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Pristine poly(butylene adipate-co-terephthalate) (PBAT) is a biodegradable aliphatic-aromatic copolyester that shows no photoluminescent features. The radio induction of photoluminescence (PL) properties in PBAT, after exposure to high doses of gamma radiation, was firstly reported in 2014. These new PL properties have great potential for applications at “in vitro” imaging of human cancer, bio-imaging devices and radiation dosimetry. In this paper, we report the radio induction of photoluminescence (PL) properties in PBAT, after exposure to low energy UV irradiation. In this investigation, films of PBAT, produced by the wire-bar coating technique, were exposed to UV radiation for periods of time ranging from 50 to 500 hours. The PL emission analysis revealed that UV irradiation performed under O2 rich air atmosphere enhances the PL output when compared to irradiations performed in the air. FTIR data confirm that the mechanism behind the UV photo-induction of PL features are similar to the mechanism suggested for gamma radio-induction PL emission. The PL intensity x Spectral Irradiance relationship and RGB color components, the green (G) and blue (B) components, can be used to perform 2D UV dosimetry. The high quantum yield emission of UV-induced PL near 500 nm observed in PBAT is a very interesting finding because it involves the development of a new cheap biodegradable photoluminescent polymer that finds application in drug delivery, bio-imaging devices and also in 2D dosimetry.

In this work, we report evidences of the improvement of X-ray attenuation efficiency by the addition of a very small amount of Graphene Oxide (GO) in polymer-based nanocomposite. Poly(vinylidene fluoride) (PVDF) homopolymer and barium sulfate (BaSO4) nanoparticles were mixed. PVDF/BaSO4 nanocomposite was found to attenuate 9.14% of a 20 kV X-ray beam. The addition of only 4.0 wt % of GO nanosheets to the nanocomposite improved this X-Ray attenuation efficiency to 24.56%. The respective linear attenuation coefficients (μ) were 39.9 cm−1 and 54.4 cm−1, respectively. The X-ray attenuation gradually decreases until 6.71% and 17.62%, respectively, for the X-ray beam with higher energy (100 kV). Fourier transform infrared data revealed that, due to the lack of the bending vibration modes of CF2 molecule at 656 cm−1, 688 cm−1, 723 cm−1, 776 cm−1and 796 cm−1, characteristics of the γ-crystalline phase of PVDF the nanocomposites casted from solution are mostly in the β-ferroelectric phase of PVDF, besides the γ-paraelectric phase. SEM micrographs were used to evaluate the dispersion state of graphene sheets and the BaSO4 nanoparticles into the polymeric matrix. UV-Vis spectrometry and Differential Scanning Calorimetry (DSC) were also performed in order to complement the structural analysis. The results confirm that the addition of graphene sheets in PVDF polymer-based nanocomposites enhances the X-ray shielding efficiency. The phenomenon is discussed in terms of the reported anomalous negative thermal expansion coefficient of graphene sheets

High-dose radiation is the main component of glioblastoma therapy. Unfortunately, radio-resistance is a common problem and a major contributor to tumor relapse. Understanding the molecular mechanisms driving response to radiation is critical for identifying regulatory routes that could be targeted to improve treatment response. We conducted an integrated analysis in the U251 and U343 glioblastoma cell lines to map early alterations in the expression of genes at three levels: transcription, splicing, and translation in response to ionizing radiation. Changes at the transcriptional level were the most prevalent response. Downregulated genes are strongly associated with cell cycle and DNA replication and linked to a coordinated module of expression. Alterations in this group are likely driven by decreased expression of the transcription factor FOXM1 and members of the E2F family. Genes involved in RNA regulatory mechanisms were affected at the mRNA, splicing, and translation levels, highlighting their importance in radiation-response. We identified a number of oncogenic factors, with an increased expression upon radiation exposure, including BCL6, RRM2B, IDO1, FTH1, APIP, and LRIG2 and lncRNAs NEAT1 and FTX. Several of these targets have been previously implicated in radio-resistance. Therefore, antagonizing their effects post-radiation could increase therapeutic efficacy. Our integrated analysis provides a comprehensive view of early response to radiation in glioblastoma. We identify new biological processes involved in altered expression of various oncogenic factors and suggest new target options to increase radiation sensitivity and prevent relapse.

