Body size evolution is a central theme in evolutionary biology. Particularly the question of when and how smaller body sizes can evolve continues to interest evolutionary ecologists, because most life history models, and the empirical evidence, document that large body size is favoured by natural and sexual selection in most (even small) organisms and environments at most times. How, then, can such a large range of body size and life history syndromes evolve and coexist in nature?

The paper by Coulson et al. lifts this question to the level of the population, a relatively novel approach using so-called integral projection (simulation) models (IPMs) (as opposed to individual-based or game theoretical models). As is well outlined by (anonymous) Reviewer 1, and following earlier papers spearheading this approach in other life history contexts, the authors use the well-known carrying capacity (K) of population biology as the ultimate fitness parameter to be maximized or optimized (rather than body size per se), to ultimately identify factors and conditions promoting the evolution of extreme body sizes in nature. They vary (individual or population) size-structured growth trajectories to observe age and size at maturity, surivorship and fecundity/fertility schedules upon evaluating K (see their Fig. 1). Importantly, trade-offs are introduced via density-dependence, either for adult reproduction or for juvenile survival, in two (of several conceivable) basic scenarios (see their Table 2). All other relevant standard life history variables (see their Table 1) are assumed density-independent, held constant or zero (as e.g. the heritability of body size).

The authors obtain evidence for disruptive selection on body size in both scenarios, with small size and a fast life history evolving below a threshold size at maturity (at the lowest K) and large size and a slow life history beyond this threshold (see their Fig. 2). Which strategy wins ultimately depends on the fitness benefits of delaying sexual maturity (at larger size and longer lifespan) at the adult stage relative to the preceeding juvenile mortality costs, in agreement with classic life history theory (Roff 1992, Stearns 1992). The modeling approach can be altered and refined to be applied to other key life history parameters and environments. These results can ultimately explain the evolution of smaller body sizes from large body sizes, or vice versa, and their corresponding life history syndromes, depending on the precise environmental circumstances.

All reviewers agreed that the approach taken is technically sound (as far as it could be evaluated), and that the results are interesting and worthy of publication. In a first round of reviews various clarifications of the manuscript were suggested by the reviewers. The new version was substantially changed by the authors in response, to the extent that it now is a quite different but much clearer paper with a clear message palatable for the general reader. The writing is now to the point, the paper's focus becomes clear in the Introduction, Methods & Results are much less technical, the Figures illustrative, and the descriptions and interpretations in the Discussion are easy to follow.

In general any reader may of course question the choice and realism of the scenarios and underlying assumptions chosen by the authors for simplicity and clarity, for instance no heritability of body size and no cost of reproduction (other than mortality). But this is always the case in modeling work, and the authors acknowledge and in fact suggest concrete extensions and expansions of their approach in the Discussion.

References

Coulson T., Felmy A., Potter T., Passoni G., Montgomery R.A., Gaillard J.-M., Hudson P.J., Travis J., Bassar R.D., Tuljapurkar S., Marshall D.J., Clegg S.M. (2022) Density-dependent environments can select for extremes of body size. bioRxiv, 2022.02.17.480952, ver. 3 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.02.17.480952

​​Durability of plant resistance to diploid pathogen Hirohisa Kishino Based on the population genetic and epidemiologic model, Saubin et al. (2021) report that the resistant hosts generated by the breeding based on the gene-for-gene interaction is durable much longer against diploid pathogens than haploid pathogens. The avr allele of pathogen that confers the resistance is genetically recessive. The heterozygotes are not recognized by the resistant hosts and only the avr/avr homozygote is adaptive. As a result, the trajectory of avr allele frequency becomes more stochastic due to genetic drift. Although the paper focuses on the evolution of standing polymorphism, it seems obvious that the adaptive mutations in pathogen have much larger probability of being deleted from the population because the individuals own the avr allele mostly in the form of heterozygote at the initial phase after the mutation. Since only few among many models of plant resistance deployment study the case of diploid pathogen and the contribution of the pathogen life cycle, this work will add an important intellect to the literature (Rimbaud et al. 2021).

