Changes In Gene Frequencies Research Articles

F. W. Allendorf and G. Luikart, Conserving Global Biodiversity? Conservation and the Genetics of Populations

Conservation and the Genetics of Populations is the second major text that deals with the relatively young discipline of Conservation Genetics, with publication arriving some five years after that of the field's inaugural text (Frankham et al. 2002). The discipline has not been without contro- versy, with continuing debate among those who implement conservation strategy as to how important genetic consid- erations are likely to be, particularly in the short term. While the authors acknowledge this debate, they do not dwell on it, pointing out that the book's aim is to provide an understanding of the principles of conservation genetics, and ways of applying them in real-world situations; it is not an argument for the value of genetics to conservation per se. Having fairly recently completed the (seemingly) never-ending undergrad and graduate route myself, this text would have been very welcome during that time, as it provides a truly comprehensive and accessible guide to the discipline. The target audience of the book is advanced under- graduate and graduate students, conservation biologists and practitioners. The book presents well, with very good illustrations, a 'guest box' in each chapter authored by leading workers in the field (e.g., Louis Bernatchez, James Crow, Loren Rieseberg, Robert Vrijenhoek, Robin Waples, and 22 others), and problem sets at the end of each chapter. Each chapter opens with a couple of relevant quotations, many from 'giants' in the field—a nice touch (for the mathematically-challenged, see Dobzhansky's remarks on Sewall Wright's work in the Appendix). Case studies provide a good mix of both classical and recent advances in conservation genetics. An associated website provides solutions to the problems (in printable PDF format), alongside example data sets and several basic software programs to illustrate methods of data analysis and popu- lation genetic processes (e.g., Hardy-Weinberg test). The book comprises 20 chapters divided into three sections. The first, the Introduction, opens with a brief 'what and how', that is, what should we conserve and how are we going to go about doing so. Subsequent chapters in this section deal with variation in natural populations, both phenotypic and genetic, and the assessment and application thereof in conservation; with genetic variation being fur- ther subdivided into two chapters, the first on chromosomal and protein variation, the second on DNA variation. This provides a good background to the discipline and an overview of the tools of the trade, and how to apply them appropriately. The chapter on DNA variation concludes with a short overview of recent developments that could potentially revolutionise the field, such as population genomics and DNA arrays. However, one other develop- ment that may well contribute significantly to conservation genetics and population genetic theory in general, the growing field of 'ancient DNA' (e.g., to understand the significance of changes in gene frequencies over time), is not covered at all in this book. Part II deals with Mechanisms of Evolutionary Change and provides much of the theoretical genetics background to the more applied final section of the book. This section provides comprehensive chapters on Hardy-Weinberg, Small populations and genetic drift, Effective population size, Natural selection, Population subdivision, Multiple loci, Quantitative genetics, and Mutation. The first three chapters get to the heart of the problem—the loss of genetic

Detection of marker–QTL associations by studying change in marker frequencies with selection

The value of selective genotyping for the detection of QTL has already been studied from a theoretical point of view but with the assumption of a negligible contribution (r2P) of the QTL to the phenotypic variance. For predicting change in gene frequency, we show that this assumption is only valid for r2P less than 0.05 and for a proportion selected higher than 1%. Therefore, we develop a study of the optimization of selective genotyping without assumption on QTL effect, with selection either of both tails (bidirectional genotyping or BSG) or only one tail (unidirectional genotyping or USG). For a given population size of phenotyped plants the optimal proportion selected for selective genotyping is around 30% for each tail. For the same investment as in ANOVA, by investing more in phenotyping than in genotyping when the cost ratio of genotyping to phenotyping is higher than 1, the optimal proportion selected appears to be between 10 and 20% for each tail. It is mainly affected by the cost ratio and decreases when the cost ratio increases. At this optimum, BSG is competitive with ANOVA, or even more powerful, when the cost ratio is higher than 1. USG can also be competitive when the cost ratio is higher than 2. Using experimental data from two populations of about 300 F4 inbred families of maize, it was verified that BSG at the optimum gives the same results as ANOVA or is better whereas USG is less powerful or equivalent.

