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Alan G Fix

Publications and source records attributed to Alan G Fix.

4 recordsLinked to original sources

Rapid deployment of the five founding Amerind mtDNA haplogroups via coastal and riverine colonization.

Numerous studies of variation in mtDNA in Amerindian populations established that four haplogroups are present throughout both North and South America. These four haplogroups (A, B, C, and D) and perhaps a fifth (X) in North America are postulated to be present in the initial founding migration to the Americas. Furthermore, studies of ancient mtDNA in North America suggested long-term regional continuity of the frequencies of these founding haplogroups. Present-day tribal groups possess high frequencies of private mtDNA haplotypes (variants within the major haplogroups), consistent with early establishment of local isolation of regional populations. Clearly these patterns have implications for the mode of colonization of the hemisphere. Recently, the earlier consensus among archaeologists for an initial colonization by Clovis hunters arriving through an ice-free corridor and expanding in a "blitzkrieg " wave was shown to be inconsistent with extensive genetic variability in Native Americans; a coastal migration route avoids this problem. The present paper demonstrates through a computer simulation model how colonization along coasts and rivers could have rapidly spread the founding lineages widely through North America.

Computer Simulation↗

Simulating hemoglobin history.

In one of the truly classic works in anthropological genetics, Frank Livingstone established the interrelationships between agriculture, mosquito ecology, malaria, and, consequently, the frequencies of sickle cell hemoglobin in West Africa. A major inference from Livingstone's study was the recency of malaria as a selective agent in human populations, only becoming significant after the adoption of agriculture in the last few thousand years. Clines of the abnormal hemoglobin alleles might therefore represent continuing waves of advance of adaptive alleles. In order to model the complex interaction of several hemoglobin alleles, selection, and gene flow spreading adaptive mutants, Livingstone turned to computer simulation. Numerous insights concerning the competitive increase of different alleles (hemoglobins S, C, and E and thalassemia), the rate of allele spread under different migration scenarios, including the potential importance of long-range migration, came out of these studies. These experiments also stimulated others to search for mechanisms that might increase the diffusion rate of hemoglobin variants, including kin-structured migration and epidemic disease selection. Recent molecular studies have substantiated major aspects of Livingstone's work (including the recent origin of falciparum malaria) and posed challenges to some of his assumptions (such as the number of mutations to hemoglobins S and E). But whatever the fate of his specific hypotheses, his emphasis on the interaction of genetics, ecology, and culture stands as a model for the anthropological approach to the understanding of human variation and evolution.

Alleles↗

Colonization models and initial genetic diversity in the Americas.

The mode and tempo of colonization of the Americas established the initial pattern of continental genetic diversity. Despite a long history of study, the process of settlement remains controversial in terms of date, rate, and pattern. While there is agreement that Asia was the source population, several different models have been proposed for the colonization process. A classic model postulates a rapid spread of population ("blitzkrieg") from a small band of hunters entering through the corridor between the continental ice sheets circa 11,000 years B.P. Colonization occurred as a wave of expansion across the land masses of North and South America. An alternative model envisions the original colonists initially limiting settlement to the coastline, using boats, and entering the Americas at an earlier date, circa 13,500 B.P. Range expansion along this linear habitat from North to South America could be rapid without requiring population saturation of entire continental regions. These models have markedly different implications for genetic variation among Native Americans. The blitzkrieg colonization process would have generated multiple founder effects leading to extreme loss of genetic variation. Computer simulation of this model shows nearly complete fixation in 30 generations. Simulation of the coastal model, on the other hand, requires less extreme demographic assumptions and maintains substantial genetic variability after 100 generations. Although with the coastal model continental interiors are occupied less rapidly than with the blitzkrieg model, the coastal model allows earlier entry and rapid expansion to the southern limits of the hemisphere.

Emigration and Immigration↗

Kin-structured migration: causes and consequences.

Migration among local populations classically has been seen as the principal process retarding genetic microdifferentiation. However, as Sewall Wright pointed out long ago, migration may also act as a random differentiating force. In fact, when migrants comprise a biological kin group, migration may be considered a component of genetic drift. The causes of kin-structured migration (KSM) lie in the common, if not universal, tendency for kin to associate and cooperate. However, similar to genetic drift, KSM has its greatest effect in smaller populations and is most apparent in low-density fission-fusion societies such as the Yanomamo of South America and the Semai of Malaysia, and less salient in higher density, low-mobility populations such as those of the New Guinea Highlands. The evolutionary consequences of KSM begin with increased genetic variation among populations. Such intergroup variation provides a basis for group selection. The origin of larger-scale geographic differentiation can arise from kin-structured migrant groups colonizing new regions. Waves of colonizing kin-structured founder groups may produce gene frequency clines, mimicking demic diffusion and natural selection. Finally, because kin structuring reduces the effective size of a population, it may be speculated that the extremely small effective size inferred for ancestral populations of Homo sapiens may be an artifact of kin-structured demographically larger populations.

Anthropology, Physical↗