Models of animal coalitions and their implications for human evolution.

Social interaction is a prime driver for the evolution of animal behaviour. Dyadic interaction, in particular, has been the focus of intensive research on the evolution of mutualistic, altruistic, selfish or spiteful behaviours. Meanwhile, triadic interaction has been the minimal framework for the study of animal coalition as observed in some species of primates, as well as in carnivores and cetaceans, where two or more individuals act jointly against a third party in a competitive context. Previous mathematical models of animal coalition have either failed to explain the observed diversity in the configuration of coalition or presumed fine-tuned decision-making that may be unrealistic for non-human animals. To approach these issues, the present study develops a new model that is fairly simple, but still able to account for the observed diversity in animal coalitions. Analysis of the model specifies key parameters affecting the predicted types of coalition: the nature of the benefit being contested, the cost-to-benefit ratio associated with fighting and the synergistic effect in coalition formation. Additionally, the model is used to evaluate the social selection hypothesis, which claims that coalition formation induced social selection favouring reduced aggression and lower fighting abilities during human evolution.

Cultural niche construction with application to fertility control: A model for education and social transmission of contraceptive use.

The evolution of a cultural trait may be affected by niche construction, or changes in the selective environment of that trait due to the inheritance of other cultural traits that make up a cultural background. This study investigates the evolution of a cultural trait, such as the acceptance of the idea of contraception, that is both vertically and horizontally transmitted within a homogeneous social network. Individuals may conform to the norm, and adopters of the trait have fewer progeny than others. In addition, adoption of this trait is affected by a vertically transmitted aspect of the cultural background, such as the preference for high or low levels of education. Our model shows that such cultural niche construction can facilitate the spread of traits with low Darwinian fitness while providing an environment that counteracts conformity to norms. In addition, niche construction can facilitate the 'demographic transition' by making reduced fertility socially accepted.

Application of a Markovian ancestral model to the temporal and spatial dynamics of cultural evolution on a population network.

Cultural macroevolution concerns a long-term evolutionary process involving transmission of non-genetic or cultural traits between populations as well as birth and death of populations. To understand the spatial dynamics of cultural macroevolution, we present a one-locus model of cultural diffusion in which a cultural trait is transmitted on a network of populations. Borrowing the method of ancestral backward process from population genetics, our model explores the lineage of a trait variant sampled in the present generation to quantify when and where the variant was invented. Mathematical analysis of the model enables us to predict the distribution of cultural age in each population of the network, estimate the frequencies of trait variants originating from given populations, and discuss the time it takes for a trait variant to diffuse between a given pair of populations. We also perform numerical analysis on random scale-free network of populations to investigate the effect of network topology and innovation rate on the age and origin of variants in each population. The result suggests that trait variants are more likely to derive from a population with higher innovation rate. Our numerical analysis also shows that trait variants invented in populations with higher network-centrality values are likely to be maintained at a higher frequency and transmitted to other populations in a shorter time period.

γ-Secretase Activity Is Associated with Braak Senile Plaque Stages.

Amyloid ß-proteins (Aßs) Aß1-42 and Aß1-43 are converted via two product lines of γ-secretase to Aß1-38 and Aß1-40. This parallel stepwise processing model of γ-secretase predicts that Aß1-42 and Aß1-43, and Aß1-38 and Aß1-40 are proportional to each other, respectively. To obtain further insight into the mechanisms of parenchymal Aß deposition, these four Aß species were quantified in insoluble fractions of human brains (Brodmann areas 9 to 11) at various Braak senile plaque (SP) stages, using specific enzyme-linked immunosorbent assays. With advancing SP stages, the amounts of deposited Aß1-43 in the brain increased proportionally to those of Aß1-42. Similarly, the amounts of deposited Aß1-38 correlated with those of Aß1-40. Surprisingly, the ratios of deposited Aß1-38/Aß1-42 and Aß1-40/Aß1-43 were proportional and discriminated the Braak SP stages accurately. This result indicates that the generation of Aß1-38 and Aß1-40 decreased and the generation of Aß1-42 and Aß1-43 increased with advancing SP stages. Thus, Aßs deposition might depend on γ-secretase activity, as it does in the cerebrospinal fluid. Here, the extracted γ-secretase from Alzheimer disease brains generates an amount of Aß1-42 and Aß1-43 compared with cognitively normal brains. This refractory γ-secretase localized in detergent-solubilized fractions from brain cortices. But activity modulated γ-secretase, which decreases Aß1-42 and Aß1-43 in the cerebrospinal fluid, localized in detergent-insoluble fractions. These drastic alterations reflect Aß situation in Alzheimer disease brains.