Changes in disease gene frequency over time with differential genotypic fitness and various control strategies

A spreadsheet model was constructed to describe the change in allelic frequency over time for a lethal recessive mutation in an animal population. The model allowed relative fitness to differ between genotypes, between sexes, and over time. Whereas a lethal recessive allele is naturally eliminated very slowly from a population, a small selective disadvantage of the heterozygote results in a large increase in the rate of elimination. With selective advantage of the heterozygote through linkage with a production trait or pleiotropy, the allele is never naturally eliminated but tends toward a stable equilibrium frequency. The model was used to investigate various alternative control programs based on the detection of heterozygotes by genotyping and their exclusion from breeding. The programs (genotyping males only, genotyping males and 50% of females, and genotyping all breeding animals) were modeled for various initial heterozygote frequencies, and the results were described in terms of the number of generations, number of tests, and number of culls required to reduce the heterozygote frequency to a predefined level. The model can be used to compare the feasibility and cost of various control strategies and to illustrate clearly to breeders the expected outcomes, as well as the danger of prematurely terminating a control program when there is a selective advantage of the heterozygote.

Natural selection and climate change: temperature‐linked spatial and temporal trends in gene frequency in Fagus sylvatica

Rapid increases in global temperature are likely to impose strong directional selection on many plant populations, which must therefore adapt if they are to survive. Within populations, microgeographic genetic differentiation of individuals with respect to climate suggests that some populations may adapt to changing temperatures in the short-term through rapid changes in gene frequency. We used a genome scan to identify temperature-related adaptive differentiation of individuals of the tree species Fagus sylvatica. By combining molecular marker and dendrochronological data we assessed spatial and temporal variation in gene frequency at the locus identified as being under selection. We show that gene frequency at this locus varies predictably with temperature. The probability of the presence of the dominant marker allele shows a declining trend over the latter half of the 20th century, in parallel with rising temperatures in the region. Our results show that F. sylvatica populations may show some capacity for an in situ adaptive response to climate change. However as reported ongoing distributional changes demonstrate, this response is not enough to allow all populations of this species to persist in all of their current locations.

Mendel's Impact

ArgumentI wish to propose that the history of genetics reflects the history of the concept of reductionism in the life sciences. Reductionism is the thesis that explanation of laws or phenomena in one realm by those of another realm are always likely to be successful as explanations. By 1900 reduction of biology to the laws of chemistry and physics was not self evident: Although bottom-up preformationist explanations were largely inadequate for development, top-down epigenetic hypotheses often adopted metaphysical assumptions. Similarly, top-down theories of evolution as dependent on the accumulated impact of the past confronted those of bottom-up notions of fitness of specific traits that are relevant for future evolution. Mendel's 1865 methodological reductionist study of inheritance of traits was embraced in 1900 as evidence for reduction at the conceptual level. With the achievements of research of the mechanisms of inheritance, genetics became increasingly genocentric in its explanatory arsenal of development, and accordingly it was in conflict with the top-down, life-as-organized-systems' notions of embryology. Similarly, evolution was conceptually reduced to changes of gene-frequencies in populations. It was, however, precisely the increasing attempts to ground the bottom-up approach at the molecular level that eventually pushed conceptual reductionism to its crisis. Modern developments of molecular and computational methods finally forced, or allowed, researchers to apply bottom-up methodologies to top-down systems' analyses.

The molecular genetics of the melanocortin pathway and energy homeostasis

The CNS melanocortin pathway plays an important role in the control of body weight. Two papers in this issue of Cell Metabolism, Lee et al., 2006 and Biebermann et al., 2006, suggest that beta MSH--a product of POMC processing--plays an unanticipated role in this pathway in humans.

根井の標準遺伝距離を用いたｎｅｕｔｒａｌｉｔｙを含む問題でのＧＡの進化ダイナミクス解析

Neutrality, which is caused by highly redundant mappings from genotype to phenotype or from phenotype to fitness, has been recognized as an important factor for artificial genetic search. However, this research field has still been trying to overcome the difficulties of analyzing evolutionary dynamics at the level of phenotype space or fitness space for about ten years. On the other hand, considering that population genetics explains the change of gene frequency in a population, that is, dynamics at the level of genotype space, we expect that various techniques developed in population genetics might be useful for analyzing dynamics of artificial evolution. In this paper, we apply the Nei's standard genetic distance to artificial evolution. Several computer simulations are systematically conducted by applying a standard genetic algorithm to a tunably neutral NK landscape in order to clarify the characteristics of the Nei's standard genetic distance in genetic algorithms. The results prove several consistencies with the (nearly) neutral theory of molecular evolution.

