars. Say you have a evolutionary trade-off between exploration and exploitation, with one extreme being useful in some extreme environmental niche (say food is abundant) and the other strategy useful in the opposed environmental niche (say food is scare) . The trait that gets stabilized should have a bell cure distribution so that the a species can survive even if environment leans toward one extreme. The way to archive this could be by having distribution of frequency of different alleles; or it can be via CNV mechanism. You may have some gentic loci for exploration and have a single popular gene allele that codes for exploration at that loci and CNVs that cause deletions here will lead to more exploitation while CNVs that are duplications will lead to more exploration. Thus, by CNV mechanism one can have more of good thing or less of a good thing, good depending on context (i.e context says what is ‘good’).
To take the example of 16p13.11 – it seems it is somehow related to mental retardation/ creativity/intelligence. A deletion at this site causes mental retardation/multiple congenital anomalies.=, while duplications have benign effects. I would conjecture that duplications (associated with ADHD and schizophrenia) may actually increase intelligence/ creativity. That woudl fit with the diametrical model and the finding that ADHD kids are more creative nd develop language more readily than autistic kids of same age.
I am pasting the background and findings from the abstract below:
Large, rare chromosomal deletions and duplications known as copy number variants (CNVs) have been implicated in neurodevelopmental disorders similar to attention-deficit hyperactivity disorder (ADHD). We aimed to establish whether burden of CNVs was increased in ADHD, and to investigate whether identified CNVs were enriched for loci previously identified in autism and schizophrenia.
Data for full analyses were available for 366 children with ADHD and 1047 controls. 57 large, rare CNVs were identified in children with ADHD and 78 in controls, showing a significantly increased rate of CNVs in ADHD (0·156 vs 0·075; p=8·9×10?5). This increased rate of CNVs was particularly high in those with intellectual disability (0·424; p=2·0×10?6), although there was also a significant excess in cases with no such disability (0·125, p=0·0077). An excess of chromosome 16p13.11 duplications was noted in the ADHD group (p=0·0008 after correction for multiple testing), a finding that was replicated in the Icelandic sample (p=0·031). CNVs identified in our ADHD cohort were significantly enriched for loci previously reported in both autism (p=0·0095) and schizophrenia (p=0·010).
To some the fact that ADHD had the same loci as both Autism and Schizophrenia may speak against there being a diametrical relation; however the same was claimed when initially it was found that autism and schizophrenia CNVs were at the same loci; only after looking at the nature of CNV’s (whether duplications or deletions) were the researchers able to identify the diametrical nature of the CNV’s
I haven’t read the full paper yet (waiting for someone to send me the paper) and as and when I get my hands on the full paper, I’ll update this blog post with more details.
Williams, N., Zaharieva, I., Martin, A., Langley, K., Mantripragada, K., Fossdal, R., Stefansson, H., Stefansson, K., Magnusson, P., & Gudmundsson, O. (2010). Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis The Lancet DOI: 10.1016/S0140-6736(10)61109-9