Showing papers by "Jean Clobert published in 2001"

Does clutch size evolve in response to parasites and immunocompetence

Abstract: Parasites have been argued to influence clutch size evolution, but past work and theory has largely focused on within-species optimization solutions rather than clearly addressing among-species variation. The effects of parasites on clutch size variation among species can be complex, however, because different parasites can induce age-specific differences in mortality that can cause clutch size to evolve in different directions. We provide a conceptual argument that differences in immunocompetence among species should integrate differences in overall levels of parasite-induced mortality to which a species is exposed. We test this assumption and show that mortality caused by parasites is positively correlated with immunocompetence measured by cell-mediated measures. Under life history theory, clutch size should increase with increased adult mortality and decrease with increased juvenile mortality. Using immunocompetence as a general assay of parasite-induced mortality, we tested these predictions by using data for 25 species. We found that clutch size increased strongly with adult immunocompetence. In contrast, clutch size decreased weakly with increased juvenile immunocompetence. But, immunocompetence of juveniles may be constrained by selection on adults, and, when we controlled for adult immunocompetence, clutch size decreased with juvenile immunocompetence. Thus, immunocompetence seems to reflect evolutionary differences in parasite virulence experienced by species, and differences in age-specific parasite virulence appears to exert opposite selection on clutch size evolution.

Perspectives on the Study of Dispersal Evolution

Abstract: In this chapter, we stress the gaps in our knowledge about dispersal evolution and suggest several promising research directions. (i) Both empirical and theoretical studies illustrate how different causes may result in the evolution of dispersal behaviour. Integrative approaches that study the interactions between these causes are, however, rare. Theoretical expectations must be clarified by a careful comparison with existing models and their specific assumptions. The importance and evolutionary significance of plasticity for dispersal has also been largely neglected. (ii) The evolution of dispersal cannot be understood simply as a change in a single trait. Changes in dispersal rate alter the demographic functioning of populations and their genetic structure, which, in turn, modify the selective pressures on dispersal. Theoretical studies incorporating both types of feed-back are rare, and empirical investigations of such interactions almost absent. Similarly, selective interactions between the evolution of dispersal and life histories are yet largely unexplored. (iii) Knowledge about the determinism and ontogeny of dispersal behaviour is likely to alter predictions concerning its evolution. This includes information ranging from the genetic determinism of dispersal, the effects of hormones on physiology and behaviour, and maternal effects, to the particular environmental cues used by individuals to asses habitat quality. (iv) Experimental evolution should provide information about the relative importance of different causes of the evolution of dispersal, the interaction between demography and the evolution of dispersal, and the joint evolution of other traits. These experiments may also indicate, from comparison of lines before and after selection, which are the genes and/or physiological mechanisms involved in dispersal behaviour.

The contribution of phenotypic plasticity to adaptation in lacerta vivipara

Abstract: Correlation between intraspecific phenotypic variability and variation of environmental conditions could reflect adaptation. Different phenotypes may result from differential expression of a genotype in different environments (phenotypic plasticity) or from expression of different genotypes (genetic diversity). Populations of Lacerta vivipara exhibit larger adult body length, lower age at maturity, higher fecundity, and smaller neonatal size in humid habitats compared to dry habitats. We conducted reciprocal transplants of juvenile L. vivipara to test for the genetic or plastic origin of this variation. We captured gravid females from four populations that differed in the relative humidity of their habitats, and during the last 2 to 4 weeks of gestation, we manipulated heat and water availability under laboratory conditions. Juveniles were released into the different populations and families were divided to compare growth rate and survival of half-sibs in two environments. Growth rate and survival were assessed using capture-recapture techniques. Growth rate was plastic in response to postnatal conditions and did not differ between populations of origin. Survival differed between populations of origin, partially because of differences in neonatal body length. The response of juvenile body length and body condition to selection in the different habitats was affected by the population of origin. This result cannot be simply interpreted in terms of adaptation; however, phenotypic plasticity of fecundity or juvenile size most probably resulted in adaptive reproductive strategies. Adaptation to the habitat by means of genetic specialization was not detected. Further investigation is needed to discriminate between genetic and long-term maternal effects.

Diagnosing the environmental causes of the decline in Grey Partridge Perdix perdix survival in France

Abstract: We studied Grey Partridge Perdix perdix mortality during breeding to identify the environmental causes of a long-term decline in adult survival. We radiotagged and monitored daily from mid-March to mid-September 1009 females on ten contrasting study sites in 1995-97. Simultaneously, we recorded habitat features and estimated the abundance of Hen and Marsh Harriers Circus cyaneus and C. aeruginosus, Red Fox Vulpes vulpes and mustelids. We experimentally tested whether scavenging could have biased predation rates. We also examined, through the necropsy of 80 carcasses of Grey Partridge, whether disease, parasites or poisoning could have been ultimate causes of high predation rates. The survival rate of radiotagged females during spring and summer ranged from 0.25 to 0.65 across study areas. Mortality peaked in May, June and July when females were laying and incubating. The direct negative impact of farming practices was low (6%). Predation was the main proximate cause of female mortality during breeding (73%) and determined the survival rate, suggesting no compensation by other causes of mortality. Ground carnivores were responsible for 64% of predation cases, and raptors for 29%, but this proportion varied across study sites. Disease and poisoning did not appear to favour predation, and scavenging was not likely to have substantially overestimated predation rates. The predation rate on breeding females was positively correlated with the abundance of Hen and Marsh Harriers, suggesting an additional mortality in areas where harriers were abundant. The proportion of raptor predation was linearly related to harrier abundance. The predation rate was not correlated with the abundance of the Red Fox and mustelids. A potential density-dependent effect on the predation rate was confounded by the abundance of harriers. We found no convincing relationship between the predation rate and habitat features, but we observed a positive relationship between the abundance of Hen and Marsh Harriers and the mean field size. This suggested that habitat characteristics may contribute to high predation rates through predator abundance or habitat-dependent predation.