Ectopic Expression Induces Abnormal Somatodendritic Distribution of Tau in the Mouse Brain.

Tau is a microtubule (MT)-associated protein that is localized to the axon. In Alzheimer's disease, the distribution of tau undergoes a remarkable alteration, leading to the formation of tau inclusions in the somatodendritic compartment. To investigate how this mislocalization occurs, we recently developed immunohistochemical tools that can separately detect endogenous mouse and exogenous human tau with high sensitivity, which allows us to visualize not only the pathological but also the pre-aggregated tau in mouse brain tissues of both sexes. Using these antibodies, we found that in tau-transgenic mouse brains, exogenous human tau was abundant in dendrites and somata even in the presymptomatic period, whereas the axonal localization of endogenous mouse tau was unaffected. In stark contrast, exogenous tau was properly localized to the axon in human tau knock-in mice. We tracked this difference to the temporal expression patterns of tau. Endogenous mouse tau and exogenous human tau in human tau knock-in mice exhibited high expression levels during the neonatal period and strong suppression into the adulthood. However, human tau in transgenic mice was expressed continuously and at high levels in adult animals. These results indicated the uncontrolled expression of exogenous tau beyond the developmental period as a cause of mislocalization in the transgenic mice. Superresolution microscopic and biochemical analyses also indicated that the interaction between MTs and exogenous tau was impaired only in the tau-transgenic mice, but not in knock-in mice. Thus, the ectopic expression of tau may be critical for its somatodendritic mislocalization, a key step of the tauopathy.SIGNIFICANCE STATEMENT Somatodendritic localization of tau may be an early step leading to the neuronal degeneration in tauopathies. However, the mechanisms of the normal axonal distribution of tau and the mislocalization of pathological tau remain obscure. Our immunohistochemical and biochemical analyses demonstrated that the endogenous mouse tau is transiently expressed in neonatal brains, that exogenous human tau expressed corresponding to such tau expression profile can distribute into the axon, and that the constitutive expression of tau into adulthood (e.g., human tau in transgenic mice) results in abnormal somatodendritic localization. Thus, the expression profile of tau is tightly associated with the localization of tau, and the ectopic expression of tau in matured neurons may be involved in the pathogenesis of tauopathy.

A demographic test of accidental versus intentional island colonization by Pleistocene humans.

This study evaluates the hypothesis that some documented cases of long-distance sea crossing by the Late Pleistocene Homo sapiens occurred as a result of accidental drifting, rather than by intentional seafaring. For that purpose, we use an existing computer simulation framework, with some modifications, to investigate the likelihood that a planned or unplanned island colonization by a small group of individuals will persist to establish a viable population. Within the original framework, planned colonization was operationally characterized as being initiated by equal numbers of unrelated young men and women, whereas for unplanned colonization, those who migrate inadvertently were regarded in effect as a random sample of the whole population. Here, we consider a different scenario for unplanned colonization, which we believe is more relevant to sea crossing by the Late Pleistocene humans, that is, we assume that unplanned colonization occurs when members of households on watercrafts with limited voyaging capabilities are drifted away by ocean currents and washed up on a distant island. We also extend the previous analysis by considering a broader range of combinations of fertility and mortality schedules that individuals are assumed to follow. Our simulations suggest the following: (1) colonization of an island by ten or fewer unrelated young men and women can be successful within the feasible range of fertility and mortality levels; (2) in comparison, the likelihood of success for unplanned colonization is considerably smaller for the same range of fertility and mortality levels; and (3) there exists a small range of parameter combinations for which unplanned colonization has a non-negligible prospect of success even without assuming recurrent accidental drifts to the same island, and thus, the accidental colonization scenario cannot be totally excluded. In addition, we find that the minimum founding population required for successful colonization varies substantially depending on the fertility and mortality levels.

Cultural and evolutionary dynamics with best-of-k learning when payoffs are uncertain.

