Selection on Visual Opsin Genes in Diurnal Neotropical Frogs and Loss of the SWS2 Opsin in Poison Frogs.

Amphibians are ideal for studying visual system evolution because their biphasic (aquatic and terrestrial) life history and ecological diversity expose them to a broad range of visual conditions. Here, we evaluate signatures of selection on visual opsin genes across Neotropical anurans and focus on three diurnal clades that are well-known for the concurrence of conspicuous colors and chemical defense (i.e., aposematism): poison frogs (Dendrobatidae), Harlequin toads (Bufonidae: Atelopus), and pumpkin toadlets (Brachycephalidae: Brachycephalus). We found evidence of positive selection on 44 amino acid sites in LWS, SWS1, SWS2, and RH1 opsin genes, of which one in LWS and two in RH1 have been previously identified as spectral tuning sites in other vertebrates. Given that anurans have mostly nocturnal habits, the patterns of selection revealed new sites that might be important in spectral tuning for frogs, potentially for adaptation to diurnal habits and for color-based intraspecific communication. Furthermore, we provide evidence that SWS2, normally expressed in rod cells in frogs and some salamanders, has likely been lost in the ancestor of Dendrobatidae, suggesting that under low-light levels, dendrobatids have inferior wavelength discrimination compared to other frogs. This loss might follow the origin of diurnal activity in dendrobatids and could have implications for their behavior. Our analyses show that assessments of opsin diversification in across taxa could expand our understanding of the role of sensory system evolution in ecological adaptation.

Conservation of Nematocida microsporidia gene expression and host response in Caenorhabditis nematodes.

Microsporidia are obligate intracellular parasites that are known to infect most types of animals. Many species of microsporidia can infect multiple related hosts, but it is not known if microsporidia express different genes depending upon which host species is infected or if the host response to infection is specific to each microsporidia species. To address these questions, we took advantage of two species of Nematocida microsporidia, N. parisii and N. ausubeli, that infect two species of Caenorhabditis nematodes, C. elegans and C. briggsae. We performed RNA-seq at several time points for each host infected with either microsporidia species. We observed that Nematocida transcription was largely independent of its host. We also observed that the host transcriptional response was similar when infected with either microsporidia species. Finally, we analyzed if the host response to microsporidia infection was conserved across host species. We observed that although many of the genes upregulated in response to infection are not direct orthologs, the same expanded gene families are upregulated in both Caenorhabditis hosts. Together our results describe the transcriptional interactions of Nematocida infection in Caenorhabditis hosts and demonstrate that these responses are evolutionarily conserved.

Role of the Ubi-p63E gene in the germline stem cell niche of the Drosophila testis / 医学研究生学报

Objective Whether the Ubi-p63E gene regulates spermatogenesis and tumorigenesis remains unclear. This study aimed to explore the regulatory effect of Ubi-p63E on germline stem cells (GSC) in the GSC niche of the Drosophila testis. Methods We used the UAS-Gal4 system for knockdown of the Ubi-p63E gene in the specific GSCs of the Drosophila testis and divided the male flies for this experiment into three groups: control (wild-type W1118 flies), nos>Ubi-p63E RNAi (knockdown of the Ubi-p63E gene in the early germ cells), and tj>Ubi-p63E RNAi (knockdown of the Ubi-p63E gene in the cystoblasts). We determined the fertility rate of the flies by fertility tests and examined the effect of Ubi-p63E on the Drosophila testis in the GSC niche by immunofluorescence staining. Results Fertility tests manifested a significantly lower rate of fertility in the nos>Ubi-p63E RNAi and tj>Ubi-p63E RNAi groups than in the control (0.00% and 4.12% vs 97.26%, P < 0.01). Morphologically abnormal testes were observed in the nos>Ubi-p63E RNAi and tj>Ubi-p63E RNAi groups, only 22.77% and 18.86% as long as the testes of the control flies. Immunofluorescence staining revealed no morphologically normal testes in the tj>Ubi-p63E RNAi group, but quite a few masses of abnormal cells, and mostly Vasa-positive cells. Conclusion The Ubi-p63E gene affects the self-renewal ability of GSCs in the GSC niche of the Drosophila testis as well as the differentiation of GSCs via cystoblasts, and consequently leads to the formation of germ cell tumors.