From the study of host-parasite interaction in flax rust Melampsora lini, Flor (1942, 1955) showed that the host resistance is formed by the interaction of a host resistance gene and a corresponding pathogen gene. This gene-for-gene hypothesis has been supported by experimental evidence and has served as a basis of the methods of molecular breeding targeting the dominant R genes. However, modern agriculture provides the pathogen populations with the homogeneous environments and laid strong selection pressure on them. As a result, the newly developed resistant plants face the risk of immediate resistance breakdown (Möller and Stukenbrock 2017).

Currently, quantitative resistance is getting attention as characters as a potential target for long-life (mild) resistant breeds (Lannou, 2012). They are polygenic and controlled partly by the same genes that mediate qualitative resistance but mostly by the genes that encode defense-related outputs such as strengthening of the cell wall or defense compound biosynthesis (Corwin and Kliebenstein, 2017). Progress of molecular genetics may overcome the technical difficulty (Bakkeren and Szabo, 2020). Saubin et al. (2021) notes that the pattern of genetic inheritance of the pathogen counterparts that respond to the host traits is crucial regarding with the durability of the resistant hosts. The resistance traits for which avr alleles are predicted to be recessive may be the targets of breeding.

References

Bakkeren, G., and Szabo, L. J. (2020) Progress on molecular genetics and manipulation of rust fungi. Phytopathology, 110, 532-543. https://doi.org/10.1094/PHYTO-07-19-0228-IA

Corwin, J. A., and Kliebenstein, D. J. (2017) Quantitative resistance: more than just perception of a pathogen. The Plant Cell, 29, 655-665. https://doi.org/10.1105/tpc.16.00915

Flor, H. H. (1942) Inheritance of pathogenicity in a cross between physiological races 22 and 24 of Melampsova lini. Phytopathology, 35. Abstract.

Flor, H. H. (1955) Host-parasite interactions in flax rust-its genetics and other implications. Phytopathology, 45, 680-685.

Lannou, C. (2012) Variation and selection of quantitative traits in plant pathogens. Annual review of phytopathology, 50, 319-338. https://doi.org/10.1146/annurev-phyto-081211-173031

Möller, M. and Stukenbrock, E. H. (2017) Evolution and genome architecture in fungal plant pathogens. Nature Reviews Microbiology. 15, 756–771. https://doi.org/10.1038/nrmicro.2017.76

Rimbaud, L., Fabre, F., Papaïx, J., Moury, B., Lannou, C., Barrett, L. G., and Thrall, P. H. (2021) Models of Plant Resistance Deployment. Annual Review of Phytopathology, 59. https://doi.org/10.1146/annurev-phyto-020620-122134

Saubin, M., De Mita, S., Zhu, X., Sudret, B. and Halkett, F. (2021) Impact of ploidy and pathogen life cycle on resistance durability. bioRxiv, 2021.05.28.446112, ver. 4 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2021.05.28.446112

Sirtuin proteins are class III histone deacetylases that are involved in a variety of fundamental biological functions mostly related to aging. These proteins are located in different subcellular compartments and are associated with different biological functions such as metabolic regulation, stress response, and cell cycle control [1]. In mammals, the sirtuin gene family is composed of seven paralogs (SIRT1-7) grouped into four classes [2]. Due to their involvement in maintaining cell cycle integrity, sirtuins have been studied as a way to understand fundamental mechanisms governing longevity [1]. Indeed, the downregulation of sirtuin genes with aging seems to explain much of the pathophysiology that accumulates with aging [3]. Biomedical studies have thus explored the potential therapeutic implications of sirtuins [4] but whether they can effectively be used as molecular targets for the treatment of human diseases remains to be demonstrated [1]. Despite this biomedical interest and some phylogenetic analyses of sirtuin paralogs mostly conducted in mammals, a comprehensive evolutionary analysis of the sirtuin gene family at the scale of vertebrates was still lacking.