The Flaviviridae virus family was named after the Yellow-fever virus, and the latin term flavi means “of golden color”. Dengue, caused by Dengue virus (DENV), is one of the most important infectious diseases worldwide. A sensitive and differential diagnosis is crucial for patient management, especially due to the occurrence of serological cross-reactivity to other co-circulating flaviviruses. This became particularly important with the emergence of Zika virus (ZIKV) in areas were DENV seroprevalence was already high. We developed a sensitive and specific diagnostic test based on gold nanorods (GNR) functionalized with DENV proteins as nanosensors. These were able to detect as little as one picogram of anti-DENV monoclonal antibodies and highly diluted DENV-positive human sera. The nanosensors could differentiate DENV-positive sera from other flavivirus-infected patients, including ZIKV, and were even able to distinguish which DENV serotype infected individual patients. Readouts are obtained in ELISA-plate spectrophotometers without the need of specific devices.

High-dose radiation is the main component of glioblastoma therapy. Unfortunately, radio-resistance is a common problem and a major contributor to tumor relapse. Understanding the molecular mechanisms driving response to radiation is critical for identifying regulatory routes that could be targeted to improve treatment response. We conducted an integrated analysis in the U251 and U343 glioblastoma cell lines to map early alterations in the expression of genes at three levels: transcription, splicing, and translation in response to ionizing radiation. Changes at the transcriptional level were the most prevalent response. Downregulated genes are strongly associated with cell cycle and DNA replication and linked to a coordinated module of expression. Alterations in this group are likely driven by decreased expression of the transcription factor FOXM1 and members of the E2F family. Genes involved in RNA regulatory mechanisms were affected at the mRNA, splicing, and translation levels, highlighting their importance in radiation-response. We identified a number of oncogenic factors, with an increased expression upon radiation exposure, including BCL6, RRM2B, IDO1, FTH1, APIP, and LRIG2 and lncRNAs NEAT1 and FTX. Several of these targets have been previously implicated in radio-resistance. Therefore, antagonizing their effects post-radiation could increase therapeutic efficacy. Our integrated analysis provides a comprehensive view of early response to radiation in glioblastoma. We identify new biological processes involved in altered expression of various oncogenic factors and suggest new target options to increase radiation sensitivity and prevent relapse.

Adipocytes possess remarkable adaptive capacity to respond to nutrient excess, fasting or cold exposure, and they are thus an important cell type for the maintenance of proper metabolic health. Although the endoplasmic reticulum (ER) is a critical organelle for cellular homeostasis, the mechanisms that mediate adaptation of the ER to metabolic challenges in adipocytes are unclear. Here we show that brown adipose tissue (BAT) thermogenic function requires an adaptive increase in proteasomal activity to secure cellular protein quality control, and we identify the ER-localized transcription factor nuclear factor erythroid 2-like 1 (Nfe2l1, also known as Nrf1) as a critical driver of this process. We show that cold adaptation induces Nrf1 in BAT to increase proteasomal activity and that this is crucial for maintaining ER homeostasis and cellular integrity, specifically when the cells are in a state of high thermogenic activity. In mice, under thermogenic conditions, brown-adipocyte-specific deletion of Nfe2l1 (Nrf1) resulted in ER stress, tissue inflammation, markedly diminished mitochondrial function and whitening of the BAT. In mouse models of both genetic and dietary obesity, stimulation of proteasomal activity by exogenously expressing Nrf1 or by treatment with the proteasome activator PA28α in BAT resulted in improved insulin sensitivity. In conclusion, Nrf1 emerges as a novel guardian of brown adipocyte function, providing increased proteometabolic quality control for adapting to cold or to obesity.

Genomic analyses have become an important tool to identify new avenues for therapy. This is especially true for cancer types with extremely poor outcomes, since our lack of effective therapies offers no tangible clinical starting point to build upon. The highly malignant brain tumor glioblastoma (GBM) exemplifies such a refractory cancer, with only 15 month average patient survival. Analyses of several hundred GBM samples compiled by the TCGA (The Cancer Genome Atlas) have produced an extensive transcriptomic map, identified prevalent chromosomal alterations, and defined important driver mutations. Unfortunately, clinical trials based on these results have not yet delivered an improvement on outcome. It is, therefore, necessary to characterize other regulatory routes known for playing a role in tumor relapse and response to treatment. Alternative splicing affects more than 90% of the human coding genes and it is an important source for transcript variation and gene regulation. Mutations and alterations in splicing factors are highly prevalent in multiple cancers, demonstrating the potential for splicing to act as a tumor driver. As a result, numerous genes are expressed as cancer-specific splicing isoforms that are functionally distinct from the canonical isoforms found in normal tissue. These include genes that regulate cancer-critical pathways such as apoptosis, DNA repair, cell proliferation, and migration. Splicing defects can even induce genomic instability, a common characteristic of cancer, and a driver of tumor evolution. Importantly, components of the splicing machinery are targetable; multiple drugs can inhibit splicing factors or promote changes in splicing which could be exploited to begin improving clinical outcomes. Here, we review the current literature and present a case for exploring RNA processing as therapeutic route for the treatment of GBM.

