West Nile Virus and California Breeding Bird Declines

Since it was first detected in 1999, West Nile virus (WNV) quickly spread, becoming the dominant vector-borne disease in North America. Sometimes fatal to humans, WNV is even more widespread among birds, with hundreds of species known to be susceptible to WNV infection in North America alone. However, despite considerable mortality and local declines observed in American crows (Corvus brachyrhynchos), there has been little evidence of a large regional association between WNV susceptibility and population declines of any species. Here we demonstrate a correlation between susceptibility to WNV measured by large-scale testing of dead birds and two indices of overall population change among bird species following the spread of WNV throughout California. This result was due primarily to declines in four species of Corvidae, including all species in this family except common ravens (Corvus corax). Our results support the hypothesis that susceptibility to WNV may have negative population consequences to most corvids on regional levels. They also provide confirmation that dead animal surveillance programs can provide important data indicating populations most likely to suffer detrimental impacts due to WNV.     

Potential causes of arrested succession in Kibale National Park, Uganda: growth and mortality of seedlings

Recent studies suggest that regeneration following large-scale disturbance in Kibale National Park, Uganda, is slow or possibly arrested. Here, data is provided on the growth and mortality of seedlings in the forest understory, treefall gaps, and in large gaps that suggest that this pattern of arrested succession can be attributed partially to the fact that this East African community lacks aggressive colonizing tree species. Growth and mortality rates were contrasted for seedlings of six tree species planted in the understory, small gaps, and large gaps for 36 months. Data suggest that species are adapted to gaps of particular sizes. For example, Uvariopsis congensis grew faster in the understory than in small gaps, whereas Warburgia ugandensis had the lowest mortality rate and highest growth rate in large gaps. Seedlings (n=170) of 15 species were transplanted to assess the response of the tree community to large gap conditions. The limited survival of seedlings in large gaps relative to the understory suggests that only a small proportion of the tree community in this forest regenerates best in gaps larger than those created by the collapse of a single tree. These findings differ from a number of studies conducted in other geographical regions, and suggests that tree communities differ with respect to the proportion of tree species adapted to gaps of particular sizes. This may relate to variation among regions in their history of disturbance and thus frequency of gap formation, size of gaps, and the duration of periods of release. Such variation could imply the existence of a corresponding pattern among tropical forests of differential vulnerability to human disturbance, which tends to create many large gaps.     

Src-inducible association of CrkL with procaspase-8 promotes cell migration

Procaspase-8, the zymogen form of the apoptosis-initiator caspase-8, undergoes phosphorylation following integrin-mediated cell attachment to an extracellular matrix substrate. Concordant with cell attachment to fibronectin, a population of procaspase-8 becomes associated with a peripheral insoluble compartment that includes focal complexes and lamellar microfilaments. Phosphorylation of procaspase-8 both impairs its maturation to the proapoptotic form and can promote cell migration. Here we show that the cytoskeletal adaptor protein CrkL promotes caspase-8 recruitment to the peripheral spreading edge of cells, and that the catalytic domain of caspase-8 directly interacts with the SH2 domain of CrkL. We show that the interaction is abolished by shRNA-mediated silencing of Src, in Src-deficient MEFs, and by pharmacologic inhibitors of the kinase. The results provide insight into how tyrosine kinases may act to coordinate the suppression caspase-8 mediated apoptosis, while promoting cell invasion.