Evolutionary developmental biology of notothenioid fishes through the genomic looking glass


Meeting Abstract

69.3  Saturday, Jan. 5  Evolutionary developmental biology of notothenioid fishes: through the genomic looking glass DETRICH, H.W.*; YAN, Y.L.; TITUS, T.; ALLARD, C.; ALBERTSON, R.C.; POSTLETHWAIT, J.H.; Northeastern Univ., Boston; Univ. of Oregon, Eugene; Univ. of Oregon, Eugene; Northeastern Univ., Boston; Univ. of Massachusetts, Amherst; Univ. of Oregon, Eugene iceman@neu.edu

Comparative genomics provides a global perspective of the evolutionary changes in developmental programs that control phenotypic diversity among related organisms, and many of these naturally adaptive phenotypes mimic deleterious human diseases. Some Antarctic fish provide an evolutionary mutant model for osteopenic diseases of elderly humans. Ancestral notothenioid fish were benthic and lacked a swim bladder, an organ of buoyancy. As the Southern Ocean cooled to -1.9°C, notothenioids filled pelagic niches left vacant by local extinction of other species by evolving strategies to reduce body density, including decreases in bone mineral density in several clades. To identify genes causing the adaptive demineralization of bone in Antarctic fish, which may be orthologous to genes responsible for low bone mineral density in aging humans, we are comparing the molecular genetics of skeletal development in embryos of the robustly ossified, benthic Bullhead notothen, Notothenia coriiceps, and of the osteopenic, benthopelagic Blackfin icefish, Chaenocephalus aceratus. First, we have generated reference transcriptomes for the two species by sequencing total cDNA from multiple bones and soft tissues by RNAseq. Second, we have cultured embryos of the two species and sampled them at intervals to obtain stage-specific total mRNA. Cross-comparison of the reference-normalized developmental cDNA samples will enable us to identify the molecular-genetic basis of the evolution of osteopenia by the icefish, and our results may provide clues to age-related osteopenia in humans. Support: NSF grant ANT-0944517 (HWD); NIH grant R01AG031922 (JHP, HWD, RCA).

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