A new study investigates how microRNAs affect the binding of proteins to RNA.

Background Melanoma is the most lethal type of skin cancer. Since chemoresistance is a significant barrier, identification of regulators affecting chemosensitivity is necessary in order to create new forms of intervention. Prohibitin 1 (PHB1) can act as anti-apoptotic or tumor suppressor molecule, depending on its subcellular localization. Our recent data shown that accumulation of PHB1 protects melanoma cells from chemotherapy-induced cell death. Lacking of post-transcriptional regulation of PHB1 could explain this accumulation. Interestingly, most of melanoma patients have down-regulation of microRNA-195. Here, we investigate the role of miR-195, its impact on PHB1 expression, and on chemosensitivity in melanoma cells. Methods TCGA-RNAseq data obtained from 341 melanoma patient samples as well as a panel of melanoma cell lines were used in an expression correlation analysis between PHB1 and predicted miRNAs. miR-195 impact on PHB1 mRNA and protein levels and relevance of this regulation were investigated in UACC-62 and SK-MEL-5 melanoma lines by RT-qPCR and western blot, luciferase reporter and genetic rescue experiments. Cell proliferation, cell-cycle analysis and caspase 3/7 assay were performed to investigate the potential action of miR-195 as chemosensitizer in melanoma cells treated with cisplatin and temozolomide. Results Analysis of the TCGA-RNAseq revealed a significant negative correlation (Pearson) between miR-195 and PHB1 expression. Moreover, RT-qPCR data showed that miR-195 is down-regulated while PHB1 is up-regulated in a collection of melanoma cells. We demonstrated that miR-195 regulates PHB1 directly by RT-qPCR and western blot in melanoma cells and luciferase assays. To establish PHB1 as a relevant target of miR-195, we conducted rescue experiments in which we showed that PHB1 transgenic expression could antagonize the suppressive effect miR-195 on the proliferation of melanoma cells. Finally, transfection experiments combined with drug treatments performed in the UACC-62 and SK-MEL-5 melanoma cells corroborated miR-195 as potential anti-proliferative agent, with potential impact in sensitization of melanoma cell death. Conclusions This study support the role of miR-195 as anti-proliferative miRNA via targeting of PHB1 in melanoma cells. Electronic supplementary material The online version of this article (10.1186/s12885-017-3721-7) contains supplementary material, which is available to authorized users.

