Recent advances in technology and in the ability to acquire, store, and analyze complex biological data sets have provided an unprecedented understanding of the mechanisms regulating living organisms' development and responses to the environment. We are gaining the insights required for rational modification of these organisms toward specific purposes. Microarrays provide an early example of the productive integration of high-throughput technologies with biological inquiry. In this article we discuss the development of this popular platform and its application in crop science and agriculture.

Pest risk maps are powerful visual communication tools to describe where invasive alien species might arrive, establish, spread, or cause harmful impacts. These maps inform strategic and tactical pest management decisions, such as potential restrictions on international trade or the design of pest surveys and domestic quarantines. Diverse methods are available to create pest risk maps, and can potentially yield different depictions of risk for the same species. Inherent uncertainties about the biology of the invader, future climate conditions, and species interactions further complicate map interpretation. If multiple maps are available, risk managers must choose how to incorporate the various representations of risk into their decisionmaking process, and may make significant errors if they misunderstand what each map portrays. This article describes the need for pest risk maps, compares pest risk mapping methods, and recommends future research to improve such important decision-support tools.

Some aspects of habitat seem to enhance the spread of disease whereas others inhibit it. Here, we illustrate and identify mechanisms that connect habitat to epidemiology using a case study of disease in plankton. We see a pronounced relationship between the basin shapes of lakes and fungal (Metschnikowia bicuspidata) disease in the Zooplankton grazer Daphnia dentifera. As we work through seven mechanisms that could explain why Daphnia in some lakes are sicker, we can eliminate some hypotheses (i.e., those relating an index of lake productivity to disease through host density, links between resource quality and transmission rate, and variation in host susceptibility) and find support for others involving food-web actors (e.g., selective predation on infected hosts by fishes, “sloppy predation” by an invertebrate, a possible dilution effect in V-shaped lakes). Furthermore, we identify physical mechanisms (gravity currents, turbulence) that could lead to greater transport of fungal spores to habitat occupied by Daphnia hosts in U-shaped lakes. These results highlight how habitat structure, through its effects on food-web structure and physical processes, can shape wildlife disease.

Charles Darwin, who was married to his first cousin, Emma Wedgwood, was one of the first experimentalists to demonstrate the adverse effects of inbreeding and to question the consequences of consanguineous mating. He documented the phenomenon of inbreeding depression for numerous plant species, and this caused him to worry about the health of his own children, who were often ill. To determine whether Darwin's fears were justified, we constructed a pedigree of the Darwin/Wedgwood dynasty from the large quantity of genealogical information published on these families. The inbreeding coefficients (F) computed from the pedigree show that Darwin's children were subject to a moderate level of inbreeding (F = 0.0630), and the progeny of related families had still higher inbreeding values (e.g., F = 0.1255 for the progeny of Henry Wedgwood, Emma Wedgwood's brother). The analysis of a sample of 25 Darwin/Wedgwood families belonging to four consecutive generations shows a statistically significant positive association between child mortality (death at or before the age of 10 years) and inbreeding coefficient detected by means of nonparametric tests (τ = 0.309, P = 0.040). Our findings suggest that the high childhood mortality experienced by the Darwin progeny (3 of his 10 children died at age 10 or younger) might be a result of increased homozygosity of deleterious recessive alleles produced by the consanguineous marriages within the Darwin/Wedgwood dynasty.

Hybridization in the wild between closely related species is not unusual. In some cases, hybridization may prove beneficial for a rare taxon. Under certain conditions, however, a rare taxon can be driven rapidly to extinction by hybridizing with a more common taxon. This problem is urgent because human activities are increasingly bringing together cross-compatible species that were previously geographically isolated. US conservation policy has yet to address how to deal with hybrid-derived individuals whose ancestry includes an endangered species. Developing sound science-based conservation policy that addresses hybridization requires cross-disciplinary social-science and life-science research to address the following two questions: (1) How do human decisions with regard to species protection, trade, transportation, land use, and other factors affect the opportunities for, and rates of hybridization between, rare species and more common relatives? and (2) How do the positive or negative perceived values regarding hybrids and hybrid-derived individuals compare with values regarding their nonhybridized counterparts from social, cultural, economic, and environmental perspectives? In this article we explore the ways to inform such policy using a multidisciplinary approach.