Fitting different visual models to behavioral patterns of parasitic egg rejection along a natural egg color gradient in a cavity-nesting host species.

Avian brood parasites lay their eggs in other birds' nests, and hosts can mitigate the fitness cost of raising unrelated offspring by rejecting parasitic eggs. A visually-based cognitive mechanism often thought to be used by hosts to discriminate the foreign egg is to compare it against the hosts' own eggshell by size, shape, maculation, and/or ground coloration (i.e.

Rearing a virulent common cuckoo is not extra costly for its only cavity-nesting host.

Virulent brood parasites refrain from arduous parental care, often kill host progeny and inflict rearing costs upon their hosts. Quantifying the magnitude of such costs across the whole period of care (from incubation through to parasite fledgling independence) is essential for understanding the selection pressures on hosts to evolve antiparasitic defences. Despite the central importance of such costs for our understanding of coevolutionary dynamics, they have not yet been comprehensively quantified in any host of any avian brood parasite.

First-Time Migration in Juvenile Common Cuckoos Documented by Satellite Tracking.

Being an obligate parasite, juvenile common cuckoos Cuculus canorus are thought to reach their African wintering grounds from Palearctic breeding grounds without guidance from experienced conspecifics but this has not been documented. We used satellite tracking to study naïve migrating common cuckoos. Juvenile cuckoos left breeding sites in Finland moving slowly and less consistently directed than adult cuckoos.

The common redstart as a suitable model to study cuckoo-host coevolution in a unique ecological context.

Background: Co-evolutionary arms-races result in spatio-temporally dynamic relationships between interacting species, e.g., brood parasites and their avian hosts.

Ancient origin and maternal inheritance of blue cuckoo eggs.

Maternal inheritance via the female-specific W chromosome was long ago proposed as a potential solution to the evolutionary enigma of co-existing host-specific races (or 'gentes') in avian brood parasites. Here we report the first unambiguous evidence for maternal inheritance of egg colouration in the brood-parasitic common cuckoo Cuculus canorus. Females laying blue eggs belong to an ancient (∼2.

A shared chemical basis of avian host-parasite egg colour mimicry.

Avian brood parasites lay their eggs in other birds' nests and impose considerable fitness costs on their hosts. Historically and scientifically, the best studied example of circumventing host defences is the mimicry of host eggshell colour by the common cuckoo (Cuculus canorus). Yet the chemical basis of eggshell colour similarity, which impacts hosts' tolerance towards parasitic eggs, remains unknown.

Alternative mechanisms of increased eggshell hardness of avian brood parasites relative to host species.

Obligate brood parasitic birds lay their eggs in nests of other species and parasite eggs typically have evolved greater structural strength relative to host eggs. Increased mechanical strength of the parasite eggshell is an adaptation that can interfere with puncture ejection behaviours of discriminating hosts. We investigated whether hardness of eggshells is related to differences between physical and chemical traits from three different races of the parasitic common cuckoo Cuculus canorus, and their respective hosts.

A host-race of the cuckoo Cuculus canorus with nestlings attuned to the parental alarm calls of the host species.

The common cuckoo has several host-specific races, each with a distinctive egg that tends to match its host's eggs. Here, we show that the host-race specializing on reed warblers also has a host-specific nestling adaptation. In playback experiments, the nestling cuckoos responded specifically to the reed warbler's distinctive 'churr' alarm (given when a predator is near the nest), by reducing begging calls (likely to betray their location) and by displaying their orange-red gape (a preparation for defence).

The timSL mutant affects a restricted portion of the Drosophila melanogaster circadian cycle.

The circadian rhythm genes period (per) and timeless (tim) are central to contemporary studies on Drosophila circadian rhythms. Mutations in these genes give rise to arrhythmic or period-altered phenotypes, and per and tim gene expression is under clock control. per and tim proteins (PER and TIM) also undergo circadian changes in level and phosphorylation state.

CYCLE is a second bHLH-PAS clock protein essential for circadian rhythmicity and transcription of Drosophila period and timeless.

We report the identification, characterization, and cloning of another novel Drosophila clock gene, cycle (cyc). Homozygous cyc flies are completely arrhythmic. Heterozygous cyc/+ flies are rhythmic but have altered periods, indicating that the cyc locus has a dosage effect on period.

The timSL mutant of the Drosophila rhythm gene timeless manifests allele-specific interactions with period gene mutants.

To identify new components of the Drosophila circadian clock, we screened chemically mutagenized flies for suppressors or enhancers of the long periods characteristic of the period (per) mutant allele perL. We isolated a novel mutant that maps to the rhythm gene timeless (tim). This novel allele, timSL, alters the temporal pattern of perL protein nuclear localization and restores temperature compensation to perL flies.

Dosage compensation of the period gene in Drosophila melanogaster.

The period (per) gene is located on the X chromosome of Drosophila melanogaster. Its expression influences biological clocks in this fruit fly, including the one that subserves circadian rhythms of locomotor activity. Like most X-linked genes in Drosophila, per is under the regulatory control of gene dosage compensation.

Phase shifting of the circadian clock by induction of the Drosophila period protein.

Virtually all organisms manifest circadian (24-hour) rhythms, governed by an ill-defined endogenous pacemaker or clock. Several lines of evidence suggest that the Drosophila melanogaster period gene product PER is a clock component. If PER were central to the time-keeping mechanism, a transient increase in its concentration would cause a stable shift in the phase of the clock.

The analysis of new short-period circadian rhythm mutants suggests features of D. melanogaster period gene function.

A number of new period gene (per) mutants were generated by in vitro mutagenesis and germ line transformation. Missense mutations were made at amino acid 589, which is altered in the 19 h short-period (per(s)) mutant, and insertion mutations were generated with peptides commonly used for epitope tagging. Most of these new per mutants had short behavioral rhythms.

Molecular transfer of a species-specific behavior from Drosophila simulans to Drosophila melanogaster.

Drosophila males modulate the interpulse intervals produced during their courtship songs. These song cycles, which are altered by mutations in the clock gene period, exhibit a species-specific variation that facilitates mating. We have used chimeric period gene constructs from Drosophila melanogaster and Drosophila simulans in germline transformation experiments to map the genetic control of their song rhythm difference to a small segment of the amino acid encoding information within this gene.

Mutational analysis of simian virus 40 small-t antigen.

Several point mutations in the simian virus 40 (SV40) small-t antigen have been analyzed for their effects on protein stability, transformation, transactivation, and binding of two cellular proteins. All mutations which affected cysteine residues in two cysteine clusters produced highly unstable small-t antigens. Four point mutations outside these clusters and one in-frame deletion mutant, dl890, produced stable proteins but reduced transformation efficiency.

Viral growth, origin binding, and p53 binding properties of simian virus 40 large T antigen transformation and replication mutants.

The viability, p53 binding, and SV40 origin binding of a series of SV40 large T antigen point mutants, which map to the amino terminal one-third of the molecule, were examined. Two mutants which yield small plaques were found to have altered kinetics of replication upon infection of permissive cells. Mutants which did not bind to the origin of replication were not able to replicate, but the reverse was not always true.

Replication and transformation functions of in vitro-generated simian virus 40 large T antigen mutants.

We used sodium bisulfite mutagenesis to introduce point mutations within the early region of the simian virus 40 genome. Seventeen mutants which contained amino acid changes in the amino-terminal half of the large T antigen coding sequence were assayed for their ability to replicate viral DNA and to induce transformation in the established rodent cell line Rat-3. The mutants fell into four basic classes with respect to these two biological functions.