The biology of acute myelogenous leukemia (AML) is characterized by a block in differentiation, increase in proliferation and inhibition of apoptosis, all of which when combined lead to an expansion of leukemic blasts.1 AML therapy cures ~20% of those affected,2 highlighting the need for a better understanding of leukemia biology in order to identify novel therapeutic targets. The Wilms’ tumor 1 (WT1) gene has an oncogenic role in leukemogenesis and its overexpression correlates with a poor prognosis.3 WTAP is a highly conserved protein that partners with WT14,5 to function as a switch gene, regulating the balance between quiescence and proliferation.6 WTAP-null mice exhibit embryonic lethality.7 WTAP has been recently described as an oncogenic factor in gliomas.8 We hypothesized that alterations in WTAP, whose role in leukemogenesis is unknown, might provide an alternate means of modulating the WT1 pathway in AML. We performed a series of experiments to test this possibility. First, we examined WTAP expression in several primary AML samples observing increased levels of WTAP in AML compared with normal peripheral blood mononuclear cells (Figure 1a) as well as in AML cell lines (data not shown). Next, the WTAP expression levels were determined in 511 newly diagnosed AML patients using the reverse-phase protein array (RPPA) technique. In comparison with normal bone marrow CD34+ cells, WTAP expression in bulk AML cells was above normal levels in 32% of patients (Figure 1b). Although WTAP levels were not associated with individual cytogenetic abnormalities, some specific molecular mutations such as NPM1 and FLT3-ITD were found to have significant correlation (P ≤ 0.05) with WTAP expression (Supplementary Figure 1A). In addition, RPPA analysis showed that WTAP levels were positively correlated (R > |0.2|) with levels of various cell proliferation-related proteins (cyclins and Hsp90), antiapoptotic proteins (Bcl-2 and Bax), oncoproteins (FLI1) and proteins important for stem cell functions such as Myc and Ash2L (Supplementary Figure 1B). To assess the functional significance of increased WTAP expression, its expression was silenced in K562 and HL-60 cells, leading to a significant reduction (P ≤ 0.05) in proliferation (Figure 1c), and clonogenic survival (P ≤ 0.01) (Figure 1d). Similar effects on proliferation were observed in the AML cell line OCI-AML3 and in primary AML cells (Supplementary Figure 1C), suggesting a pro-proliferative role for WTAP in AML. WTAP knockdown alone did not induce apoptosis but markedly increased (P ≤ 0.01) the extent of apoptosis following etoposide treatment (Figure 1e). These results provide evidence for an association between the increased expression of WTAP and chemoresistance in AML. Figure 1 Expression of WTAP in AML and effect of WTAP silencing on AML cell behavior. (a) Peripheral blood mononuclear cells from normal donors (NL) and AML patients (AML) were obtained by Ficoll–Paque density centrifugation, and protein extracts were ... To examine the role of WTAP in AML progression in vivo, we performed tumor xenograft experiments in nude mice. As shown in Figure 1f, the growth rates and masses of tumors derived from WTAP-knockdown cells were significantly reduced (P ≤ 0.01) compared with control. To complement this analysis, the in vitro transforming activity of WTAP was examined by investigating its effects on growth of the Ba/F3 cell line. This line depends on interleukin 3 (IL-3) for survival and proliferation, but this dependence can be released by the transgenic expression of suitable oncogenes.9 Whereas control Ba/F3 cells were not viable in the absence of IL-3 at 72 h, WTAP-expressing Ba/F3 cells were able to maintain growth factor-independent proliferation, as demonstrated by significantly higher (P ≤ 0.01) number of viable cells (Figure 1g), suggesting that WTAP harbors oncogenic activity. The aberrant cellular proliferation and terminal differentiation block of myeloid cells are two hallmarks of AML.10 Having shown that WTAP regulates growth and survival, we investigated whether WTAP has a role in myeloid cell differentiation. As shown in Figure 1h, knockdown of WTAP promoted phorbol 12-myristate 13-acetate (PMA)-induced myeloid differentiation, as revealed by an increase in the expression of myeloid differentiation markers CD11b and CD14 compared with control cells. These results suggest that increased expression of WTAP in AML not only supports cell proliferation but also induces the differentiation block. Our RPPA analysis suggested a link between WTAP and mammalian target of rapamycin (mTOR) expression; and given that the mTOR pathway is deregulated in a number of cancers including AML,11 we hypothesized a putative regulatory role of WTAP on mTOR activity in AML. As shown in Figure 1i, WTAP knockdown induced a decrease in the phosphorylation levels of mTOR and its downstream effector p70 ribosomal subunit 6 kinase (pS6K) compared with control shRNA. To further understand the participation of WTAP in leukemogenesis, we performed transcriptomic analysis with RNA-Seq on WTAP knockdown in K562 cells. Gene ontology analysis indicated that cell adhesion and regulation of cell proliferation are the most enriched functionalities (Supplementary Figure 1D and Supplementary Table 2). Among the most relevant genes affected by WTAP with recognized roles in leukemia are CD4, CD44, CEBPA, CSF1R, MPO, ABCG2, TCL1A, CYP1A1, CYP3A4, FGFR1, PTPRC (CD45), CD83, CD86, CD9 and CCR4. Consistent with its described role in RNA processing, we determined that WTAP knockdown affected exon usage of 93 genes, including important factors such as MLL and MSI2. Interestingly, we also observed that WTAP affects the processing of its own transcript, very likely via polyA site selection. Complete analysis can be accessed in GEO ({"type":"entrez-geo","attrs":{"text":"GSE46718","term_id":"46718"}}GSE46718—http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?token=jbkjjswaqscegjsa Fisher’s exact test) in their mRNA levels as determined by RNA-Seq. Mutations of WTAP were not observed in the TCGA analysis of AML.12 Therefore, the etiology of increased WTAP expression in AML remains unexplained. We next sought to determine the potential mechanism that may contribute to an increase in WTAP expression in AML. The molecular chaperone Hsp90 maintains the stability of many tumor-promoting oncoproteins,13 including WT1.14 Keeping in mind the connection between WT1 and WTAP, we investigated the potential interaction between Hsp90 and WTAP. First, we determined that WTAP co-immunoprecipitates with Hsp90 (Figure 2a), whereas treatment with the Hsp90 inhibitor ganetespib significantly reduced the binding of Hsp90 to WTAP. Therefore, formation of the WTAP–Hsp90 complex is dependent on the chaperoning activity of Hsp90. Studies have shown that Hsp90 client proteins shift the primary chaperone association from Hsp90 to Hsp70 following inhibition of Hsp90 activity.15 Accordingly, our results showed that ganetespib treatment increased WTAP association with Hsp70 (Figure 2a). Furthermore, the GST pull-down assay showed a direct interaction between WTAP and Hsp90 (Figure 2b). To understand the functional significance of the association of Hsp90 with WTAP, we investigated the effects of Hsp90 inhibitors on WTAP protein stability. Ganetespib treatment promoted the degradation of WTAP in K562 (CML), MV4-11 (AML) and Kasumi-1 (AML) cell lines, previously shown to be highly sensitive to ganetespib (Figure 2c).16 Marked reduction in WTAP expression was similarly observed in blasts exposed to ganetespib (Figure 2d). Furthermore, ganetespib inhibited AML tumor growth in nude mice, as we reported previously,14 and WTAP expression in xenograft tumors (Figure 2e). Inhibition of Hsp90 induces polyubiquitination and proteasomal degradation of Hsp90 client proteins.17 We confirmed that pretreatment with proteasomal inhibitor bortezomib largely prevented ganetespib-induced degradation of WTAP (Figure 2f), and higher levels of ubiquitinated WTAP were observed in the presence of the combination of bortezomib and ganetespib compared with either agent alone (Figure 2g). Together, these data show that ganetespib-mediated degradation of WTAP is dependent on the ubiquitin-proteasome pathway, very similar to other bonafide Hsp90 client proteins. Figure 2 Hsp90 associates with WTAP and is necessary for its stability. (a) The K562 cells were treated with vehicle (−) or Hsp90 inhibitor, ganetespib (1 µm for 6 h) followed by immunoprecipitation (IP) with IgG and WTAP antibody. The immunoprecipitates ... In summary, our study shows that WTAP has an important role in abnormal proliferation and arrested differentiation of leukemia cells, and WTAP is a novel client protein of Hsp90. Therefore, WTAP may be a promising novel therapeutic target in AML. Further investigation aimed to elucidate the mechanism of action of WTAP is warranted.