Social learning not only takes the form of random copying of other individuals, but also involves learners' choice of what to learn or from whom to learn. Best-of-k learning refers to a kind of success-biased social learning strategy in which a learner randomly samples k exemplars from the population and imitates the most "successful" one, or the one gaining the highest payoff. While it is intuitive that best-of-k learning can promote the spread of superior variants and thereby enable cumulative cultural evolution, a previous mathematical analysis has shown that it may sometimes result in maladaptive cultural evolution when the payoffs associated with cultural variants vary stochastically. If so, best-of-k learners may be selectively disfavored and in the long run replaced by unbiased learners, who simply copy someone chosen at random. Here we develop new mathematical models that are more simplified and mathematically tractable than the previous model to achieve a fuller analysis of cultural and evolutionary dynamics involving best-of-k learning and stochastic payoffs. We find that best-of-k learning, unlike unbiased learning, can facilitate the invasion of an on average inferior variant that sometimes gives a very high payoff, destabilize a population fixed with a variant that is on average superior but occasionally results in a very low payoff, and maintain cultural polymorphism at equilibrium. Considering gene-culture coevolution of learning rules and cultural variants, under the assumption that social learning is always faithful, it is shown that a population of best-of-k learners at the culturally polymorphic state can always be invaded by unbiased learners and eventually converges to a culturally monomorphic state. Nonetheless, we show that best-of-k learning can be stable against invasion by unbiased learning if social learning is sometimes combined with individual learning.

The effect of sexual selection on phenotypic diversification among human populations: A simulation study.

Despite the generally low level of inter-population genetic differentiation in humans as compared with great apes, it has long been acknowledged that there is a considerable amount of geographic variations in human phenotypes, for example, skin pigmentation, cranial morphology, and soft-tissue facial morphology, to name but a few. Indeed, recent studies have suggested that the extent of inter-population diversity in some human phenotypes is greater than expected from random drift alone. Such an excess of phenotypic diversity is often attributed to adaptation to local environment. However, this account is valid only if populations differ in some ecological aspects that elicit differential selection acting on a given phenotypic feature. Another long-standing hypothesis is the sexual selection hypothesis, which claims that phenotypic diversity arises and/or is maintained owing to variations in preference for mating partners. In this paper, we explore the plausibility of the sexual selection hypothesis by means of computer simulations, in which the inter-population diversity of a quantitative trait is evaluated against the expectation from random drift, using the QST-FST comparison. As possible driving factors of sexual selection, we consider two types of mate-choice preference: preference for the population average and preference for a culturally-transmitted arbitrary trend. Our simulations suggest that sexual selection can, under certain circumstances, maintain and/or generate a detectable amount of inter-population phenotypic diversity, even when populations are ecologically identical and loosely connected to each other by mutual migration. Since mating decisions in humans are considerably affected by social learning, human mate-choice preference may be more readily diversified between populations than in other animals. We suggest, therefore, that some of the observed human phenotypic variations may be better understood as a product of cultural, rather than ecological, diversification.

Alanine substitutions in the GXXXG motif alter C99 cleavage by γ-secretase but not its dimerization.

The amyloid ß (Aß) protein is a major component of senile plaques, one of the neuropathological hallmarks of Alzheimer's disease. Amyloidogenic processing of amyloid precursor protein (APP) by ß- and γ-secretases leads to production of Aß. APP contains tandem triple repeats of the GXXXG motif in its extracellular juxtamembrane and transmembrane regions. It is reported that the GXXXG motif is related to protein-protein interactions, but it remains controversial whether the GXXXG motif in APP is involved in substrate dimerization and whether dimerization affects γ-secretase-dependent cleavage. Therefore, the relationship between the GXXXG motifs, substrate dimerization, and γ-secretase-dependent cleavage sites remains unclear. Here, we applied blue native poly acrylamide gel electrophoresis to examine the effect of alanine substitutions within the GXXXG motifs of APP carboxyl terminal fragment (C99) on its dimerization and Aß production. Surprisingly, alanine substitutions in the motif failed to alter C99 dimerization in detergent soluble state. Cell-based and solubilized γ-secretase assays demonstrated that increasing alanine substitutions in the motif tended to decrease long Aß species such as Aß42 and Aß43 and to increase in short Aß species concomitantly. Our data suggest that the GXXXG motif is crucial for Aß production, but not for C99 dimerization.

Evolution of group-wise cooperation: Is direct reciprocity insufficient?

