Abstract
Individual levels of genetic variation can be a key factor for survival and pathogen resistance of wild vertebrate populations. It was recently shown that California sea lions pups that were infected with Uncinaria and were homozygous at a particular microsatellite, Hg 4.2 were more likely to develop anemia.1 Similar results were found for a related species, the New Zealand sea lion, suggesting heterosis for a more robust blood coagulation process.2 However, the generalities and processes underlying such a possibility remain unclear. Due to the current knowledge on their common diseases and associated clinical parameters, and to the large numbers of animals that strand every year and are admitted to The Marine Mammal Center for rehabilitation, the California sea lion is a good model to investigate aspects of genetic susceptibility to disease and the mechanisms that underlie such patterns. Here we examined various blood parameters, including circulating levels of platelets, hematocrit, and erythrocyte counts, related to blood coagulation, in 967 California sea lions stranded and admitted to the Marine Mammal Center between 1994 and 2005 in order to determine whether Hg 4.2 heterozygosity or allele identity plays a role in shaping the blood parameters for each disease condition. A series of generalized linear models that included genetic parameters, sex and age as explanatory variables for 11 well characterized causes of stranding (leptospirosis, domoic acid, parasitic infection, urogenital carcinoma, bacterial infection, malnutrition, pneumonia, trauma and septicemia) showed that heterozygosity at Hg 4.2 significantly influenced levels of platelets for individuals with leptospirosis (GLM n = 231 , p = 0.03) and parasitic infection ( GLM n = 12 , p = 1.003), but did not affect blood counts of neutrophils, hemoglobin, hematocrit, erythrocyte, monocyte, eosinophil, leucocyte, lymphocyte and mean corpuscular hemoglobin. Allele identity did not appear to play a role for the platelet levels recorded (p > 0.05 for all models). Our results are congruent with previous findings in California sea lions and New Zealand sea lion, and suggest that microsatellite Hg 4.2 lies within a genetic region that is relevant to platelets function or genesis. An in silico alignment of the microsatellite's flanking sequences revealed high similarity to the canine gene SEMA5B. This region is characterized by having seven thrombospondin repeats (type 1 and type 1-like), which are proteins known to be involved in platelet aggregation.3 Further work will be needed to determine whether Hg 4.2 is located within SEMA5B in California sea lions and to establish the functional significance of Hg 4.2 allele variants for platelet function.
* Presenting author
+ Student presenter
Literature Cited
1. Acevedo-Whitehouse K, Petetti L, Duignan P, Castinel A. 2009. Hookworm infection, anaemia and genetic variability of the New Zealand sea lion. Proceeding of the Royal Society B. 276:3523–3529
2. Acevedo-Whitehouse K, Spraker TR, Lyons E, Melin SR, Gulland F, DeLong RL, Amos W. 2006. Contrasting effects of heterozygosity on survival and hookworm resistance in California sea lion pups. Molecular Ecology. 15:1973–1982
3. Simantov R, Silverstein RL. 2003. CD36: A Critical anti-angiogenic receptor. Frontiers in Bioscience 8: s874–882