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Acetylation of the ɛ -amino group of a lysine residue was first discovered with histones in 1968, but the responsible enzymes, histone acetyltransferases and deacetylases, were not identified until the mid-1990s. In the past decade, knowledge about this modification has exploded, with targets rapidly expanding from histones to transcription factors and other nuclear proteins, and then to cytoskeleton, metabolic enzymes, and signaling regulators in the cytoplasm. Thus, protein lysine acetylation has emerged as a major post-translational modification to rival phosphorylation. In this issue of Oncogene , 19 articles review various aspects of the enzymes governing lysine acetylation, especially about their intimate links to cancer. To introduce the articles, we highlight here four central themes: (i) multisubunit enzymatic complexes; (ii) non-histone substrates in diverse cellular processes; (iii) interplay of lysine acetylation with other regulatory mechanisms, such as noncoding RNA-mediated gene silencing and activation; and (iv) novel therapeutic strategies and preventive measures to combat cancer and other human diseases.

Generating ion-photon entanglement is a crucial step for scalable trapped-ion quantum networks. To avoid the crosstalk on memory qubits carrying quantum information, it is common to use a different ion species for ion-photon entanglement generation such that the scattered photons are far off-resonant for the memory qubits. However, such a dual-species scheme can be subject to inefficient sympathetic cooling due to the mass mismatch of the ions. Here we demonstrate a trapped-ion quantum network node in the dual-type qubit scheme where two types of qubits are encoded in the S and F hyperfine structure levels of 171 Yb + ions. We generate ion photon entanglement for the S -qubit in a typical timescale of hundreds of milliseconds, and verify its small crosstalk on a nearby F -qubit with coherence time above seconds. Our work demonstrates an enabling function of the dual-type qubit scheme for scalable quantum networks. In ion-photon quantum network platforms, usually memory qubits and communication qubits are encoded in ions of different species. Here, instead, the authors show how to realise ion-photon entanglement within the same-species-dual-encoding scheme.

Two-dimensional (2D) ion crystals may represent a promising path to scale up qubit numbers for ion trap quantum information processing. However, to realize universal quantum computing in this system, individually addressed high-fidelity two-qubit entangling gates still remain challenging due to the inevitable micromotion of ions in a 2D crystal as well as the technical difficulty in 2D addressing. Here we demonstrate two-qubit entangling gates between any ion pairs in a 2D crystal of four ions. We use symmetrically placed crossed acousto-optic deflectors (AODs) to drive Raman transitions and achieve an addressing crosstalk error below 0.1%. We design and demonstrate a gate sequence by alternatingly addressing two target ions, making it compatible with any single-ion addressing techniques without crosstalk from multiple addressing beams. We further examine the gate performance versus the micromotion amplitude of the ions and show that its effect can be compensated by a recalibration of the laser intensity without degrading the gate fidelity. Our work paves the way for ion trap quantum computing with hundreds to thousands of qubits on a 2D ion crystal. Quantum gates in 2D ion crystals are more challenging than in 1D. Here, the authors use their 2D ion trap platform and acousto-optical deflectors to demonstrate a 2-qubit gate that can stand the ion micromotion in such configuration.

Although significant advances have recently been made in the diagnosis and treatment of cervical carcinoma, the long-term survival rate for advanced cervical cancer remains low. Therefore, an urgent need exists to both uncover the molecular mechanisms and identify potential therapeutic targets for the treatment of cervical cancer. MicroRNAs (miRNAs) have important roles in cancer progression and could be used as either potential therapeutic agents or targets. miR-506 is a component of an X chromosome-linked miRNA cluster. The biological functions of miR-506 have not been well established. In this study, we found that miR-506 expression was downregulated in approximately 80% of the cervical cancer samples examined and inversely correlated with the expression of Ki-67, a marker of cell proliferation. Gain-of-function and loss-of-function studies in human cervical cancer, Caski and SiHa cells, demonstrated that miR-506 acts as a tumor suppressor by inhibiting cervical cancer growth in vitro and in vivo . Further studies showed that miR-506 induced cell cycle arrest at the G1/S transition, and enhanced apoptosis and chemosensitivity of cervical cancer cell. We subsequently identified Gli3, a hedgehog pathway transcription factor, as a direct target of miR-506 in cervical cancer. Furthermore, Gli3 silencing recapitulated the effects of miR-506, and reintroduction of Gli3 abrogated miR-506-induced cell growth arrest and apoptosis. Taken together, we conclude that miR-506 exerts its anti-proliferative function by directly targeting Gli3. This newly identified miR-506/Gli3 axis provides further insight into the pathogenesis of cervical cancer and indicates a potential novel therapeutic agent for the treatment of cervical cancer.