Background Glioblastoma (GBM) is the most common and aggressive type of brain tumor. Currently, GBM has an extremely poor outcome and there is no effective treatment. In this context, genomic and transcriptomic analyses have become important tools to identify new avenues for therapies. RNA-binding proteins (RBPs) are master regulators of co- and post-transcriptional events; however, their role in GBM remains poorly understood. To further our knowledge of novel regulatory pathways that could contribute to gliomagenesis, we have conducted a systematic study of RBPs in GBM. Results By measuring expression levels of 1542 human RBPs in GBM samples and glioma stem cell samples, we identified 58 consistently upregulated RBPs. Survival analysis revealed that increased expression of 21 RBPs was also associated with a poor prognosis. To assess the functional impact of those RBPs, we modulated their expression in GBM cell lines and performed viability, proliferation, and apoptosis assays. Combined results revealed a prominent oncogenic candidate, SNRPB, which encodes core spliceosome machinery components. To reveal the impact of SNRPB on splicing and gene expression, we performed its knockdown in a GBM cell line followed by RNA sequencing. We found that the affected genes were involved in RNA processing, DNA repair, and chromatin remodeling. Additionally, genes and pathways already associated with gliomagenesis, as well as a set of general cancer genes, also presented with splicing and expression alterations. Conclusions Our study provides new insights into how RBPs, and specifically SNRPB, regulate gene expression and directly impact GBM development. Electronic supplementary material The online version of this article (doi:10.1186/s13059-016-0990-4) contains supplementary material, which is available to authorized users.

