A time to die

A theory of dying is proposed. The evidence and arguments are presented which suggest that the lifespan of mammals is regulated by a biological clock which, in turn acts on the endocrines to produce failure of two specific target tissues, the immune and circulatory systems. Failure of these two systems can account for the similarity among mammals of the final diseases recorded at autopsy. A newly described pituitary factor is used as an example of a possible endocrine mechanism by which the body might control its own demise.     

Adhesion-mediated mechanosensitivity: a time to experiment, and a time to theorize

Adhesion-mediated signaling provides cells with information about multiple parameters of their microenvironment, including mechanical characteristics. Often, such signaling is based on a unique feature of adhesion structures: their ability to grow and strengthen when force is applied to them, either from within the cell or from the outside. Such adhesion reinforcement is characteristic of integrin-mediated cell-matrix adhesions, but may also operate in other types of adhesion structures. Though the amount of knowledge about adhesion-mediated signaling is growing rapidly, the mechanisms underlying force-dependent regulation of junction assembly are largely unknown. Experiments have been carried out that have started to uncover the major signaling pathways involved in the response of adhesion sites to force. Theoretical models have also been used to address the physical mechanisms underlying adhesion-mediated mechanosensing.     

Population structure attributable to reproductive time: isolation by time and adaptation by time

Many populations are composed of a mixture of individuals that reproduce at different times, and these times are often heritable. Under these conditions, gene flow should be limited between early and late reproducers, even within populations having a unimodal temporal distribution of reproductive activity. This temporal restriction on gene flow might be called "isolation by time" (IBT) to acknowledge its analogy with isolation by distance (IBD). IBD and IBT are not exactly equivalent, however, owing to differences between dispersal in space and dispersal in time. We review empirical studies of natural populations that provide evidence for IBT based on heritabilities of reproductive time and on molecular genetic differences associated with reproductive time. When IBT is present, variation in selection through the reproductive season may lead to adaptive temporal variation in phenotypic traits [adaptation by time (ABT)]. We introduce a novel theoretical model that shows how ABT increases as (i) selection on the trait increases; (ii) environmental influences on reproductive time decrease; (iii) the heritability of reproductive time increases; and (iv) the temporal distribution of reproductive activity becomes increasingly uniform. We then review empirical studies of natural populations that provide evidence for ABT by documenting adaptive temporal clines in phenotypic traits. The best evidence for IBT and ABT currently comes from salmonid fishes and flowering plants, but we expect that future work will show these processes are more widespread.     

It's time to flower: the genetic control of flowering time

In plants, successful sexual reproduction and the ensuing development of seeds and fruits depend on flowering at the right time. This involves coordinating flowering with the appropriate season and with the developmental history of the plant. Genetic and molecular analysis in the small cruciform weed, Arabidopsis, has revealed distinct but linked pathways that are responsible for detecting the major seasonal cues of day length and cold temperature, as well as other local environmental and internal signals. The balance of signals from these pathways is integrated by a common set of genes to determine when flowering occurs. Excitingly, it has been discovered that many of these same genes regulate flowering in other plants, such as rice. This review focuses on recent advances in how three of the signalling pathways (the day-length, vernalisation and autonomous pathways) function to control flowering.     

Optimal time to emerge from refuge

Factors affecting emergence by prey that enter refuges when approached by predators have been studied intensively, but only two theoretical models predict how long prey should remain in a refuge before emerging. We argue that prey can make better decisions than allowed by one model; the other model describes cases in which predators wait for prey to emerge. We present optimality models that permit prey to select a time to emerge that maximizes fitness. When in a refuge, a prey cannot obtain benefits outside; emerging too soon can be catastrophic, but delaying emergence entails loss of fitness. If predators resume foraging quickly rather than engaging in strategic waiting games, current theory suggests that prey emerge when the costs of remaining in a refuge and of emerging are equal. However, prey often can do better by emerging at the time maximizing fitness rather than when benefits equal costs (i.e. when prey break even). Optimal emergence time depends on initial fitness, benefits lost by remaining in refuge, and the decay rate of predation risk. Benefits lost if a prey is killed are modelled separately from benefits that contribute to lifetime fitness, even if the prey is killed (individual reproduction, altruism). Fitness of prey emerging at the optimal emergence time may be greater than, equal to or less than initial fitness. Break-even and optimality models base predictions on the opposing effects of risk and loss of benefits. Thus, many empirically verified predictions are identical at the ordinal level although differing quantitatively. Optimality models provide novel testable predictions for the effects of initial fitness, benefits, and, for ectotherms, the rate of cooling in refuge. They predict earlier emergence for equal retainable benefits than for those lost upon death.  © 2007 The Linnean Society of London, Biological Journal of the Linnean Society , 2007, 91 , 375–382.