In this preprint, Opazo and collaborators [5] took advantage of the increasing availability of whole-genome sequences for species representing all main groups of vertebrates to unravel the evolution of the sirtuin gene family. To do so, they undertook a phylogenomic approach in its original sense aimed at improving functional predictions by evolutionary analysis [6] in order to inventory the full vertebrate sirtuin gene repertoire and reconstruct its precise duplication history. Harvesting genomic databases, they extracted all predicted sirtuin proteins and performed phylogenetic analyses based on probabilistic inference methods. Maximum likelihood and Bayesian analyses resulted in well-resolved and congruent phylogenetic trees dividing vertebrate sirtuin genes into three major clades. These analyses also revealed an additional eighth paralog that was previously overlooked because of its restricted phyletic distribution. This newly identified sirtuin family member (named SIRT8) was recovered with unambiguous statistical support as a sister-group to the SIRT3 clade. Comparative genomic analyses based on conserved gene synteny confirmed that SIRT8 was present in all sampled non-amniote vertebrate genomes (cartilaginous fish, bony fish, coelacanth, lungfish, and amphibians) except cyclostomes. SIRT8 has thus most likely been lost in the last common ancestor of amniotes (mammals, reptiles, and birds). Discovery of such previously unknown genes in vertebrates is not completely surprising given the plethora of high-quality genomes now available. However, this study highlights the importance of considering a broad taxonomic sampling to infer evolutionary patterns of gene families that have been mostly studied in mammals because of their potential importance for human biology.

Based on its phylogenetic position as closely related to SIRT3 within class I, it could be predicted that the newly identified SIRT8 paralog likely has a deacetylase activity and is probably located in mitochondria. To test these evolutionary predictions, Opazo and collaborators [5] conducted further bioinformatics analyses and functional experiments using the elephant shark (Callorhinchus milii) as a model species. RNAseq expression data were analyzed to determine tissue-specific transcription of sirtuin genes in vertebrates, including SIRT8 found to be mainly expressed in the ovary, which suggests a potential role in biological processes associated with reproduction. The elephant shark SIRT8 protein sequence was used with other vertebrates for comparative analyses of protein structure modeling and subcellular localization prediction both pointing to a probable mitochondrial localization. The protein localization and its function were further characterized by immunolocalization in transfected cells, and enzymatic and functional assays, which all confirmed the prediction that SIRT8 proteins are targeted to the mitochondria and have deacetylase activity. The extensive experimental efforts made in this study to shed light on the function of this newly discovered gene are both rare and highly commendable.

Overall, this work by Opazo and collaborators [5] provides a comprehensive phylogenomic study of the sirtuin gene family in vertebrates based on detailed evolutionary analyses using state-of-the-art phylogenetic reconstruction methods. It also illustrates the power of adopting an integrative comparative approach supplementing the reconstruction of the duplication history of the gene family with complementary functional experiments in order to elucidate the function of the newly discovered SIRT8 family member. These results provide a reference phylogenetic framework for the evolution of sirtuin genes and the further functional characterization of the eight vertebrate paralogs with potential relevance for understanding the cellular biology of aging and its associated diseases in human.

References

[1] Vassilopoulos A, Fritz KS, Petersen DR, Gius D (2011) The human sirtuin family: Evolutionary divergences and functions. Human Genomics, 5, 485. https://doi.org/10.1186/1479-7364-5-5-485

[2] Yamamoto H, Schoonjans K, Auwerx J (2007) Sirtuin Functions in Health and Disease. Molecular Endocrinology, 21, 1745–1755. https://doi.org/10.1210/me.2007-0079

[3] Morris BJ (2013) Seven sirtuins for seven deadly diseases ofaging. Free Radical Biology and Medicine, 56, 133–171. https://doi.org/10.1016/j.freeradbiomed.2012.10.525

[4] Bordo D Structure and Evolution of Human Sirtuins. Current Drug Targets, 14, 662–665. http://dx.doi.org/10.2174/1389450111314060007

