Climate change in our backyards: the reshuffling of North America's winter bird communities

Much of the recent changes in North American climate have occurred during the winter months, and as result, overwintering birds represent important sentinels of anthropogenic climate change. While there is mounting evidence that bird populations are responding to a warming climate (e.g., poleward shifts) questions remain as to whether these species‐specific responses are resulting in community‐wide changes. Here, we test the hypothesis that a changing winter climate should favor the formation of winter bird communities dominated by warm‐adapted species. To do this, we quantified changes in community composition using a functional index – the Community Temperature Index (CTI) – which measures the balance between low‐ and high‐temperature dwelling species in a community. Using data from Project FeederWatch, an international citizen science program, we quantified spatiotemporal changes in winter bird communities (n = 38 bird species) across eastern North America and tested the influence of changes in winter minimum temperature over a 22‐year period. We implemented a jackknife analysis to identify those species most influential in driving changes at the community level and the population dynamics (e.g., extinction or colonization) responsible for these community changes. Since 1990, we found that the winter bird community structure has changed with communities increasingly composed of warm‐adapted species. This reshuffling of winter bird communities was strongest in southerly latitudes and driven primarily by local increases in abundance and regional patterns of colonization by southerly birds. CTI tracked patterns of changing winter temperature at different temporal scales ranging from 1 to 35 years. We conclude that a shifting winter climate has provided an opportunity for smaller, southerly distributed species to colonize new regions and promote the formation of unique winter bird assemblages throughout eastern North America.     

The life-cycle of the asexual ostracod Darwinula stevensoni (Brady & Robertson, 1870) (Crustacea,Ostracoda) in a temporate pond

The life-cycle of the ancient asexual ostracod Darwinula stevensoni was studied during 1 year in a eutrophic pond in Belgium. The reproductive period of this species started in March and was effectively completed by September of the same year. All changes in population structure took place during the spring and summer months and a rapid turnover of the instars was observed. The life-cycle of Darwinula stevensoni appears to take one year or less in Belgium and this is considerably shorter than the 4 years which had been reported previously from subarctic populations. The difference to the present study is most likely temperature-related. Maximal densities of D. stevensoni were observed in June and July and attained 10⁵ ind. m^–2. During winter, densities were lower with a mean of 10⁴ ind. m^–2. Consequently, the calculated population size of each month was high throughout the year. Together with the low mutation rate, such a large population size could effectively counteract the stochastic loss of mutation-free genotypes as predicted by Muller's ratchet. D. stevensoni is a brooder; the maximum number of embryos and juvenile instars (up to third stage) found within a single female was 11.     

Using DNA barcoding to differentiate invasive Dreissena?species (Mollusca,Bivalvia)

The zebra mussel (Dreissena polymorpha) and the quagga mussel (Dreissena rostriformis bugensis) are considered as the most competitive invaders in freshwaters of Europe and North America. Although shell characteristics exist to differentiate both species, phenotypic plasticity in the genus Dreissena does not always allow a clear identification. Therefore, the need to find an accurate identification method is essential. DNA barcoding has been proven to be an adequate procedure to discriminate species. The cytochrome c oxidase subunit I mitochondrial gene (COI) is considered as the standard barcode for animals. We tested the use of this gene as an efficient DNA barcode and found that it allow rapid and accurate identification of adult Dreissena individuals.     

Genetic studies of the leptin receptor gene in morbidly obese French Caucasian families

Family studies have shown that in some populations up to 75% of the variation of body mass index can be explained by genetic factors. However, in humans, no major obesity gene has been identified to date. In contrast, there are a number of genetically well defined animal models for obesity. In two of those models (ob/ob and db/db), defects in the same pathway are responsible for obesity. Recently, some evidence has been found for the OB gene also being involved in human obesity. In this study we investigated the potential role of the OB receptor (OBR) in the etiology of massive obesity in humans using familial linkage analyses and case-control association studies. The typing of two microsatellite markers (D1S198 and D1S209), flanking the OBR gene, in 256 sib pairs showed no evidence for linkage with obesity. In order to be able to detect small gene effects, association studies with a 3′-UTR insertion/deletion polymorphism were carried out. The results of these analyses remained non-significant (χ² = 3.442, P = 0.18). However, subjects heterozygous for the insertion/deletion polymorphism showed a slight trend towards lower insulin values 30 min after an oral glucose load compared to homozygous individuals (P = 0.02). In summary, our results do not support a major role of the human OBR gene in the development of morbid obesity in our population. Received: 4 December 1996 / Accepted: 25 June 1997     

Structural and functional characterization of the N-terminal acetyltransferase Naa50

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Cell cycle regulation of Greatwall kinase nuclear localization facilitates mitotic progression

Cell division requires the coordination of critical protein kinases and phosphatases. Greatwall (Gwl) kinase activity inactivates PP2A-B55 at mitotic entry to promote the phosphorylation of cyclin B–Cdk1 substrates, but how Gwl is regulated is poorly understood. We found that the subcellular localization of Gwl changed dramatically during the cell cycle in Drosophila. Gwl translocated from the nucleus to the cytoplasm in prophase. We identified two critical nuclear localization signals in the central, poorly characterized region of Gwl, which are required for its function. The Polo kinase associated with and phosphorylated Gwl in this region, promoting its binding to 14-3-3ε and its localization to the cytoplasm in prophase. Our results suggest that cyclin B–Cdk1 phosphorylation of Gwl is also required for its nuclear exclusion by a distinct mechanism. We show that the nucleo-cytoplasmic regulation of Gwl is essential for its functions in vivo and propose that the spatial regulation of Gwl at mitotic entry contributes to the mitotic switch.     

Comparative Functional Analysis of ZFP36 Genes during Xenopus Development

ZFP36 constitutes a small family of RNA binding proteins (formerly known as the TIS11 family) that target mRNA and promote their degradation. In mammals, ZFP36 proteins are encoded by four genes and, although they show similar activities in a cellular RNA destabilization assay, there is still a limited knowledge of their mRNA targets and it is not known whether or not they have redundant functions. In the present work, we have used the Xenopus embryo, a model system allowing gain- and loss-of-function studies, to investigate, whether individual ZFP36 proteins had distinct or redundant functions. We show that overexpression of individual amphibian zfp36 proteins leads to embryos having the same defects, with alteration in somites segmentation and pronephros formation. In these embryos, members of the Notch signalling pathway such as hairy2a or esr5 mRNA are down-regulated, suggesting common targets for the different proteins. We also show that mouse Zfp36 protein overexpression gives the same phenotype, indicating an evolutionary conserved property among ZFP36 vertebrate proteins. Morpholino oligonucleotide-induced loss-of-function leads to defects in pronephros formation, reduction in tubule size and duct coiling alterations for both zfp36 and zfp36l1, indicating no functional redundancy between these two genes. Given the conservation in gene structure and function between the amphibian and mammalian proteins and the conserved mechanisms for pronephros development, our study highlights a potential and hitherto unreported role of ZFP36 gene in kidney morphogenesis.