Summary During adaptive radiations, animals colonize diverse environments, which requires adaptation in multiple phenotypic traits [1]. Because hormones mediate the dynamic regulation of suites of phenotypic traits [2–4], evolutionary changes in hormonal signaling pathways might contribute to adaptation to new environments. Here, we report changes in the thyroid hormone signaling pathway in stream-resident ecotypes of threespine stickleback fish (Gasterosteus aculeatus), which have repeatedly evolved from ancestral marine ecotypes [5–8]. Stream-resident fish exhibit a lower plasma concentration of thyroid hormone and a lower metabolic rate, which is likely adaptive for permanent residency in small streams. The thyroid stimulating hormone-β2 (TSHβ2) gene exhibited significantly lower mRNA expression in pituitary glands of stream-resident sticklebacks relative to marine sticklebacks. Some of the difference in TSHβ2 transcript levels can be explained by cis-regulatory differences at the TSHβ2 gene locus. Consistent with these expression differences, a strong signature of divergent natural selection was found at the TSHβ2 genomic locus. By contrast, there were no differences between the marine and stream-resident ecotypes in mRNA levels or genomic sequence in the paralogous TSHβ1 gene. Our data indicate that evolutionary changes in hormonal signaling have played an important role in the postglacial adaptive radiation of sticklebacks.

Massive scleractinian corals of the genus Porites are important reef builders in the Indo-Pacific, and they are more resistant to thermal stress than other stony corals, such as the genus Acropora. Because coral health and survival largely depend on the interaction between a coral host and its symbionts, it is important to understand the molecular interactions of an entire “coral holobiont”. We simultaneously sequenced transcriptomes of Porites australiensis and its symbionts using the Illumina Hiseq2000 platform. We obtained 14.3 Gbp of sequencing data and assembled it into 74,997 contigs (average: 1,263 bp, N50 size: 2,037 bp). We successfully distinguished contigs originating from the host (Porites) and the symbiont (Symbiodinium) by aligning nucleotide sequences with the decoded Acropora digitifera and Symbiodinium minutum genomes. In contrast to previous coral transcriptome studies, at least 35% of the sequences were found to have originated from the symbionts, indicating that it is possible to analyze both host and symbiont transcriptomes simultaneously. Conserved protein domain and KEGG analyses showed that the dataset contains broad gene repertoires of both Porites and Symbiodinium. Effective utilization of sequence reads revealed that the polymorphism rate in P. australiensis is 1.0% and identified the major symbiotic Symbiodinium as Type C15. Analyses of amino acid biosynthetic pathways suggested that this Porites holobiont is probably able to synthesize most of the common amino acids and that Symbiodinium is potentially able to provide essential amino acids to its host. We believe this to be the first molecular evidence of complementarity in amino acid metabolism between coral hosts and their symbionts. We successfully assembled genes originating from both the host coral and the symbiotic Symbiodinium to create a snapshot of the coral holobiont transcriptome. This dataset will facilitate a deeper understanding of molecular mechanisms of coral symbioses and stress responses.

11beta-Hydroxysteroid dehydrogenases (11beta-HSDs) are important steroidogenic enzymes for catalyzing the interconversion of active glucocorticoid (cortisol and corticosterone) and inert 11-keto forms (cortisone and 11-dehydrocorticosterone) in mammals. In teleosts, 11beta-HSD also plays a role in the production of the predominant androgen, 11-ketotestosterone, in male fish. In this study we cloned cDNAs encoding rainbow trout 11beta-HSD (rt11beta-HSD) from testes and head kidney. The predicted amino acid sequence, hydrophobicity analysis, and transient transfection assays with rt11beta-HSD in HEK293 cells showed that rt11beta-HSD is a homolog of mammalian 11beta-HSD type 2. rt11beta-HSD transcripts are present in steroidogenic tissues and in a number of other tissues. Strong in situ hybridization signals for rt11beta-HSD transcripts were found in Leydig cells of testes, in thecal cells of the early vitellogenic ovarian follicles, and in thecal and granulosa cells of the midvitellogenic and postovulatory follicles. Weaker signals were also found in head kidney interrenal cells from juvenile rainbow trout. Seasonal changes in rt11beta-HSD transcripts in testes showed a pattern similar to that of stress-induced serum cortisol levels, but not to serum androgen levels. High levels of rt11beta-HSD transcripts were found in ovarian follicles from late vitellogenesis through ovulation. These results raise the possibility of a role for rt11beta-HSD in the protection of developing gonads from the inhibitory effects of stress-induced cortisol.

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