Project description:BackgroundThe main aim of the study was to analyse the influence of fleshy fruits (plums) on the post-metamorphic growth and feeding behaviour of the green toad Bufotes viridis. We tested the following two hypotheses: (1) juveniles of the green toad are characterised by faster growth in conditions involving fallen plums Prunus cerasifera due to the associated presence of more varied food such as invertebrates; (2) green toads exhibit more active feeding behaviour in the presence of fleshy fruits.MethodsA total of 120 fresh metamorphs of the green toad were randomly assigned to one of four groups: two experimental groups with fleshy plums and two other groups as controls (without fruits). Each group was kept in an enclosure to which wild invertebrates had free access. Each individual toad was measured for snout-vent length (mm) and body mass (g) every other day for 30 days. In order to determine whether fallen plums influence the feeding behaviour of toads, the number of active and hidden (under an artificial shelter) individuals was also noted.ResultsThe results showed that green toads from both enclosures with plums were characterised by more rapid growth than individuals from the control treatments. Simultaneously, in the enclosure with fleshy fruits, greater species richness of wild invertebrates was observed. No differences in active feeding behaviour were noted between control groups and groups with plums.DiscussionFleshy fruits, upon falling, attract many types of invertebrates; thus they may represent good dietary supplements for fresh amphibian metamorphs. Therefore, the presence of fruit trees close to a breeding site might influences the post-metamorphic growth of amphibians, but not their feeding behaviour. The presence of insects associated with fallen fruit seems to favour the occurrence of amphibian populations, which is particularly important, since, due to political and social pressure, numbers of fruit trees are currently being reduced. To our knowledge, no previous study has investigated the potential influence of the presence of fruit trees on the growth and behaviour of anurans.

Project description:Intracellular Ca2+ release through the Inositol 1,4,5-Triphosphate Receptor (InsP3R) is a feature of all multicellular organisms in which it shapes the temporal and spatial aspects of calcium signaling in cells, affecting several developmental and physiological processes. Mutants in the InsP3R gene of Drosophila (itpr) exhibit a range of defects which include growth defects and larval lethality.The Drosophila Insulin-like peptides (ILPs) are encoded by multigene families that are expressed in the brain and other tissues. Upon secretion, these peptides likely serve as hormones, neurotransmitters, and growth factors. In Drosophila melanogaster, molecular genetic studies have revealed Drosophila ILPs as elements of a conserved insulin signaling pathway, and as in other animal models, it appears to play a key role in metabolism, growth, reproduction, and aging. Previous work from our group has shown that InsP3R function can be rescued by ectopically expressing InsP3R in dilp cells or can be compensated by altering the activity of Sarco-Endoplasmic Reticulum Calcium-ATPase (SERCA). To understand the molecular basis of larval lethality and growth defect in Drosophila InsP3R mutants and to decipher possible cross talk of itpr gene with other signaling pathways we have carried out genome wide microarray experiments. We have compared the transcript profiles of i) itpr mutant larvae and wild type larvae, ii) dilp rescue larvae with itpr mutant larvae iii) itpr and SERCA double mutant larvae with itpr mutant larvae. By this we have identified genes whose levels are altered in itpr mutants and are restored towards wild type in dilp rescue larvae with itpr mutant larvae and itpr and SERCA double mutants. Our experiments help in identify genes that are regulated by changes in intracellular Ca2+ in the context of larval viability may contribute to the better understanding of the major human pathologies caused by calcium misbalance or by dysregulation of the insulin/IGF pathway. The 8x60k array AMADID: 27326 slide was scanned immediately by PerkinElmer Scan array Gx Microarray scanner. The Scan array software (PerkinElmer) was used for grid wise normalization of array images. Three were used with Mutant, three for Dilp Rescue and two for Kum Rescue experiments . The data was analysed by GeneSpring GX Agilent . The differential expression was considered if the Log 2 mean of at least -1 for the down regulated genes and +1 for the upregulated genes. We considered only the genes that were reproducible from biological triplicates for Mutant, biological treplicates for Dilp Rescue and biological duplicates for Kum Rescue.

Project description:Intracellular Ca2+ release through the Inositol 1,4,5-Triphosphate Receptor (InsP3R) is a feature of all multicellular organisms in which it shapes the temporal and spatial aspects of calcium signaling in cells, affecting several developmental and physiological processes. Mutants in the InsP3R gene of Drosophila (itpr) exhibit a range of defects which include growth defects and larval lethality.The Drosophila Insulin-like peptides (ILPs) are encoded by multigene families that are expressed in the brain and other tissues. Upon secretion, these peptides likely serve as hormones, neurotransmitters, and growth factors. In Drosophila melanogaster, molecular genetic studies have revealed Drosophila ILPs as elements of a conserved insulin signaling pathway, and as in other animal models, it appears to play a key role in metabolism, growth, reproduction, and aging. Previous work from our group has shown that InsP3R function can be rescued by ectopically expressing InsP3R in dilp cells or can be compensated by altering the activity of Sarco-Endoplasmic Reticulum Calcium-ATPase (SERCA). To understand the molecular basis of larval lethality and growth defect in Drosophila InsP3R mutants and to decipher possible cross talk of itpr gene with other signaling pathways we have carried out genome wide microarray experiments. We have compared the transcript profiles of i) itpr mutant larvae and wild type larvae, ii) dilp rescue larvae with itpr mutant larvae iii) itpr and SERCA double mutant larvae with itpr mutant larvae. By this we have identified genes whose levels are altered in itpr mutants and are restored towards wild type in dilp rescue larvae with itpr mutant larvae and itpr and SERCA double mutants. Our experiments help in identify genes that are regulated by changes in intracellular Ca2+ in the context of larval viability may contribute to the better understanding of the major human pathologies caused by calcium misbalance or by dysregulation of the insulin/IGF pathway.

Dataset Information

Population admixture and high larval viability among urban toads.

Publications

Population admixture and high larval viability among urban toads.

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