In 2007, David S. Wilson and Edward O. Wilson (27) pointed out that, Richard Dawkins had admitted that, contrary to what he had claimed in his book The Selfish Gene (1976) (7), the idea that only the gene is a fundamental unit of selection cannot be used as an argument against the notion of group selection. This elicited a sharp denial from Dawkins (30), which was followed by an explanatory reply by Wilson and Wilson (33) and another vehement denial by Dawkins (34). I analyse the prehistory of this surprisingly complex and convoluted dispute and subsequently disentangle it. My conclusion is that much of it is based on a series of misunderstandings. First, Wilson's and Wilson's (27) original interpretation of Dawkins' selfish gene argument was incorrect. Second, in their explanatory reply (33), they distinguished between two kinds of group selection: the idea that groups can be units of selection (theoretical group selection) and the idea that group selection plays a functional role in evolution (functional group selection). They clarified that their claim concerned theoretical group selection, not functional group selection. Third, that clarified claim was correct and not correct. It was incorrect because Dawkins has never explicitly acknowledged that he had erred by developing his selfish gene theory as an implicit argument against this kind of group selection. However, the distinction that he made, by 1978, between two kinds of unit of selection, replicators (genes) and vehicles (somas), does imply such an acknowledgment since it holds that groups can be units of selection (vehicles). In this important sense, Wilson's and Wilson's clarified claim (33) was correct. Fourth, Dawkins' second denial (34) concerned functional group selection, not theoretical group selection.
{"title":"Did dawkins recant his selfish gene argument against group selection?","authors":"Koen B Tanghe","doi":"10.19272/202311402005","DOIUrl":"10.19272/202311402005","url":null,"abstract":"<p><p>In 2007, David S. Wilson and Edward O. Wilson (27) pointed out that, Richard Dawkins had admitted that, contrary to what he had claimed in his book The Selfish Gene (1976) (7), the idea that only the gene is a fundamental unit of selection cannot be used as an argument against the notion of group selection. This elicited a sharp denial from Dawkins (30), which was followed by an explanatory reply by Wilson and Wilson (33) and another vehement denial by Dawkins (34). I analyse the prehistory of this surprisingly complex and convoluted dispute and subsequently disentangle it. My conclusion is that much of it is based on a series of misunderstandings. First, Wilson's and Wilson's (27) original interpretation of Dawkins' selfish gene argument was incorrect. Second, in their explanatory reply (33), they distinguished between two kinds of group selection: the idea that groups can be units of selection (theoretical group selection) and the idea that group selection plays a functional role in evolution (functional group selection). They clarified that their claim concerned theoretical group selection, not functional group selection. Third, that clarified claim was correct and not correct. It was incorrect because Dawkins has never explicitly acknowledged that he had erred by developing his selfish gene theory as an implicit argument against this kind of group selection. However, the distinction that he made, by 1978, between two kinds of unit of selection, replicators (genes) and vehicles (somas), does imply such an acknowledgment since it holds that groups can be units of selection (vehicles). In this important sense, Wilson's and Wilson's clarified claim (33) was correct. Fourth, Dawkins' second denial (34) concerned functional group selection, not theoretical group selection.</p>","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10465687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Although most discussions on the origin and evolution of insect wings and metamorphosis have assumed that the ancestors of winged insects were terrestrial, it now seems possible that they were actually aquatic. Changing the basic assumptions affects our interpretations of the origin of metamorphosis and our understanding of insect diversity. It is argued that the ancestors of winged insects were similar to primitive mayflies, developing from aquatic larvae into terrestrial adults, and that metamorphosis originated as an inevitable consequence of an amphibiotic life cycle. It is suggested that the first pupae resembled those of Megaloptera.
{"title":"Origin of insect wings, metamorphosis, pupae and the maj or insect orders.","authors":"Robert Bligh Toms","doi":"10.19272/202311402006","DOIUrl":"https://doi.org/10.19272/202311402006","url":null,"abstract":"<p><p>Although most discussions on the origin and evolution of insect wings and metamorphosis have assumed that the ancestors of winged insects were terrestrial, it now seems possible that they were actually aquatic. Changing the basic assumptions affects our interpretations of the origin of metamorphosis and our understanding of insect diversity. It is argued that the ancestors of winged insects were similar to primitive mayflies, developing from aquatic larvae into terrestrial adults, and that metamorphosis originated as an inevitable consequence of an amphibiotic life cycle. It is suggested that the first pupae resembled those of Megaloptera.</p>","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10165580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fabien Génin, Hajarimanitra Rambeloarivony, Daniele Silvestro, Judith C Masters
Based on the Recognition Concept of species, the specific-mate contact model posits that mating systems develop as combinations of two fundamental courtship strategies that we interpret here in terms of behavioural heterochrony: territorial mate-attraction evolved as an effect of peramorphosis whereas group-living mate-seeking evolved as an effect of paedomorphosis. We tested this hypothesis on primates in a phylogenetic and paleo-climatic context. Our results suggest that primate promiscuity (both males and females are mate-seekers) evolved with group-living from ancestral pair-living monogamy (both males and females are mate-attractors) in the Palaeogene, as the result of a slowdown in growth (neoteny) caused by increased environmental predictability. A secondary return to territorial monogamy probably evolved as the result of accelerated growth driven by seasonality (acceleration). Polygamy evolved in the Neogene during periods of forest fragmentation and environmental unpredictability. Small monogamous ancestors evolved seasonal polyandry (female attraction) as an effect of truncated development (progenesis). Large promiscuous, neotenic ancestors evolved non-seasonal polygyny (male attraction) as an effect of prolonged development (hypermorphosis) in males. We conclude that social heterochrony offers alternative explanations for the coevolution of life history and mating be-haviour; and we discuss the implications of our model for human social evolution.
