Abstract
Some allelic variants of the serotonin transporter linked polymorphic region (5-HTTLPR) result in lower levels of expression of the serotonin transporter gene (SLC6A4). These low-expressing (LE) alleles are associated with mental-health disorders in a minority of humans that carry them. Humans are not the only primates that exhibit this polymorphism; other species, including some monkeys, also have LE and high-expressing (HE) variants of 5-HTTLPR. We propose a behavioral genetic framework to explain the adaptive evolution of this polymorphism in primates, including humans. We hypothesize that both LE and HE alleles are maintained by balancing selection in species characterized by short-term fluctuations in social competition levels. More specifically, we propose that LE carriers benefit from their hypervigilant tendencies during periods of elevated competition, whereas HE homozygotes cope best when competition levels do not deviate from the norm. Thus, both alleles have long-term benefits when competition levels tend to vary substantially over relatively short timescales within a social group. We describe this hypothesis in detail and outline a series of predictions to test it. Some of these predictions are supported by findings in the current literature, while others remain areas of future research.
Highlights
Understanding the neurobiological mechanisms that shape the production of behavior is a fundamental goal of neuroscience
Humans have two common versions of 5-HTTLPR, a “short” (S) allele, which consists of 14 tandem repeats, and a “long” (L) allele, which consists of 16 tandem repeats (Nakamura et al, 2000)
We propose the following framework; as with previous authors, we suggest that 5-HTTLPR is associated with an individual’s ability to cope with intra-group competition
Summary
Understanding the neurobiological mechanisms that shape the production of behavior is a fundamental goal of neuroscience. A genetic variant that has received considerable attention in recent years is the serotonin transporter linked polymorphic region (5-HTTLPR), which is a promoter sequence that regulates the expression of the serotonin transporter gene (SLC6A4) (Canli and Lesch, 2007; Homberg and Lesch, 2011). Some rare versions of the L allele, i.e., those characterized by additional single nucleotide mutations, result in reduced amounts of 5-HTT (Hu et al, 2006). Given this complexity, we use the terms “low-expressing” and “high-expressing” to refer to functional variants of 5-HTTLPR
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