Group-wise cooperation, or cooperation among three or more individuals, is an integral part of human societies. It is likely that group-wise cooperation also played a crucial role in the survival of early hominins, who were confronted with novel environmental challenges, long before the emergence of Homo sapiens. However, previous theoretical and empirical studies, focusing mainly on modern humans, have tended to suggest that evolution of cooperation in sizable groups cannot be explained by simple direct reciprocity and requires some additional mechanisms (reputation, punishment, etc.), which are cognitively too demanding for early hominins. As a partial resolution of the paradox, our recent analysis of a stochastic evolutionary model, which considers the effect of random drift, has revealed that evolution of group-wise cooperation is more likely to occur in larger groups when an individual's share of the benefit produced by one cooperator does not decrease with increasing group size (i.e., goods are non-rivalrous). In this paper, we further extend our previous analysis to explore possible consequences of introducing rare mistakes in behavior or imperfect information about behavior of others on the model outcome. Analyses of the extended models show that evolution of group-wise cooperation can be facilitated by large group size even when individuals intending to cooperate sometimes fail to do so or when all the information about the past behavior of group members is not available. We argue, therefore, that evolution of cooperation in sizable groups does not necessarily require other mechanisms than direct reciprocity if the goods to be produced via group-wise cooperation are non-rivalrous.

γ-Secretase associated with lipid rafts: multiple interactive pathways in the stepwise processing of ß-carboxyl-terminal fragment.

γ-Secretase generates amyloid ß-protein (Aß), a pathogenic molecule in Alzheimer disease, through the intramembrane cleavage of the ß-carboxyl-terminal fragment (ßCTF) of ß-amyloid precursor protein. We previously showed the framework of the γ-secretase cleavage, i.e. the stepwise successive processing of ßCTF at every three (or four) amino acids. However, the membrane integrity of γ-secretase was not taken into consideration because of the use of the 3-[(3-cholamidopropyl)dimethylammonio]-2-hydroxy-1-propanesulfonic acid-solubilized reconstituted γ-secretase system. Here, we sought to address how the membrane-integrated γ-secretase cleaves ßCTF by using γ-secretase associated with lipid rafts. Quantitative analyses using liquid chromatography-tandem mass spectrometry of the ßCTF transmembrane domain-derived peptides released along with Aß generation revealed that the raft-associated γ-secretase cleaves ßCTF in a stepwise sequential manner, but novel penta- and hexapeptides as well as tri- and tetrapeptides are released. The cropping of these peptides links the two major tripeptide-cleaving pathways generating Aß40 and Aß42 at several points, implying that there are multiple interactive pathways for the stepwise cleavages of ßCTF. It should be noted that Aß38 and Aß43 are generated through three routes, and γ-secretase modulator 1 enhances all the three routes generating Aß38, which results in decreases in Aß42 and Aß43 and an increase in Aß38. These observations indicate that multiple interactive pathways for stepwise successive processing by γ-secretase define the species and quantity of Aß produced.

Identification of key amino acids responsible for the distinct aggregation properties of microtubule-associated protein 2 and tau.

The carboxyl-terminal sequence of tau composes the framework for its intracellular inclusions that appear in diverse neurodegenerative disorders known as tauopathies. However, microtubule-associated protein 2 (MAP2), which contains a homologous carboxyl-terminal sequence of tau, is undetectable in the mature tau inclusions. The mechanisms underlying this phenomenon have remained largely unknown. Here, we show that tau and MAP2 have different aggregation properties: tau aggregates to form filaments but MAP2 remains to be granules. Exchanging (221) YKPV(224) of tau (0N3R) near the PHF6 motif for (340) TKKI(343) of MAP2c profoundly changed aggregation properties, suggesting that the YKPV motif is important for filament formation, whereas the TKKI motif is for granule formation. Thus, these minimal sequences may determine the different fates of tau and MAP2 in the formation of inclusions in tauopathies. Tau and microtubule-associated protein 2 (MAP2) are homologous microtubule-associated proteins in neurons. So far, it is largely unknown why tau but not MAP2 is selectively involved in the filamentous inclusions (neurofibrillary tangles, NFT) formation in tauopathies, including Alzheimer's disease. In this study, we found that the difference of only two amino acids in tau and MAP2 sequences may determine their different fates in tauopathies. These results may lead to the elucidation of tau deregulation in pathological conditions.

Modulation of lipid kinase PI4KIIα activity and lipid raft association of presenilin 1 underlies γ-secretase inhibition by ginsenoside (20S)-Rg3.

