Does observed fertility maximize fitness among New Mexican men?

Our objective is to test an optimality model of human fertility that specifies the behavioral requirements for fitness maximization in order (a) to determine whether current behavior does maximize fitness and, if not, (b) to use the specific nature of the behavioral deviations from fitness maximization towards the development of models of evolved proximate mechanisms that may have maximized fitness in the past but lead to deviations under present conditions. To test the model we use data from a representative sample of 7,107 men living in Albuquerque, New Mexico, between 1990 and 1993. The model we test proposes that low fertility in modern settings maximizes number of grandchildren as a result of a trade-off between parental fertility and next generation fertility. Results do not show the optimization, although the data do reveal a trade-off between parental fertility and offspring education and income. We propose that two characteristics of modern economies have led to a period of sustained fertility reduction and to a corresponding lack of association between income and fertility. The first is the direct link between costs of investment and wage rates due to the forces of supply and demand for labor in competitive economies. The second is the increasing emphasis on cumulative knowledge, skills, and technologies in the production of resources. Together they produce historically novel conditions. These two features of modern economies may interact with evolved psychological and physiological mechanisms governing fertility and parental investment to produce behavior that maximizes the economic productivity of lineages at the expense of fitness. If cognitive processes evolved to track diminishing returns to parental investment and if physiological processes evolved to regulate fertility in response to nutritional state and patterns of breast feeding, we might expect non-adaptive responses when returns from parental investment do not diminish until extremely high levels are reached. With high economic payoffs from parental investment, people have begun to exercise cognitive regulation of fertility through contraception and family planning practices. Those cognitive processes maynot have evolved to handle fitness trade-offs between fertility and parental investment. A preliminary presentation of this data was published in R. I. M. Dunbar, ed.,Human Reproduction Decisions: Biological and Social Perspectives. New York: St. Martin’s Press, 1995. Support for the research project, “Male Fertility and Parenting in New Mexico,” began with two seed grants from the University of New Mexico’s Biomedical Research Grants Program, 1988 and 1989, and one from the University of New Mexico Research Allocations Committee, 1988. Further seed money as well as interim funding came from the William T. Grant Foundation (#89130589 and #91130501). The major support for the project came from the National Science Foundation from 1990 to 1993 (#BNS-9011723 and #DBS-911552). Both National Science Foundation grants included Research Experience for Undergraduates supplements. Hillard S. Kaplan is an Associate Professor of Anthropology at the University of New Mexico. His earlier research and publications focused on food sharing, time allocation, parental investment, and reproductive strategies among Ache hunter-gatherers in Paraguay, Machiguenga and Piro forager-horticulturalists in Peru, and villagers of several ethnicities in Botswana. New research and theory concern fertility, parental investment, and mating strategies in developed and developing nations. This research formulates a new theory of reproductive decision-making and the demographic transition, integrating human capital and parental investment theory in a synthesis of economic and evolutionary approaches. Jane B. Lancaster is a Professor of Anthropology at the University of New Mexico. Her research and publications are on human reproductive biology and behavior, especially human parental investment; women’s reproductive biology of pregnancy, lactation, and child-spacing; and male fertility and investment in children. Current research with Hillard S. Kaplan is on male life history strategies among a large sample of men in New Mexico. She has coedited three books on human parental investment:School-Age Pregnancy and Parenthood (with B. Hamburg),Parenting across the Life Span (with J. Altmann, A. Rossi, and L. Sherrod), andOffspring Abuse and Neglect (with R. Gelles). She is scientific editor of a quarterly journal,Human Nature: An Interdisciplinary, Biosocial Perspective published by Aldine de Gruyter. She is also a council member of the newly formed Human Behavior and Evolution Society. John A. Bock is Andrew W. Mellon Post-Doctoral Fellow in Epidemiology and Population Health at the National Centre for Epidemiology and Population Health, The Australian National University. His research focuses on the allocation of parental investment and the determinants of children’s activities, integrating aspects of economic and evolutionary theory. He has ongoing field research with Bantu and Bushmen agro-pastoralists and forager-horticulturalists in the Okavango Delta, Botswana. He is also collaborating with Lancaster and Kaplan on the determinants of progeny distribution and homosexuality among New Mexican men. Sara E. Johnson is a Ph.D. candidate at the University of New Mexico. Her major research trajectory focuses on trade-offs in life history characters. Her research experience includes participation in a study of variation in growth and development among children in a multi-ethnic community in the Okavango Delta, Botswana, in addition to her dissertation work on individual variation in growth and mortality among juvenile baboons. She is collaborating with Lancaster and Kaplan on the association between survival and fertility among Albuquerque men.     