Phenotypic accommodation: adaptive innovation due to developmental plasticity

Phenotypic accommodation is adaptive adjustment, without genetic change, of variable aspects of the phenotype following a novel input during development. Phenotypic accommodation can facilitate the evolution of novel morphology by alleviating the negative effects of change, and by giving a head start to adaptive evolution in a new direction. Whether induced by a mutation or a novel environmental factor, innovative morphological form comes from ancestral developmental responses, not from the novel inducing factor itself. Phenotypic accommodation is the result of adaptive developmental responses, so the novel morphologies that result are not "random" variants, but to some degree reflect past functionality. Phenotypic accommodation is the first step in a process of Darwinian adaptive evolution, or evolution by natural selection, where fitness differences among genetically variable developmental variants cause phenotype-frequency change due to gene-frequency change.

Microevolution and mega-icebergs in the Antarctic.

Microevolution is regarded as changes in the frequencies of genes in populations over time. Ancient DNA technology now provides an opportunity to demonstrate evolution over a geological time frame and to possibly identify the causal factors in any such evolutionary event. Using nine nuclear microsatellite DNA loci, we genotyped an ancient population of Adélie penguins (Pygoscelis adeliae) aged approximately 6,000 years B.P. Subfossil bones from this population were excavated by using an accurate stratigraphic method that allowed the identification of individuals even within the same layer. We compared the allele frequencies in the ancient population with those recorded from the modern population at the same site in Antarctica. We report significant changes in the frequencies of alleles between these two time points, hence demonstrating microevolutionary change. This study demonstrates a nuclear gene-frequency change over such a geological time frame. We discuss the possible causes of such a change, including the role of mutation, genetic drift, and the effects of gene mixing among different penguin populations. The latter is likely to be precipitated by mega-icebergs that act to promote migration among penguin colonies that typically show strong natal return.

Long‐term responses, changes in genetic variances and inbreeding depression from 122 generations of selection on increased litter size in mice

Data on mice selected for litter size over 122 generations have been analysed in order to reveal the effect of long-term selection on responses and changes in variances over a long selection period. Originally, three lines were established from the same base population, namely an H line selected for large litter size, an L line selected for small litter size and a K line without selection. In generation 122, the mean number of pups born alive (NBA) was 22 for the H line and 11 for the K line. Phenotypic response to selection is reduced over generations, but crossing of plateaued lines increased responses and realized heritabilities. Both realized heritabilities and heritabilities from residual maximal likelihood (REML) analyses were, in general, calculated from generation (-1)-44 (period 1), 45-70 (period 2) and 71-122 (period 3) separately. Realized heritabilities were in general smaller than heritabilities estimated from mixed model analysis. An overall estimate of heritability for NBA was found to be 0.19 (+/- 0.01) by REML analysis. Additive variance is constant over all periods in the high line and the control line, but is reduced over periods in the low line. The reduction of additive variance in the low line could probably be explained by changes in gene frequencies. In all lines, environmental variances increased over periods. Inbreeding reduced the mean litter size by 0.72 (+/- 0.10) pups per 10% increase in inbreeding, with substantial variance between periods and lines.

Developmental plasticity and the origin of species differences.

Speciation is the origin of reproductive isolation and divergence between populations, according to the "biological species concept" of Mayr. Studies of reproductive isolation have dominated research on speciation, leaving the origin of species differences relatively poorly understood. Here, I argue that the origin of species differences, and of novel phenotypes in general, involves the reorganization of ancestral phenotypes (developmental recombination) followed by the genetic accommodation of change. Because selection acts on phenotypes, not directly on genotypes or genes, novel traits can originate by environmental induction as well as mutation, then undergo selection and genetic accommodation fueled by standing genetic variation or by subsequent mutation and genetic recombination. Insofar as phenotypic novelties arise from adaptive developmental plasticity, they are not "random" variants, because their initial form reflects adaptive responses with an evolutionary history, even though they are initiated by mutations or novel environmental factors that are random with respect to (future) adaptation. Change in trait frequency involves genetic accommodation of the threshold or liability for expression of a novel trait, a process that follows rather than directs phenotypic change. Contrary to common belief, environmentally initiated novelties may have greater evolutionary potential than mutationally induced ones. Thus, genes are probably more often followers than leaders in evolutionary change. Species differences can originate before reproductive isolation and contribute to the process of speciation itself. Therefore, the genetics of speciation can profit from studies of changes in gene expression as well as changes in gene frequency and genetic isolation.

