Developing Habitat Models for Waterbirds in Urban Wetlands: A Log-linear Approach

Up to 95% of wetlands in southwestern Ontario, Canada, have been drained and converted to other land uses since the mid-1800s. Remaining wetlands now exist within a mosaic of urban and agriculture land cover and may resemble “islands” from the point of view of species that need this habitat. We investigated the relationships between waterbirds and wetland size, isolation, and adjacent forest cover and roads in 19 wetlands within and adjacent to London, Ontario. Waterbirds were grouped into resource-based guilds: Dabblers, Divers, Waders, and Gulls and Terns (because of small samples, the Passerine and Raptor guilds were dropped from the statistical analyses). Because of the high degree of multicollinearity between variables, we used log-linear analysis to develop models that explained variations in species richness in the waterbird guilds. The log-linear technique provided quantification of environmental effects in a richer way than previous research as the interplay between biophysical factors found in reality are partially captured by the inclusion of interaction in the habitat models. All of the models incorporated the biophysical variables of wetland size and adjacent wetland area, forest cover, and roads. Waterbirds in these urban and near-urban landscapes appear to be using all wetlands available to them, no matter how small or how disjunct the wetland. This has implications for wetland evaluations that may not rate wetlands in human-dominated landscapes highly enough to be protected from development

Mutations in the Caenorhabditis elegans U2AF Large Subunit UAF-1 Al= of a 3' Splice Site In Vivo

The removal of introns from eukaryotic RNA transcripts requires the activities of five multi-component ribonucleoprotein complexes and numerous associated proteins. The lack of mutations affecting splicing factors essential for animal survival has limited the study of the in vivo regulation of splicing. From a screen for suppressors of the Caenorhabditis elegans unc-93(e1500) rubberband Unc phenotype, we identified mutations in genes that encode the C. elegans orthologs of two splicing factors, the U2AF large subunit (UAF-1) and SF1/BBP (SFA-1). The uaf-1(n4588) mutation resulted in temperature-sensitive lethality and caused the unc-93 RNA transcript to be spliced using a cryptic 3′ splice site generated by the unc-93(e1500) missense mutation. The sfa-1(n4562) mutation did not cause the utilization of this cryptic 3′ splice site. We isolated four uaf-1(n4588) intragenic suppressors that restored the viability of uaf-1 mutants at 25°C. These suppressors differentially affected the recognition of the cryptic 3′ splice site and implicated a small region of UAF-1 between the U2AF small subunit-interaction domain and the first RNA recognition motif in affecting the choice of 3′ splice site. We constructed a reporter for unc-93 splicing and using site-directed mutagenesis found that the position of the cryptic splice site affects its recognition. We also identified nucleotides of the endogenous 3′ splice site important for recognition by wild-type UAF-1. Our genetic and molecular analyses suggested that the phenotypic suppression of the unc-93(e1500) Unc phenotype by uaf-1(n4588) and sfa-1(n4562) was likely caused by altered splicing of an unknown gene. Our observations provide in vivo evidence that UAF-1 can act in regulating 3′ splice-site choice and establish a system that can be used to investigate the in vivo regulation of RNA splicing in C. elegans.National Institutes of Health (Grant GM24663