BIOCHEMICAL HETEROZYGOSITY AND MORPHOLOGIC VARIATION IN A COLONY OF PAPIO HAMADRYAS HAMADRYAS BABOONS

This analysis examines the association between genetic heterozygosity and individual morphologic variation in a captive population of Papio hamadryas hamadryas consisting of 403 juveniles and adults. The population structure of the colony was artificially generated and maintained and is thus rigorously defined. Subpopulations delimited by age, sex, and degree of inbreeding are also explored. Heterozygosity, as enumerated from six simple Mendelian biochemical loci, is compared with the residual morphologic variation of each individual for each of 20 quantitative traits. Use of a sequential Bonferroni technique nullifies all significant correlations. Principal-components analysis reduces the morphometrics to a single or few significant axes in each population. The first axis of the total population contains 86.07% of the variation in the sample and the absolute values of the factor scores exhibit a significant positive correlation with heterozygosity at P < 0.05. Correcting for age- and sex-related variation in the total population with a linear model subsequently demonstrates that no significant correlation between heterozygosity and morphologic variation exists. No significant relationship is found in the inbred animals or subpopulations when age and sex are controlled. Previous studies have indicated that individuals proximal to the population mean for a specific polygenic trait exhibit a higher biochemical heterozygosity than individuals distant from the mean. The results presented here, which are based on more loci than many studies and a well-defined population, do not support this relationship. Substructuring of a population by age and sex can lead to spurious correlations with univariate or multivariate techniques. Comprehensive indices of genetic variation and rigorous statistical techniques should be used in future analyses. Studies that fail to recognize these design elements should be interpreted with caution.     

Sheep Linkage Mapping: Nineteen Linkage Groups Derived from the Analysis of Paternal Half-Sib Families

Nineteen linkage groups containing a total of 52 markers have been identified in the sheep genome after typing large paternal half-sib families. The linkage groups range in size from 2 markers showing no recombination to a group containing 6 markers covering approximately 30 cM of the sheep genome. Thirteen of the groups have been assigned to a sheep chromosome. Three groups contain markers from bovine syntenic groups U2, U7 and U29, and one other group contains a marker that has been mapped only in humans. The remaining three groups are unassigned. This information will provide a useful foundation for a genetic linkage map of sheep.     

Phytochrome-mediated effects on extracellular peroxidase activity, lignin content and bending resistance in etiolated Vicia faba epicotyls

Etiolated Vicia faba seedlings were exposed to continuous red light to investigate whether changes in extracellular peroxidase activity were correlated in time and localization with changes in extension growth and/or lignin content in the subapical region of the epicotyl. Continuous red light: (a) increased extracellular peroxidase activity after a lag of ca 0.5 h, followed by a maximum peak after 2.5 h due to slightly acidic isoforms (pI = 6–6.5, according to isoelectrofocusing gels), a minimum after 4 h and a second maximum after 8 h due to acidic isoforms (pI=4–5), (b) increased lignin content and epicotyl resistance to bending after a lag of ca 4 h, i.e. simultaneously with changes in acidic extracellular peroxidase activity, and (c) reduced extension growth to a stable rate after a lag of ca 1 h, not coinciding with the kinetics of any of the extracellular peroxidase isoforms. These effects of continuous red light were at least partially mediated by phytochrome. Tissue printing and anatomical studies revealed red light effects on extracellular peroxidase activity and lignin content mainly in the outer cortical parenchyma. The results are consistent with the involvement of phyto-chrome-mediated effects on extracellular peroxidases (acidic isoforms) in the transduction chain leading to lignin responses to red light.     