[5] Opazo JC, Vandewege MW, Hoffmann FG, Zavala K, Meléndez C, Luchsinger C, Cavieres VA, Vargas-Chacoff L, Morera FJ, Burgos PV, Tapia-Rojas C, Mardones GA (2022) How many sirtuin genes are out there? evolution of sirtuin genes in vertebrates with a description of a new family member. bioRxiv, 2020.07.17.209510, ver. 5 peer-reviewed and recommended by Peer Community in Evolutionary Biology.  https://doi.org/10.1101/2020.07.17.209510

[6] Eisen JA (1998) Phylogenomics: Improving Functional Predictions for Uncharacterized Genes by Evolutionary Analysis. Genome Research, 8, 163–167. https://doi.org/10.1101/gr.8.3.163

Heliconius butterflies are famous for their colorful wing patterns acting as a warning of their chemical defenses [1]. Most species are involved in Müllerian mimicry assemblies, as predators learn to associate common wing patterns with unpalatability and preferentially target rare variants. Such positive-frequency dependent selection homogenizes wing patterns at different localities, and in several species, all individuals within a community belong to the same morph [2]. In this respect, H. numata stands out. This species shows stable local polymorphism across multiple localities, with local populations home to up to seven distinct morphs [2]. Although a balance between migration and local positive-frequency dependent selection can allow some degree of local polymorphism, theory suggests that this occurs only when migration is within a narrow window [3].
One factor that potentially enhances local polymorphism in H. numata is disassortative mating. Mate choice assays have in fact revealed that females of this species tend to reject males with the same wing pattern [4]. However the evolution of such mating behavior and its effect on polymorphism remain unclear when selection is locally positive-frequency dependent. Using a mathematical model, Maisonneuve et al. [5] clarify the conditions that favor the evolution of disassortative mating in the complicated system of H. numata. In particular, they investigate whether the genetic basis of wing colour can favor the emergence of disassortative mating. Variation in wing pattern in H. numata is controlled by the supergene P, which is a single genomic region harboring multiple protein coding genes that have ceased to recombine due to chromosomal inversions [6]. If such remarkable genetic configuration allows for the co-adaptation of multiple loci participating to a complex phenotype such as wing color pattern, the absence of recombination can also result in the accumulation of deleterious mutations [7]. In fact, alleles at the P locus have been associated with a recessive genetic load, leading to a fitness advantage for heterozygotes at this locus [8]. Can this fitness advantage to heterozygotes lead to the evolution of disassortative mating? And if so, can such evolution lead to the maintenance of local polymorphism in spite of strong positive frequency-dependent selection?
To investigate these questions, Maisonneuve et al. [5] model evolution at two loci, one is the P locus for wing pattern, and the other influences mating behavior. The population is divided among two connected patches that differ in their butterfly communities, so that different alleles at the P locus are favored by positive frequency-dependent selection in different patches. The different alleles at the P locus are ordered in dominance relationships such that the most dominant over wing color pattern are also those with the highest load. By tracking the dynamics of haplotype frequencies in the population, the authors first show that disassortative mating readily evolves via the invasion of an allele causing females carrying it to reject males that resemble them phenotypically. Such “self-referencing” mechanism of mate choice, however, has never been reported and has been argued to be rare due to its complicated nature [9].
Maisonneuve et al. [5] then compare the evolution of disassortative mating via two alternative mechanisms: attraction and rejection. In these cases, alleles at the mating locus determine attraction to or rejection of specific phenotypes (e.g., under attraction rule, allele “B” encodes attraction to males with phenotype B). With the P and mating loci fully linked, disassortative mating can evolve under all three mechanisms (self-referencing, attraction and rejection), but tends to be less prevalent at equilibrium under attraction rule. This in turn results in the maintenance of less genetic variation under attraction compared to the other mating mechanisms. The loss of variation that occurs under attraction rules is due to a combination of dominance relationships between alleles at the P locus and the searching cost to females in finding rare types of males. When a particular wing pattern, say B, is only expressed in homozygotic form, B males are relatively rare. Females that carry the allele at the mating locus causing them to be attracted to such males then suffer a fitness cost due to lost mating opportunities. This mating allele is therefore purged, and in turn so is the recessive allele for B phenotype at the P locus. Under self-referencing and rejection rules, however, choosy females only reject males of a specific phenotype. They can therefore potentially mate with larger pool of males than females attracted to a single type. As a result, self-referencing and rejection rules are less sensitive to demographic effects and so are more conducive to disassortative mating evolution.
In their final analysis, Maisonneuve et al. [5] investigate the influence of recombination among the P and mating loci. They show that recombination has different effects on disassortative mating evolution depending on the mechanism of mate choice. Under the self-referencing rule, loose linkage leads to higher levels of disassortative mating and polymorphism than when linkage is tight. Under attraction or rejection rule, however, even very limited recombination completely inhibits the evolution of disassortative mating. This is because, with alleles at the mating locus coding for attraction/rejection to specific males, recombination breaks the association between the P and mating loci necessary for disassortative mating. By contrast, disassortative mating via a self-referencing rule does not depend on the linkage among the P and mating loci: females choose males that are different to themselves independently from the alleles they carry at the P locus.
Taken together, Maisonneuve et al.’s analyses [5] show that disassortative mating can readily evolve in a system like H. numata, but that this evolution depends on the genetic architecture of mating behavior. The architectures that are more conducive to the evolution of disassortative mating are: (1) epistatic interactions among the P and mating loci such that females are able to recognize their own phenotype and base their mating decision upon this information (self-referencing rule); and (2) full linkage among the P supergene and a mating locus that triggers rejection of a specific color pattern. While the mechanisms behind disassortative mating remain to be elucidated, assortative mating seems to rely on alleles triggering attraction to specific cues with variation in attraction and cues linked together [10]. These observations support the notion that disassortative mating is due to alleles causing rejection, in tight linkage to the P locus. If so, mating loci would in fact be part of the P supergene, thus controlling not only intricate wing color pattern but also mating behavior.
Beyond the specific system of H. numata, Maisonneuve et al.’s study [5] helps understand the evolution of disassortative mating and its association with the genetic architecture of correlated traits. In particular, Maisonneuve et al. [5] expands the role of supergenes for ecologically relevant traits to mating behavior, further bolstering the relevance of these remarkable genetic elements in the maintenance of variation in complex and elaborate phenotypes.