Neanderthals and Modern Humans: An Ecological and Evolutionary Perspective

Clive Finlayson, 2004, Cambridge University Press, Cambridge, 255 p. (Hardcover, US $85.00) ISBN: 0-521-82087-1. Ever since the first recognition, back in the pre-evolutionary days of 1856, that Neanderthal Man was a real phenomenon to be contended with and somehow to be explained, paleoanthropologists have enjoyed—if that is the right word—a thoroughly equivocal relationship with this extinct but big-brained human relative. Clearly so close to our own species Homo sapiens , but equally obviously so different, Homo neanderthalensis hovers right at the brink of what we usually think of as humanity. Ought we to see the Neanderthals as no more than a rather strange version of ourselves? Or should we view them as a distinctive evolutionary entity that needs to be understood on its own—and very different—terms? Since the middle of the last century, when paleoanthropology capitulated to the seductive simplicities of the Evolutionary Synthesis (which reduced the evolutionary process to little more than generation-by-generation gene frequency changes within lineages), students of the human fossil record have tended to display a warm-hearted ecumenicism that welcomes the Neanderthals into the embrace of Homo sapiens . For even though they are nowadays a lot more willing than they were a only a decade or two ago to admit just how morphologically distinctive the Neanderthals actually were, most paleoanthropologists remain reluctant to cede these hominids their own independent identity. Clive Finlayson, the erudite and thoughtful author of Neanderthals and Modern Humans, …

Is Delayed Childbearing Changing Gene Frequencies in Western Populations?

Experimental data and clinical observations suggest that delaying childbearing influences the biology of the mother-fetus relationship, with a negative effect on fetal development and predisposition to severe diseases such as type 1 diabetes. We reason that advanced maternal age may influence intrauterine selection, favoring genotypes that are more adapted to the intrauterine environment of less young women. In the present study we have investigated the relationship of maternal age to HP genotype and PGM1-Rh area (chromosome 1) that have been previously found to be associated with fertility and developmental parameters. HP phenotype was determined in 679 consecutive puerperae from the population of central Italy. PGM1 phenotype and Rh C phenotype were determined in 222 puerperae and 200 newborns. The HP 1,1 phenotype decreases and the HP 2,2 phenotype increases with maternal age. The proportion of phenotypes carrying both the Rh C and PGM1*1 alleles is much higher in puerperae older than 36 years than in puerperae of age 22 years. The frequency of the PGM1*1-Rh C haplotype increases and the frequency of the PGM1*2-Rh C haplotype decreases with maternal age. The changes in these genetic systems with advancing maternal age are similar in mothers and newborns. The delay of childbearing age, associated in Western countries with the fertility transition in addition to detrimental effects on intrauterine development and increased susceptibility to severe disorders, could bring about changes in the genetic composition of a population.

A quantitative genetics model for viability selection

Viability selection will change gene frequencies of loci controlling fitness. Consequently, the frequencies of marker loci linked to the viability loci will also change. In genetic mapping, the change of marker allelic frequencies is reflected by the departure from Mendelian segregation ratio. The non-Mendelian segregation of markers has been used to map viability loci along the genome. However, current methods have not been able to detect the amount of selection (s) and the degree of dominance (h) simultaneously. We developed a method to detect both s and h using an F2 mating design under the classical fitness model. We also developed a quantitative genetics model for viability selection by proposing a continuous liability controlling the viability of individuals. With the liability model, mapping viability loci has been formulated as mapping quantitative trait loci. As a result, nongenetic systematic environmental effects can be easily incorporated into the model and subsequently separated from the genetic effects of the viability loci. The quantitative genetic model has been verified with a series of Monte Carlo simulation experiments.