Amyloid ß-peptide (Aß) pathology is an invariant feature of Alzheimer disease, preceding any detectable clinical symptoms by more than a decade. To this end, we seek to identify agents that can reduce Aß levels in the brain via novel mechanisms. We found that (20S)-Rg3, a triterpene natural compound known as ginsenoside, reduced Aß levels in cultured primary neurons and in the brains of a mouse model of Alzheimer disease. The (20S)-Rg3 treatment induced a decrease in the association of presenilin 1 (PS1) fragments with lipid rafts where catalytic components of the γ-secretase complex are enriched. The Aß-lowering activity of (20S)-Rg3 directly correlated with increased activity of phosphatidylinositol 4-kinase IIα (PI4KIIα), a lipid kinase that mediates the rate-limiting step in phosphatidylinositol 4,5-bisphosphate synthesis. PI4KIIα overexpression recapitulated the effects of (20S)-Rg3, whereas reduced expression of PI4KIIα abolished the Aß-reducing activity of (20S)-Rg3 in neurons. Our results substantiate an important role for PI4KIIα and phosphoinositide modulation in γ-secretase activity and Aß biogenesis.

Evolution of social behavior in finite populations: a payoff transformation in general n-player games and its implications.

The evolution of social behavior has been the focus of many theoretical investigations, which typically have assumed infinite populations and specific payoff structures. This paper explores the evolution of social behavior in a finite population using a general n-player game. First, we classify social behaviors in a group of n individuals based on their effects on the actor's and the social partner's payoffs, showing that in general such classification is possible only for a given composition of strategies in the group. Second, we introduce a novel transformation of payoffs in the general n-player game to formulate explicitly the effects of a social behavior on the actor's and the social partners' payoffs. Third, using the transformed payoffs, we derive the conditions for a social behavior to be favored by natural selection in a well-mixed population and in the presence of multilevel selection.

Spatial evolution of human cultures inferred through Bayesian phylogenetic analysis.

Spatial distribution of human culture reflects both descent from the common ancestor and horizontal transmission among neighbouring populations. To analyse empirically documented geographical variations in cultural repertoire, we will describe a framework for Bayesian statistics in a spatially explicit model. To consider both horizontal transmission and mutation of the cultural trait in question, our method employs a network model in which populations are represented by nodes. Using algorithms borrowed from Bayesian phylogenetic analysis, we will perform a Markov chain Monte Carlo (MCMC) method to compute the posterior distributions of parameters, such as the rate of horizontal transmission and the mutation rates among trait variants, as well as the identity of trait variants in unobserved populations. Besides the inference of model parameters, our method enables the reconstruction of the genealogical tree of the focal trait, provided that the mutation rate is sufficiently small. We will also describe a heuristic algorithm to reduce the dimension of the parameter space explored in the MCMC method, where we simulate the coalescent process in the network of populations. Numerical examples show that our algorithms compute the posterior distribution of model parameters within a practical computation time, although the posterior distribution tends to be broad if we use uninformative priors.

Central nervous system-specific deletion of transcription factor Nrf1 causes progressive motor neuronal dysfunction.

Cap'n'Collar (CNC) proteins heterodimerize with small Maf proteins and regulate the transcription of various genes. Small Maf-deficient mice develop severe neurodegeneration, and it remains unclear whether CNC proteins are involved in this process. In this study, we examined the contribution of Nrf1, one of the CNC proteins, to neuronal homeostasis in vivo. As Nrf1 gene knockout mice are embryonic lethal, we developed a central nervous system (CNS)-specific Nrf1 knockout (CKO) mouse line using mice bearing an Nrf1(flox) allele and Nestin-Cre allele. At birth, the CKO mice appeared indistinguishable from control mice, but thereafter they showed progressive motor ataxia and severe weight loss. All Nrf1 CKO mice died within 3 weeks. These phenotypes are similar to those reported in small Maf-deficient mice, suggesting the presence of collaboration between Nrf1 and small Maf proteins. We also found aberrant accumulation of polyubiquitinated proteins in various CNS regions and apparent neuronal loss in the hippocampus of Nrf1 CKO mice. An oxidative stress marker was accumulated in the spinal cords of the mice, but the expression patterns of oxidative stress response genes regulated by Nrf2 did not change substantially. These results show that Nrf1 sustains the CNS homeostasis through regulating target genes distinct from those regulated by Nrf2.

Homogamy and imprinting-like effect on mate choice preference for body height in the current Japanese population.