References

[1] Merrill, R M, K K Dasmahapatra, J W Davey, D D Dell'Aglio, J J Hanly, B Huber, C D Jiggins, et al. (2015). The Diversification of Heliconius butterflies: What Have We Learned in 150 Years? Journal of Evolutionary Biology 28 (8), 1417–38. https://doi.org/10.1111/jeb.12672.
[2] Joron M, IR Wynne, G Lamas, and J Mallet (1999). Variable selection and the coexistence of multiple mimetic forms of the butterfly Heliconius numata. Evolutionary Ecology 13, 721– 754. https://doi.org/10.1023/A:1010875213123
[3] Joron M and Y Iwasa (2005). The evolution of a Müllerian mimic in a spatially distributed community. Journal of Theoretical Biology 237, 87–103. https://doi.org/10.1016/j.jtbi.2005.04.005
[4] Chouteau M, V Llaurens, F Piron-Prunier, and M Joron (2017). Polymorphism at a mimicry su- pergene maintained by opposing frequency-dependent selection pressures. Proceedings of the National Academy of Sciences 114, 8325–8329. https://doi.org/10.1073/pnas.1702482114
[5] Maisonneuve, L, Chouteau, M, Joron, M and Llaurens, V. (2020). Evolution and genetic architecture of disassortative mating at a locus under heterozygote advantage. bioRxiv, 616409, ver. 9 peer-reviewed and recommended by PCI Evolutionary Biology. https://doi.org/10.1101/616409
[6] Joron M, L Frezal, RT Jones, NL Chamberlain, SF Lee, CR Haag, A Whibley, M Becuwe, SW Baxter, L Ferguson, et al. (2011). Chromosomal rearrangements maintain a polymorphic super- gene controlling butterfly mimicry. Nature 477, 203. https://doi.org/10.1038/nature10341
[7] Schwander T, R Libbrecht, and L Keller (2014). Supergenes and Complex Phenotypes.” Current Biology. 24 (7), 288–94. https://doi.org/10.1016/j.cub.2014.01.056.
[8] Jay P, M Chouteau, A Whibley, H Bastide, V Llaurens, H Parrinello, and M Joron (2019). Mutation accumulation in chromosomal inversions maintains wing pattern polymorphism in a butterfly. bioRxiv. https://doi.org/ 10.1101/736504.
[9] Kopp M, MR Servedio, TC Mendelson, RJ Safran, RL Rodrıguez, ME Hauber, EC Scordato, LB Symes, CN Balakrishnan, DM Zonana, et al. (2018). Mechanisms of assortative mating in speciation with gene flow: connecting theory and empirical research. The American Naturalist 191, 1–20. https://doi.org/10.1086/694889
[10] Merrill RM, P Rastas, SH Martin, MC Melo, S Barker, J Davey, WO McMillan, and CD Jiggins (2019). Genetic dissection of assortative mating behavior. PLoS biology 17, e2005902. https://doi.org/10.1371/journal.pbio.2005902