Simulating the Effects of Dominance and Epistasis on Selection Response in the CIMMYT Wheat Breeding Program Using QuCim

Plant breeders use many different breeding methods to develop superior cultivars. However, it is difficult, cumbersome, and expensive to evaluate the performance of a breeding method or to compare the efficiencies of different breeding methods within an ongoing breeding program. To facilitate comparisons, we developed a QU-GENE module called QuCim that can simulate a large number of breeding strategies for self-pollinated species. The wheat breeding strategy Selected Bulk used by CIMMYT's wheat breeding program was defined in QuCim as an example of how this is done. This selection method was simulated in QuCim to investigate the effects of deviations from the additive genetic model, in the form of dominance and epistasis, on selection outcomes. The simulation results indicate that the partial dominance model does not greatly influence genetic advance compared with the pure additive model. Genetic advance in genetic systems with overdominance and epistasis are slower than when gene effects are purely additive or partially dominant. The additive gene effect is an appropriate indicator of the change in gene frequency following selection when epistasis is absent. In the absence of epistasis, the additive variance decreases rapidly with selection. However, after several cycles of selection it remains relatively fixed when epistasis is present. The variance from partial dominance is relatively small and therefore hard to detect by the covariance among half sibs and the covariance among full sibs. The dominance variance from the overdominance model can be identified successfully, but it does not change significantly, which confirms that overdominance cannot be utilized by an inbred breeding program. QuCim is an effective tool to compare selection strategies and to validate some theories in quantitative genetics.

Inferring phylogenies: an instant classic

Joe Felsenstein has had more positive influence on the statistical revolution of phylogenetics than any other researcher in the field. For that reason, many biologists view him as the father of statistical phylogenetics. It was with this in mind that I finally got my hands on his long-awaited book, Inferring Phylogenies. The short answer is: it delivers. In a narrow sense, Felsenstein's book could be viewed as old-fashioned, with a number of chapters devoted to 'old' methods such as parsimony and distance-based approaches. This view misses the point. No other book gives as clear and comprehensive a picture of the major problems, solved or otherwise, in phylogenetic inference. In fact, it is perhaps precisely because Felsenstein follows the progress of statistical phylogenetics from its early beginnings that the book will be so enduring. It is enjoyable to read and is written in an uncluttered way that invites the reader to understand the details, and to work them out with pen and paper when the answer is not explicitly given. Scientists should know their tools, and Felsenstein does his best to explain to tree-builders what in fact they are actually doing when they run an analysis using popular phylogeny programs like PAUP* or PHYLIP. But this book is not just about building trees. There are also chapters devoted to modeling changes in gene frequencies, genealogy-based population genetics (the coalescent) and quantitative genetics, to mention just a few. Not only is this an unrivalled reference book for users of phylogenetic methods, but it also serves as a foundation stone on which developers of phylogenetic methods can build. The nature of the material demands that the difficulty level is a bit uneven from chapter to chapter, but an effort is always made to convey the essential features of the discipline discussed. The book is well balanced, containing enough detail to suit most readers, and providing ample references for those that require more.

Fast and Slow Dynamics of Malaria and the S-gene Frequency

A mathematical model incorporating both malaria epidemics and human population genetics of the sickle-cell gene is studied. Singular perturbation techniques are used to separate the dynamics of the model into two time-scales with a faster time-scale for the epidemics and a slower time-scale for the change in gene frequencies. A complete analysis of the dynamics on the slow manifold is conducted, which provides insights into how malaria epidemics may have an impact on the maintenance of the sickle-cell gene in a population where malaria is prevalent.

Fitness and life-history traits of the two major mitochondrial DNA haplotypes of Drosophila subobscura.

Mitochondrial DNA restriction site analyses on natural populations of Drosophila subobscura have proved the existence of two common, coexisting haplotypes (I and II), as well as a set of less frequent ones derived from them. To explain this distribution, experiments to date point practically to all possible genetic mechanisms being involved in the changes of gene frequencies (cytonuclear coadaptation, direct natural selection on mtDNA and genetic drift). In an attempt to find differences that help to understand the dynamics of these haplotypes and to detect the effect of selection, we measured certain fitness components and life-history traits (egg-larva and larva-adult viabilities and developmental times, longevity, resistance to desiccation and optimal density) of the two main haplotypes I and II when maintained in laboratory population cages. As a general trend, haplotype II showed a higher net fitness than haplotype I, which explains the superiority of haplotype II over haplotype I in experimental populations but not their coexistence in nature, where additional factors must be considered.

