Integration of acoustic telemetry and GIS to identify potential spawning areas for lake trout (Salvelinus namaycush)

Locations of potential spawning areas for lake trout (Salvelinus namaycush) were predicted in Lake Opeongo, Ontario, Canada using information gained via acoustic telemetry and geographic information system (GIS) technologies. From 1998 to 2000, 18 adult lake trout (mean fork length 553 mm) implanted with acoustic transmitters (battery life 2 years) were manually tracked. For evening fall locations within the erosive zone of the lake (determined using an existing sedimentation model), habitat variables (slope, depth, and effective fetch) were summarised using GIS. Sites selected by lake trout during the spawning window were in areas of mean fetch equal to 1.5 km and mean slope of 10.6% (n = 50 fixes). We used GIS to identify areas that matched the mean habitat criteria and thus locate potential spawning areas. This model correctly identified 19 of 21 known spawning sites, as well as additional sites used by spawning females in an earlier telemetry study. Depths of traditional fall netting sites are shallow compared to areas in which telemetered lake trout were found during evenings of the spawning period (means 3.1 vs. 5.1 m, respectively). Through the use of information on spawning habitat selection gained through telemetry and knowledge of the physical characteristics of the lake, we provide an alternative means of identifying potential spawning habitat for lake trout.     

Homozygous deletion of the very low density lipoprotein receptor gene causes autosomal recessive cerebellar hypoplasia with cerebral gyral simplification

An autosomal recessive syndrome of nonprogressive cerebellar ataxia and mental retardation is associated with inferior cerebellar hypoplasia and mild cerebral gyral simplification in the Hutterite population. An identity-by-descent mapping approach using eight patients from three interrelated Hutterite families localized the gene for this syndrome to chromosome region 9p24. Haplotype analysis identified familial and ancestral recombination events and refined the minimal region to a 2-Mb interval between markers D9S129 and D9S1871. A 199-kb homozygous deletion encompassing the entire very low density lipoprotein receptor (VLDLR) gene was present in all affected individuals. VLDLR is part of the reelin signaling pathway, which guides neuroblast migration in the cerebral cortex and cerebellum. To our knowledge, this syndrome represents the first human lipoprotein receptor malformation syndrome and the second human disease associated with a reelin pathway defect.