The striking differences in species richness among lineages in the Tree of Life have long attracted much research interest. In particular, researchers have asked whether certain traits are associated with greater diversification, with a particular focus on traits under sexual selection given their direct link to mating isolation.

Polymorphism, defined as the presence of co-occurring, heritable morphs within a population, has been proposed to influence diversification rates although the effect has been proposed as both promoting or alternatively impeding speciation. The effect of polymorphism may be positive, that is facilitating speciation if polymorphism allows to broaden the ecological niche, thus enabling range expansion, or enabling maintenance of populations in variable environments. Specialized ectomorphs have been observed in several species (e.g. Kusche et al. 2015, Lattanzio and Miles 2016, Whitney et al. 2018, Scali et al. 2016). Polymorphism may also facilitate speciation if a morph is lost during the colonization of a novel area or niche, resulting in rapid divergence of the remaining morphs and reproductive isolation from the ancestral population, known as the morph speciation hypothesis (West-Eberhard 1986, Corl et al. 2010). On the other hand, polymorphism may hamper speciation through disassortative maintaining by morph, which may maintain the polymorphism through the speciation process (Jamie and Meier 2020). An example of such a process is Heliconius numata where disassortative mate preferences based on color hampers ecological speciation (Chouteau et al. 2017). Previous evidence in birds and lizards suggests polymorphism favors diversification (Corl et al. 2010b, 2012, Hugall and Stuart-Fox 2012, Brock et al. 2021).

Here, de Solan et al. (2023) test the effect of polymorphism on diversification in Lacertidae, a family of lizards containing more than 300 species distributed across Europe, Africa and Asia. The group offers a good model system to test the effect of polymorphism on speciation as it contains several species with colour polymorphism, sometimes present in both sexes but restricted to males when present in the flank. Using coloration data from the literature as well as photographs of live specimens for 295 species the authors tested whether the presence of polymorphism is associated with higher diversification rates.

While undertaking their project, another group independently tackled the same question (Brock et al. 2021), using the same model system but coming to very different conclusions. Therefore, de Solan et al. (2023) decided to also contrast their results with those of Brock et al. (2021) to determine the factors responsible for the contrasting results of both studies. The latter I consider one of the strengths of the work, given the careful re-analyses to determine the causes of the discrepancies between both studies. De Solan et al. (2023) found no association between the presence of polymorphism and diversification rates, even though they used different analytical approaches. Thus, this study is interesting as it provides results that do not support a positive effect of polymorphism on species richness. The use of a phylogeny with more limited species sampling (García-Porta et al. 2019) implied that the authors had to manually add 75 species, of which 17 were added to the tree based on information from previously published trees and 68 were added at random locations within the genus. To control for potential biases the authors repeated the analyses using a sample of trees with the imputed taxa, results were broadly concordant across the set of trees. The careful re-analysis contrasting Brock et al. (2021) and de Solan et al. (2023) results suggests the difference is mainly due to a difference in how species were coded as presenting polymorphism, which differed between the two studies, as well as a difference in the package version used to run the state-dependent diversification models. Interestingly non-parametric analyses yielded similar results across both datasets. 
 
