Screening of morphology-related genes based on predator-induced transcriptome sequencing and the functional analysis of Dagcut gene in Daphnia galeata.

High fish predation pressure can trigger "induced defense" in Daphnia species, resulting in phenotypic plasticity in morphology, behavior, or life-history traits. The molecular mechanisms of defense morphogenesis (e.g., the tail spine and helmet) in Daphnia remain unclear. In the present study, the tail spine, helmet, and body of Daphnia galeata under fish and non-fish kairomones conditions were collected for transcriptome analysis. A total of 24 candidate genes related to the morphological defense of D. galeata were identified, including 2 trypsin, one cuticle protein, 1 C1qDC protein, and 2 ferritin genes. The function of the Dagcut gene (D. galeata cuticle protein gene) in relation to tail spine morphology was assessed using RNA interference (RNAi). Compared with the EGFP (Enhanced green fluorescent protein) treatment, after RNAi, the expression levels of the Dagcut gene (D. galeata cuticle protein gene) showed a significant decrease. Correspondingly, the tail spines of the offspring produced by D. galeata after RNAi of the Dagcut gene appeared curved during the experiment. In whole-mount in situ hybridization, a clear signal site was detected on the tail spine of D. galeata before RNAi which disappeared after RNAi. Our results suggest that the Dagcut gene may play an important role in tail spine formation of D. galeata, and will provide a theoretical basis for studying the molecular mechanisms of the morphological plasticity in cladocera in the future.

Natural Selection on Exonic SNPs Shapes Allelic Expression Imbalance (AEI) Adaptability in Lung Cancer Progression.

Tumors are driven by a sequence of genetic and epigenetic alterations. Previous studies have mostly focused on the roles of somatic mutations in tumorigenesis, but how germline variants act is largely unknown. In this study, we hypothesized that allelic expression imbalance (AEI) participated in the process of germline variants on tumorigenesis. We screened single-nucleotide polymorphisms (SNPs) as representative germline variants. By using 127 patients' RNA sequencing data from paired lung cancer and adjacent normal tissues from public databases, we analyzed the effects of the functional consequence of SNPs, function and conservativeness on genes with AEI. We found that natural selection can affect AEI. Functional adaptability of genes with a high frequency of AEI and a correlation of the incidence of AEI with conservativeness were observed in both adjacent tissues and tumor tissues. Moreover, we observed a higher incidence of AEI in genes with non-synonymous SNPs than in those with synonymous SNPs. However, we also found that AEI was affected by allele expression noise, especially in tumor tissues, which led to an increased proportion of AEI, weakened the effect of natural selection and eliminated the influence of the functional consequence of SNPs on AEI. We unveiled a previously unknown adaptive regulatory mechanism in which the effect of natural selection on SNPs can be reflected in allelic expression, which provides insight into a better understanding of cancer evolution.

EDI-OCT choroidal thickness in Posner-Schlossman syndrome.

PURPOSE: To compare the choroidal thickness (CT) of the affected eyes with the contralateral eyes in the active period and in the remission period in Posner-Schlossman syndrome (PSS) using EDI-OCT. PATIENTS AND METHODS: This prospective longitudinal study included 15 patients with PSS and 15 age- and sex-matched healthy subjects. All subjects underwent complete ophthalmologic examinations, and EDI-OCT was conducted to measure macular CT (mCT) at the subfoveal locations and at 0.5, 1.0 and 2.0 mm superior, inferior, nasal and temporal to the fovea. The mean measurements at each location were used for analysis. Linear regression analysis was performed to analyse the correlation between the choroidal thickness and IOP, and the correlation between the choroidal thickness and episode time. RESULTS: The mean mCT was significantly thinner in affected eyes than in contralateral eyes in the acute phase (p = 0.010) but were not different in the remission phase (p = 0.404). The mean mCT was significantly increased in the remission phase compared to that in the acute phase in the affected eyes (p = 0.000). The mCT of healthy subjects was significantly thicker than in the affected eyes (p = 0.020) and similar to the fellow eyes of PSS patients (p = 0.357) in the acute phase. Linear regression analyses show negative correlations between the mCT changes and IOP changes in the affected eyes compared to those in the fellow eyes in the acute period (R2 = 0.396, p = 0.033) and between the mCT changes and IOP changes from the acute period to the remission period in the affected eyes (R2 = 0.372, p = 0.027). Linear regression analyses show positive correlations (age- and sex-matched) between the CT changes and episode time from the affected eyes to the fellow eyes in the acute period (R2 = 0.492, p = 0.012). CONCLUSIONS: The mCT values of the PSS-affected eyes were significantly thinner than those of the fellow eyes in the acute phase and in the remission phase, and this change was correlated with IOP reduction and episode time.

Integrative analysis reveals enhanced regulatory effects of human long intergenic non-coding RNAs in lung adenocarcinoma.

Although there is an accumulating appreciation of the key roles that long intergenic non-coding RNAs (lincRNAs) play in diverse cellular processes, our knowledge of how lincRNAs function in cancer remains sparse. Here, we present a comprehensive landscape of RNA-seq transcriptome profiles of lung adenocarcinomas and their paired normal counterparts to unravel gene regulation rules of lincRNAs. Consistent with previous findings of co-expression between neighboring protein-coding genes, lincRNAs were typically co-expressed with their neighboring genes, which was found in both cancerous and normal tissues. By building a mathematical model based on correlated gene expression, we distinguished an additional subset of lincRNAs termed "regulatory lincRNAs", representing their dominant roles in gene regulation. The number of regulatory lincRNAs was significantly higher in cancerous compared to normal tissues, and most of them positively regulated protein-coding genes in trans. Functional validation, using knockdown, determined that regulatory lincRNA, GAS5, affected its predicted protein-coding targets. Moreover, we discovered hundreds of differentially expressed regulatory lincRNAs with inclusion of some cancer-associated lincRNAs. Our integrated analysis reveals enhanced regulatory effects of lincRNAs and provides a resource for the study of regulatory lincRNAs that play critical roles in lung adenocarcinoma.