Aberrant gene expression is the cause and the consequence of tumorigenesis. A major component of gene expression is translation regulation; a process whose main players are RNA-binding-proteins (RBPs). More than 800 RBPs have been identified in the human genome and several of them have been shown to control gene networks associated with relevant cancer processes. A more systematic characterization of RBPs starts to reveal that similar to transcription factors, they can function as tumor suppressors or oncogenes. A relevant example is Musashi1 (Msi1), which is emerging as a critical regulator of tumorigenesis in multiple cancer types, including colon cancer. Msi1 is a stem marker in several tissues and is critical in maintaining the balance between self-renewal and differentiation. However, a boost in Msi1 expression can most likely lead cells towards an oncogenic pathway. In this article, we discuss the parallels between Msi1 function in normal renewal of intestinal epithelium and in colon cancer.

This paper presents a novel algorithm to successfully achieve viable integrity and authenticity addition and verification of n-frame DICOM medical images using cryptographic mechanisms. The aim of this work is the enhancement of DICOM security measures, especially for multiframe images. Current approaches have limitations that should be properly addressed for improved security. The algorithm proposed in this work uses data encryption to provide integrity and authenticity, along with digital signature. Relevant header data and digital signature are used as inputs to cipher the image. Therefore, one can only retrieve the original data if and only if the images and the inputs are correct. The encryption process itself is a cascading scheme, where a frame is ciphered with data related to the previous frames, generating also additional data on image integrity and authenticity. Decryption is similar to encryption, featuring also the standard security verification of the image. The implementation was done in JAVA, and a performance evaluation was carried out comparing the speed of the algorithm with other existing approaches. The evaluation showed a good performance of the algorithm, which is an encouraging result to use it in a real environment.

Background The obesity-associated insulin resistance has been shown to play an important role in the pathophysiology of overactive bladder in mice [1,2]. Therefore, we evaluated the beneficial effects of long-term administration of the sGC activator BAY 60-2270 in bladders from lean and obese mice. Methods Mice were fed for 12 weeks with either a standard chow diet (carbohydrate: 70%; protein: 20%; fat: 10%) or a high fat diet that induces obesity (carbohydrate: 29%; protein: 16%; fat: 55%). Lean and obese mice were orally treated with BAY 60-2770 (1 mg/kg/day, given as daily gavage

In this work we investigate the radio-degradation of MEH-PPV polymer film as a tool for measuring high doses of gamma radiation. In order to produce film samples with thickness in the micron range, we have mixed the photoluminescent poly(2-methoxy-5(2'-ethylhexyloxy)-p-phenylenevinylene) copolymer (MEH-PPV) with a biodegradable poly(butylene adipate-co-terephthalate) copolymers (PBAT). The system was irradiated with a Co-60 source with doses ranging from 1 to 1,000 kGy. Ultraviolet-visible (UV-Vis) and photoluminescence (PL) spectroscopy have been used to investigate the radiation induced changes in the absorption and photon-emission spectra of the irradiated samples. Results indicate that the PL emission intensity varies exponentially with the applied gamma radiation dose for doses ranging from 30 to 500 kGy. The unambiguous relationship between PL & Dose together with the good flexibility of the copolymer films indicate that MEH-PPV/PBAT blends have great potential for applications in high gamma dose dosimetry.

Crosses between Drosophila melanogaster females and D. simulans males produce viable hybrid females, while males are lethal. These males are rescued if they carry the D. simulans Lhr gene. This paper reports that females of the wild-type D. melanogaster population Staket do not produce viable hybrid males when crossed with D. simulans Lhr males, a phenomenon which we designate as the Staket phenotype. The agent responsible for this phenomenon was found to be the Staket X chromosome (Xmel, Stk). Analysis of the Staket phenotype showed that it is suppressed by extra copies of D. melanogaster rDNA genes and that the Xmel, Stk chromosome manifests a weak bobbed phenotype in D. melanogaster Xmel, Stk/0 males. The numbers of functional rDNA genes in Xmel, Stk and Xmel, y w (control) chromosomes were found not to differ significantly. Thus a reduction in rDNA gene number cannot account for the weak bobbed Xmel, Stk phenotype let alone the Staket phenotype. The rRNA precursor molecules transcribed from the Xmel, Stk rDNA genes seem to be correctly processed in both intraspecific (melanogaster) and interspecific (melanogaster-simulans) conditions. It is therefore suggested that the Xmel, Stk rDNA genes are inefficiently transcribed in the melanogaster-simulans hybrids.

Correction to: Leukemia (2014) 28, 1171–1174; doi:10.1038/leu.2014.16 Since the publication of this article, the authors have identified an error concerning one of the author names. D Proia should be listed as DA Proia. The corrected list is shown above. The Authors would like to apologise for any inconvenience this may have caused.