References
 
Brock, K.M., McTavish, E.J., Edwards, D.L. 2021. Colour polymorphism is a driver of diversification in the lizard family Lacertidae. Systematic Biology. 71: 24-39. https://doi.org/10.1093/sysbio/syab046
 
Chouteau, M., Llaurens, V., Piron-Prunier, F., Joron, M. 2017. Polymorphism at a mimicry supergene maintained by opposing frequency-dependent selection pressures. Proceedings of the National Academy of Sciences. 114: 8325-8329. https://doi.org/10.1073/pnas.1702482114
 
Corl, A., Davis, A.R., Kuchta, S.R., Comendant, T., Sinervo, B. 2010a. Alternative mating strategies and the evolution of sexual dimorphism in the side-blotched lizard, Uta stansburiana: a population-level comparative analysis. Evolution. 64: 79-96. https://doi.org/10.1111/j.1558-5646.2009.00791.x 
 
Corl, A., Davis, A.R., Kuchta, S.R., Sinervo, B. 2010b. Selective loss of polymorphic mating types is associated with rapid phenotypic evolution during morphic speciation. Proceedings of the National Academy of Sciences. 107: 4254-4259. https://doi.org/10.1073/pnas.0909480107
 
Corl, A., Lancaster, L.T., Sinervo, B. 2012. Rapid formation of reproductive isolation between two populations of side-blotched lizards, Uta stansburiana. Copeia. 2012: 593-602. https://doi.org/10.1643/CH-11-166

Garcia-Porta, J., Irisarri, I., Kirchner, M. et al. 2019. Environmental temperatures shape thermal physiology as well as diversification and genome-wide substitution rates in lizards. Nature Communications. 10: 4077. https://doi.org/10.1038/s41467-019-11943-x
 
Hugall, A.F., Stuart-Fox, D. 2012. Accelerated speciation in colour-polymorphic birds. Nature. 485: 631-634. https://doi.org/10.1038/nature11050
 
Jamie, G.A. and Meier, J.I. 2020. The persistence of polymorphisms across species radiations. Trends in Ecology and Evolution. 35: 795-808. https://doi.org/10.1016/j.tree.2020.04.007
 
Kusche, H., Elmer, K.R., Meyer, A. 2015. Sympatric ecological divergence associated with a colour polymorphism. BMC Biology, 13: 82. https://doi.org/10.1186/s12915-015-0192-7
 
Lattanzio, M.S. and Miles, D.B. 2016. Trophic niche divergence among colour morphs that exhibit alternative mating tactics. Royal Society Open Science. 3: 150531. https://doi.org/10.1098/rsos.150531
 
Scali, S., Sacchi, R., Mangiacotti, M., Pupin, F., Gentilli, A., Zucchi, C. Scannolo, M., Pavesi, M., Zuffi, M.A.L. 2016. Does a polymorphic species have a ‘polymorphic’ diet? A case study from a lacertid lizard. Biologcial Journal of the Linnean Society. 117: 492-502. https://doi.org/10.1111/bij.12652

de Solan T, Sinervo B, Geniez P, David P, Crochet P-A (2023) Colour polymorphism and conspicuousness do not increase speciation rates in Lacertids. bioRxiv, 2023.02.15.528678, ver. 2 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2023.02.15.528678

West-Eberhard, M.J. 1986. Alternative adaptations, speciation, and phylogeny (A review). Proceedings of the National Academy of Sciences. 83: 1388-1392. https://doi.org/10.1073/pnas.83.5.1388
 
Whitney, J.L., Donahue, M.J., Karl, S.A. 2018. Niche divergence along a fine-scale ecological gradient in sympatric colour morphs of a coral reef fish. Ecosphere. 9: e02015. https://doi.org/10.1002/ecs2.2015