The making of the minibody: An engineered β-protein for the display of conformationally constrained peptides

Conformationally constraining selectable peptides onto a suitable scaffold that enables their conformation to be predicted or readily determined by experimental techniques would considerably boost drug discovery process by reducing the gap between the discovery of a peptide lead and the design of a peptidomimetic with a more desirable pharmacological profile. With this in mind, we designed the minibody, a 61-residue β-protein aimed at retaining some desirable features of immunogloblin variable domains, such as tolerance to sequence variability in selected regions of the protein and predictability of main chain conformation of the same regions, based on the ‘canonical structures’ model. To test the ability of the minibody scaffold to support functional sites we also designed a metal binding version of the protein by suitably choosing the sequences of its loops. The minibody was produced both by chemical syntyhesis and expression in E. coli and charactgerized by size exclusion chromatography, UV CD (circular dichroism) spectroscopy and metal binding activity. All our data supported the model, but a more detailed structural characterization of the molecule was impaired by its low soubility. We were able to overcome this problem both by further; mutagenesis of the framework and by addition of a solublizing motif. The minibody is being used to select constrained human IL-6 peptidic ligands from a library displayed on the surface of the f1 bacteriophage.     

5,7-Diphenyl-3-ureidohexahydroazepin-2-ones as Cholecystokinin-B receptor ligands

A series of 5,7-diphenyl-3-ureidohexahydroazepin-2-one cholecystokinin-B (CCK-B) receptor antagonists was synthesized using Beckmann ring expansion of a suitable 2,4-diphenylcyclohexanone as a key step. SAR studies revealed the importance of the 5-aryl group for high and selective CCK-B receptor affinity, as illustrated in compound (−)-10i (CCK-B IC₅₀ = 6.8 nM).     

The molecular genetics of Alzheimer's disease

The major pathological characteristic of Alzheimer's disease (AD) is the abnormal deposition of β-amyloid peptide (Aβ) in the brain. In some early onset cases, the disease develops because of mutations in the gene coding for β-amyloid precursor protein (βAPP). However, the majority of AD families in the early onset subgroup are linked to a locus on chromosome 14. The genetic analysis and age of onset correlates of both the βAPP gene and the chromosome 14 locus are discussed. We speculate on the mechanisms by which the βAPP mutations cause the disease and discuss recent advances in βAPP processing that may be relevant to the pathogenesis of the late-onset (common) form of the disease. In addition, we review the association of theAPOE locus with late-onset familial and nonfamilial disease. Further work is required to establish the effects of this locus on disease occurrence, age of onset, and progression. The molecular pathology of ApoE in relation to AD development and the identification of the chromosome 14 gene will greatly contribute to a general pathogenic model of AD, and will clarify the role of βAPP and its derivatives.     

Identification and characterization of a chlorate-resistant mutant of Arabidopsis thaliana with mutations in both nitrate reductase structural genes NIA1 and NIA2

Mutant plants defective in the assimilation of nitrate can be selected by their resistance to the herbicide chlorate. In Arabidopsis thaliana, mutations at any one of nine distinct loci confer chlorate resistance. Only one of the CHL genes, CHL3, has been shown genetically to be a nitrate reductase (NR) structural gene (NIA2) even though two NR genes (NIA1 and NIA2) have been cloned from the Arabidopsis genome. Plants in which the NIA2 gene has been deleted retain only 10% of the wildtype shoot NR activity and grow normally with nitrate as the sole nitrogen source. Using mutagenized seeds from the NIA2 deletion mutant and a modified chlorate selection protocol, we have identified the first mutation in the NIA1 NR structural gene. nia1, nia2 double mutants have only 0.5% of wild-type shoot NR activity and display very poor growth on media with nitrate as the only form of nitrogen. The nial-1 mutation is a single nucleotide substitution that converts an alanine to a threonine in a highly conserved region of the molybdenum cofactor-binding domain of the NR protein. These results show that the NIA1 gene encodes a functional NR protein that contributes to the assimilation of nitrate in Arabidopsis.     

Replication of the promiscuous plasmid pLSI: a region encompassing the minus origin of replication is associated with stable plasmid inheritance

Deletion of a region of the promiscuous plasmid pLS1 encompassing the initiation signals for the synthesis of the plasmid lagging strand led to plasmid instability in Streptococcus pneumoniae and Bacillus subtilis. This defect could not be alleviated by increasing the number of copies (measured as double-stranded plasmid DNA) to levels similar to those of the wild-type plasmid pLS1. Our results indicate that in the vicinity of, or associated with the single-stranded origin region of pLS1 there is a plasmid component involved in its stable inheritance. Homology was found between the DNA gyrase binding site within the par region of plasmid pSC101 and the pLS1 specific recombination site RS_R.