BACKGROUND: Homogamy for body height has been repeatedly documented in Western societies. Nevertheless, the underlying mechanism is unclear and the reasons for its apparent absence in non-Western societies remain unexplained. AIM: This study investigates spousal correlation and mate preference for height in the Japanese population. SUBJECTS AND METHODS: This study analyses self-reported data on the height of individuals, their parents and their ideal marriage partners, collected by a series of questionnaires on university students. RESULTS: In contrast to a previous study, this study found a significant positive correlation between the heights of Japanese spouses, after controlling for age. It also found a positive correlation between the heights of subjects and of their ideal partners, suggesting that an individual's self-referent preference may contribute to the observed homogamy for height. However, a subject's preference is also influenced by the height of his/her opposite-sex--but not same-sex--parent, where this effect is more prominent in male subjects. CONCLUSION: This study shows that homogamy for body height is present in the current Japanese population and that it may in part result from an individual's preference. It also indicates a possible role of a sexual imprinting-like mechanism in human mate choice.

Cultural transmission of traditional songs in the Ryukyu Archipelago.

Geographic patterns of cultural variations are affected by how cultural traits are transmitted within and between populations. It has been argued that cultural traits are transmitted in different manners depending on their characteristics; for example, words for basic concepts are less liable to horizontal transmission between populations (i.e., borrowing) than other words. Here we examine the geographic variation of traditional songs in the Ryukyu Archipelago, southwestern islands of Japan, to explore cultural evolution of music with a focus on different social contexts in which songs are sung. Published scores of 1,342 traditional songs are coded using the CantoCore song classification scheme and distances between the songs are calculated from the codings. Neighbor-Net graphs of regions/islands are generated on the basis of the musical distances, and delta scores are obtained to examine the treelikeness of the networks. We also perform analysis of molecular variance (AMOVA) to evaluate the extent of musical diversification among regions/islands. Our results suggest that horizontal transmission between populations has played a greater role in the formation of musical diversity than that of linguistic diversity in the Ryukyu Archipelago and that the social context in which songs are sung has an effect on how they are transmitted within and between populations. In addition, we compare the observed patterns of song diversity among regions/islands with those of lexical and mitochondrial-DNA (mtDNA) diversity, showing that the variation of songs sung in the "work" context are associated with the linguistic variation, whereas no association is found between the musical and genetic variation.

Dissociation of ß-amyloid from lipoprotein in cerebrospinal fluid from Alzheimer's disease accelerates ß-amyloid-42 assembly.

Monoclonal 2C3 specific to ß-amyloid (Aß) oligomers (AßOs) enabled us to test our hypothesis that the alteration of lipoprotein-Aß interaction in the central nervous system (CNS) initiates and/or accelerates the cascade favoring Aß assembly. Immunoprecipitation of frontal cortex employing 2C3 unequivocally detected soluble 4-, 8-, and 12-mers in Alzheimer's disease (AD) brains. Immunoblot analysis of the entorhinal cortex employing 2C3 revealed that the accumulation of soluble 12-mers precedes the appearance of neuronal loss or cognitive impairment and is enhanced as the Braak neurofibrially tangle (NFT) stages progress. The dissociation of soluble Aß from lipoprotein particles occurs in cerebrospinal fluid (CSF), and the presence of lipoprotein-free oligomeric 2C3 conformers (4- to 35-mers) was evident, which mimic CNS environments. Such CNS environments may strongly affect conformation of soluble Aß peptides, resulting in the conversion of soluble Aß(42) monomers into soluble Aß(42) assembly. The findings suggest that functionally declined lipoproteins may accelerate the generation of metabolic conditions leading to higher levels of soluble Aß(42) assembly in the CNS.

Classes of communication and the conditions for their evolution.

Evolution of communication is conceptualized as a coevolutionary process in which evolution of signaler and that of receiver occur in an interdependent manner. Three classes of communication, mutualistic, altruistic, and exploiting, are distinguished depending on who gains a benefit or suffers a cost from successful communication. Communication is also dichotomized according to whether individuals are innately able to send and receive relevant signals or they have to acquire those signals culturally. We develop two-locus haploid models that represent the coevolutionary nature of the evolution of communication, and derive the conditions under which communicators can invade a population of non-communicators and those under which a population of communicators is evolutionarily stable against the invasion by non-communicators for each of the three classes of communication. Analysis of the models reveals that interaction among siblings enables the invasion of communication and that the optimal probability of interaction with siblings depends on the class of communication and the mode of signal transmission. In addition, cultural exploiting communication is more likely to invade a population of non-communicators than is genetic exploiting communication under certain circumstances.