{"title":"Ontogeny and phylogeny of mating behaviour: social heteroch rony in primates.","authors":"Fabien Génin, Hajarimanitra Rambeloarivony, Daniele Silvestro, Judith C Masters","doi":"10.19272/202311402002","DOIUrl":"https://doi.org/10.19272/202311402002","url":null,"abstract":"<p><p>Based on the Recognition Concept of species, the specific-mate contact model posits that mating systems develop as combinations of two fundamental courtship strategies that we interpret here in terms of behavioural heterochrony: territorial mate-attraction evolved as an effect of peramorphosis whereas group-living mate-seeking evolved as an effect of paedomorphosis. We tested this hypothesis on primates in a phylogenetic and paleo-climatic context. Our results suggest that primate promiscuity (both males and females are mate-seekers) evolved with group-living from ancestral pair-living monogamy (both males and females are mate-attractors) in the Palaeogene, as the result of a slowdown in growth (neoteny) caused by increased environmental predictability. A secondary return to territorial monogamy probably evolved as the result of accelerated growth driven by seasonality (acceleration). Polygamy evolved in the Neogene during periods of forest fragmentation and environmental unpredictability. Small monogamous ancestors evolved seasonal polyandry (female attraction) as an effect of truncated development (progenesis). Large promiscuous, neotenic ancestors evolved non-seasonal polygyny (male attraction) as an effect of prolonged development (hypermorphosis) in males. We conclude that social heterochrony offers alternative explanations for the coevolution of life history and mating be-haviour; and we discuss the implications of our model for human social evolution.</p>","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10465683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE's central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary framework. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution.
{"title":"A third way to the selected effect/causal role distinction in the great encode debate.","authors":"Ehud Lamm, Sophie Juliane Veigl","doi":"10.19272/202311402004","DOIUrl":"https://doi.org/10.19272/202311402004","url":null,"abstract":"<p><p>Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE's central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary framework. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution.</p>","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10165575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1007/978-981-19-8257-6
Makoto Sato
{"title":"Getting Started in Mathematical Life Sciences","authors":"Makoto Sato","doi":"10.1007/978-981-19-8257-6","DOIUrl":"https://doi.org/10.1007/978-981-19-8257-6","url":null,"abstract":"","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81894063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1007/978-981-19-6016-1
H. Seno
{"title":"A Primer on Population Dynamics Modeling","authors":"H. Seno","doi":"10.1007/978-981-19-6016-1","DOIUrl":"https://doi.org/10.1007/978-981-19-6016-1","url":null,"abstract":"","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75754346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1007/978-981-19-4979-1
M. Nakamaru
{"title":"Trust and Credit in Organizations and Institutions","authors":"M. Nakamaru","doi":"10.1007/978-981-19-4979-1","DOIUrl":"https://doi.org/10.1007/978-981-19-4979-1","url":null,"abstract":"","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77530800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Annah Mwikali Muli, A. Gusnanto, Jeanine Houwing-Duistermaat
In survival analysis, the effect of a covariate on the outcome is reported in a hazard rate. However, hazards rates are hard to interpret. Here we consider differences in survival probabilities instead. Using data on twins is interesting due to the fact that many observed and unobserved factors are controlled or matched. To model the correlation between twins, some authors have proposed survival models with frailties or random effects. However, there is a potential danger of bias in the estimation if the frailty distribution is misspecified. Frailties are often assumed to follow a gamma distribution. To safeguard us from the impact of the misspecification of this distribution, we consider a flexible non-parametric baseline hazard in addition to a parametric one. We will apply this methodology to the TwinsUK cohort to predict the probability of experiencing a fracture in the next five or ten years, given their bone mineral densities (BMD) and their frailty index. The models with parametric and non-parametric baseline hazards yield very close results in estimating survival probabilities and thus a choice of parametric baseline hazard is generally preferred. We find that bone mineral density is a significant predictor in the model whereas frailty index is not. Low BMD leads to a larger probability of fracture; e.g, in 10 years, the probability of fracture is 21% for low BMD group, 16% for medium BMD group and 8% for high BMD group.
{"title":"Use of shared gamma frailty model in analysis of survival data in twins.","authors":"Annah Mwikali Muli, A. Gusnanto, Jeanine Houwing-Duistermaat","doi":"10.19272/202111402005","DOIUrl":"https://doi.org/10.19272/202111402005","url":null,"abstract":"In survival analysis, the effect of a covariate on the outcome is reported in a hazard rate. However, hazards rates are hard to interpret. Here we consider differences in survival probabilities instead. Using data on twins is interesting due to the fact that many observed and unobserved factors are controlled or matched. To model the correlation between twins, some authors have proposed survival models with frailties or random effects. However, there is a potential danger of bias in the estimation if the frailty distribution is misspecified. Frailties are often assumed to follow a gamma distribution. To safeguard us from the impact of the misspecification of this distribution, we consider a flexible non-parametric baseline hazard in addition to a parametric one. We will apply this methodology to the TwinsUK cohort to predict the probability of experiencing a fracture in the next five or ten years, given their bone mineral densities (BMD) and their frailty index. The models with parametric and non-parametric baseline hazards yield very close results in estimating survival probabilities and thus a choice of parametric baseline hazard is generally preferred. We find that bone mineral density is a significant predictor in the model whereas frailty index is not. Low BMD leads to a larger probability of fracture; e.g, in 10 years, the probability of fracture is 21% for low BMD group, 16% for medium BMD group and 8% for high BMD group.","PeriodicalId":55980,"journal":{"name":"Theoretical Biology Forum","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43590946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}