The Representational Revolution

Minds are very accessible when their owners connection between pretense in children and are around, and the written record of speech and artistic achievement, and between changes to action keeps a tolerable connection with minds social structure and pretend play. Scholars such of the recent past.1 Looking further back is as Merlin Donald, Nick Humphrey, and Steven much harder. Brains decay quickly, and, for our Mithen have helped to make speculation in cogspecies, fossils indicate little more than a boring nitive anthropology respectable. Trouble would uniformity of brain size over a hundred thoucome if the speculation became dogma; that is sand years. For ideas about the minds of our very unlikely to happen in the case of the distant ancestors we are heavily reliant on the present essay. record of their nonlinguistic artifacts, so our To what genre, then, does this essay belong? reasoning in this area is very precarious. Still, A kindly view would be to see it as contributing when we focus on the astonishing cultural prodto a philosophically informed anthropology of ucts of around 30,000 years before the present art. But the fact that it brings philosophical (BP), it is hard to resist the conclusion that we ideas and modes of thought to bear on the topic are seeing what Paul Harris calls a new power does not make it a piece of philosophy of art, or of the imagination.2 What happened, and why? philosophy of anything. There may be no Steven Mithen has offered an explanation of absolute distinction between using ideas from a these dramatic cultural achievements that domain and contributing to that domain itself, appeals to assumptions about changes in human but my efforts are far toward the former end of mental architecture; I argue that, even granting the spectrum. Indeed, I end by biting the editoMithen these assumptions, his theory does not rial hand that feeds me, arguing that what I am explain what needs explaining. I suggest instead doing is not aesthetics at all. that those who believe in a cognitive revolution These are partly speculations about evolution, around this time consider two factors that may but I shall not be concerned with genetic have led to a growth in pretend play: the extenchange, or exclusively with factors that depend sion of childhood in Homo sapiens sapiens on genetic change. Changes in gene frequency (H.s.s.), and changes in diet, population density, are causal factors in some of the (putative) social organization, and child-rearing practices. events I shall be describing, but they do not All this is highly speculative, though I hope constitute any kind of explanatory bedrock. my references make clear that few of the ideas Macro-level explanations are not merely devices are my own. But it is not quite a house of cards, of convenience, pressed into service when we where failure at any level brings everything happen not to know the micro-level detail that crashing down. Some parts would survive the underpins them; they allow us to formulate true annihilation of others: my criticism of Mithen is counterfactuals that would be unavailable at the pretty much independent of anything else I say, micro level.3 We need not even assume that all as are my complaints about the use of a toothe factors we will consider here are filtered general category of the symbolic. What if the through the genome. According to Developmental timetable I am using turns out to be wrong? Systems Theory (DST), changes at the genetic There may still be merit in the ideas of a level have no privileged place in evolutionary

Non-major histocompatibility complex alloantigen genes affecting immunity

An alloantigen is a genetically determined cell-surface molecule detected by specific antisera. An identifying letter has been assigned to each genetic locus responsible for the 12 distinct families of alloantigens: A, B, C, D, E, H, I, J, K, L, P, and R. The genes of each system segregate independently of the other systems, except that the A and E are very closely linked (0.5 centimorgans). Selection experiments over numerous generations have revealed distinct changes in gene frequency of the A-E alloantigens, suggesting immune responses associated with susceptibility to coccidiosis, response to immunizations with SRBC, and selection for size of the bursa of Fabricius. Immune response effects of the C system of alloantigen genes are indicated by distinct gene frequency changes following selection for response to SRBC, selection for size of bursa of Fabricius, and macrophage nitrite production after lipopolysaccharide (LPS) stimulation. Immune response effects of the D system of antigens are indicated by data from genetic selection for response to immunization with SRBC, selection for bursa size, and macrophage nitrite and cytokine interleukin (IL)-6 production following LPS stimulation. Immune response effects of the I system genes are indicated by distinct gene frequency changes in lines selected for bursa size and within family comparisons for macrophage nitrite and cytokine IL-6 production following LPS stimulation. Effects of the L system, consisting of only 2 alleles, are indicated by the gene frequency changes following selection for bursa size, direct comparison of genotypes within families for monocyte phagocytosis, susceptibility to coccidiosis, outcome of Rous sarcomas, and immune responses to SRBC and Brucella abortus. Genotypes of the P alloantigen system were directly compared within families of fully pedigreed chicks with significant differences for monocyte phagocytosis. An experimental procedure for simultaneously testing for immune responses of genotypes of 9 of the alloantigen systems (A, B, C, D, E, H, I, L, and P) has been established by producing test progeny from a single cross of parent lines segregating for genes of each of the systems.