Nitrous acid (HONO) plays a key role in atmospheric chemistry by influencing the budget of hydroxyl radical (OH). In this study, a two-month measurement of HONO and related quantities were analyzed during a biomass burning season in 2012 at a suburban site in the western Yangtze River delta, eastern China. An overall high HONO concentration with the mean value of 0.76 ppbv (0.01 ppbv to 5.95 ppbv) was observed. During biomass burning (BB) periods, both HONO concentration and HONO/NO2 ratio were enhanced significantly (more than a factor of 2, p < 0.01) compared with non-biomass burning (non-BB) periods. A correlation analysis showed that the HONO in BB plumes was more correlated with nitrogen dioxide (NO2) than that with potassium (a tracer of BB). Estimation by the method of potassium tracing suggests a maximum contribution of 17 ± 12% from BB emission to the observed HONO concentrations, and the other over 80% of the observed nighttime HONO concentrations during BB periods were secondarily produced by the heterogeneous conversion of NO2. The NO2-to-HONO conversion rate (CHONO) in BB plumes was almost twice as that in non-BB plumes (0.0062 hr−1 vs. 0.0032 hr−1). Given that the residence time of the BB air masses was lower than that of non-BB air masses, these results suggest BB aerosols have higher NO2 conversion potentials to form HONO than non-BB aerosols. A further analysis based on comparing the surface area at similar particle mass levels and HONO/NO2 ratios at similar surface area levels suggested larger specific surface areas and higher NO2 conversion efficiencies of BB aerosols. A mixed plume of BB and anthropogenic fossil fuel (FF) emissions was observed on 10 June with even higher HONO concentrations and HONO/NO2 ratios. The strong HONO production potential (high HONO/NO2 to PM2.5 ratio) was accompanied with a high sulfate concentration in this plume, suggesting a promotion of mixed aerosols to the HONO formation. In summary, our study suggests an important role of BB in atmospheric chemistry by affecting the HONO budget. This can be especially important in eastern China, where agricultural burning plumes are inevitably mixed with urban and industrial pollution.

The genus Microichthyurus Pic 1919 is first recorded here from mainland China. Four new species are described: M. flavicollissp. nov. (China, Guizhou), M. villosipessp. nov. (China, Chongqing), M. hubeiensissp. nov. (China, Hubei) and M. elongatussp. nov. (China, Yunnan). These new species are illustrated with habitus and genital segments of both sexes, and aedeagi and internal genitalia of females. The generic diagnosis is summarized and an identification key to all Chinese Microichthyurus species is provided.

Nanometer-thick passive films, which impart superior corrosion resistance to metals, are degraded in long-term service; they are also susceptible to chloride-induced localized attack. Here we show, by engineering crystallographic configurations upon metal matrices adjacent to their passive films, we obtain great enhancement of corrosion resistance of FeCr15Ni15 single crystal in sulphuric acid, with activation time up to two orders of magnitude longer than that of the non-engineered counterparts. Meanwhile, engineering crystallography decreases the passive current density and shifts the pitting potential to noble values. Applying anodic polarizations under a transpassivation potential, we make the metal matrices underneath the transpassive films highly uneven with {111}-terminated configurations, which is responsible for the enhancement of corrosion resistance. The transpassivation strategy also works in the commercial stainless steels where both grain interior and grain boundaries are rebuilt into the low-energy configurations. Our results demonstrate a technological implication in the pretreatment process of anti-corrosion engineering. Passive films on metal surfaces provide better corrosion resistance, but they can degrade in long-term service. Here the authors demonstrate a strategy to engineer crystallographic configuration at the metal/film interface to further improve corrosion resistance.

Since the beginning of the 1980s, 33 emerging tick-borne agents have been identified in mainland China, including eight species of spotted fever group rickettsiae, seven species in the family Anaplasmataceae, six genospecies in the complex Borrelia burgdorferi sensu lato, 11 species of Babesia, and the virus causing severe fever with thrombocytopenia syndrome. In this Review we have mapped the geographical distributions of human cases of infection. 15 of the 33 emerging tick-borne agents have been reported to cause human disease, and their clinical characteristics have been described. The non-specific clinical manifestations caused by tick-borne pathogens present a major diagnostic challenge and most physicians are unfamiliar with the many tick-borne diseases that present with non-specific symptoms in the early stages of the illness. Advances in and application of modern molecular techniques should help with identification of emerging tick-borne pathogens and improve laboratory diagnosis of human infections. We expect that more novel tick-borne infections in ticks and animals will be identified and additional emerging tick-borne diseases in human beings will be discovered.

Neuroendocrine prostate cancer (NEPC) has increasingly become a clinical challenge. The mechanisms by which neuroendocrine (NE) cells arises from prostate adenocarcinoma cells are poorly understood. FOXA1 is a transcription factor of the forkhead family that is required for prostate epithelial differentiation. In this study, we demonstrated that FOXA1 loss drives NE differentiation, demarcated by phenotypical changes and NEPC marker expressions. Mechanistically, this is mediated by FOXA1 binding to the promoter of interleukin 8 ( IL-8 ), a chemokine previously shown elevated in NEPC, to directly inhibit its expression. Further, IL-8 upregulation activates the MAPK/ERK pathway, leading to ERK phosphorylation and enolase 2 (ENO2) expression. IL-8 knockdown or ERK inhibition, on the other hand, abolished FOXA1 loss-induced NE differentiation. Analysis of xenograft mouse models confirmed FOXA1 loss in NEPC tumors relative to its adenocarcinoma counterparts. Importantly, FOXA1 is downregulated in human NEPC tumors compared to primary and castration-resistant prostate cancers, and its expression is negatively correlated with that of ENO2. These findings indicate that FOXA1 transcriptionally suppresses IL-8 , the expression of which would otherwise stimulate the MAPK/ERK pathway to promote NE differentiation of prostate cancer cells. Our data strongly suggest that FOXA1 loss may play a significant role in enabling prostate cancer progression to NEPC, whereas IL-8 and MAPK/ERK pathways may be promising targets for therapeutic intervention.