Evolutionary Impacts of Chronic Cold on the Antarctic Notothenioid Chaperome and its Regulatory Mechanisms


Meeting Abstract

P2-128  Saturday, Jan. 5 15:30 – 17:30  Evolutionary Impacts of Chronic Cold on the Antarctic Notothenioid Chaperome and its Regulatory Mechanisms BILYK, KT*; CHENG, CH-C; Western Kentucky University; University of Illinois at Urbana Champaign kevin.bilyk@wku.edu

Antarctic notothenioid fishes show a variety of extraordinary physiological gains and losses driven by their evolution in the chronic cold waters of the Southern Ocean. Both these gains and losses are mirrored in the chaperome, where impacts are found both in expression at native temperatures as well as its capacity to reorganize expression in response to heat stress. While past work has suggested that greater native expression of some molecular chaperones coexists with the extraordinary loss of the Heat Shock Response (HSR), a clear understanding is lacking in the nature and extent of changes across the diverse families of molecular chaperones, and within the regulatory framework controlling their expression during periods of cellular stress. Using the basal temperate notothenioid Eleginops maclovinus as the reference ancestral notothenioid state, we found widespread increases in native expression of chaperome and key proteostasis genes in the Antarctic species Pagothenia borchgrevinki and Chionodraco rastrospinosus. However, these increases are generally small the sole exception is one ancestrally inducible member of the HSP70 gene family, which interestingly correlates with the insertion of a transposon into the gene’s 5’UTR intron. In both known copies of ancestrally-inducible HSP70 genes, canonical Heat Shock Element motifs are conserved in the proximal upstream sequence, suggesting defects leading to HSR loss reside elsewhere. Investigation of the coding sequence for the transcription factor HSF1, central in the HSR, showed that modifications among the two Antarctic species were concentrated in the regulatory and transactivation regions of the gene suggesting HSR loss may lie at the level of HSF1 activation of the cascade.

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