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Acknowledgements: The authors are grateful to the other members of the Boletta laboratory for useful discussions and to L. Tronci for helpful suggestions on data analysis. This work was supported by the Italian Ministry of Health (RF-2018-12368254; RF-2016-02361267 to A.B.; GR-2016-02364851 to C.P. and R.P.), the Italian association of patients with PKD (AIRP to A.B.), the PKD Foundation (218G18 to A.B.), the European Community (H-2020-MSCA-ITN-2019#SCiLS to A.B. and R.R.), by the Italian association for research on cancer (AIRC, IG2019-23513 to A.B.), by Q12 grant (MRC_MC_UU_12022/6 to C.F.), the European Research Council (ERC819920 to C.F.), and the CRUK Programme Foundation (Award C51061/A27453 to C.F.). The authors are grateful to S. Bramani for her continuous support. Part of this work was carried out in ALEMBIC, an advanced microscopy laboratory established by IRCCS Ospedale San Raffaele and Università Vita-Salute San Raffaele. Part of the present work was performed by M.E.S. and A.K.N. in fulfilment of the requirements for obtaining a PhD degree at Vita-Salute San Raffaele University, Milano, Italy., Funder: EC | EC Seventh Framework Programm | FP7 People: Marie-Curie Actions (FP7-PEOPLE - Specific Programme "People" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)); doi: https://doi.org/10.13039/100011264; Grant(s): H2020-MSCA-ITN-2019#SCiLS, H2020-MSCA-ITN-2019#SCiLS, Funder: EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)); doi: https://doi.org/10.13039/100011199; Grant(s): ERC819920, Depriving cells of nutrients triggers an energetic crisis, which is resolved by metabolic rewiring and organelle reorganization. Primary cilia are microtubule-based organelles at the cell surface, capable of integrating multiple metabolic and signalling cues, but their precise sensory function is not fully understood. Here we show that primary cilia respond to nutrient availability and adjust their length via glutamine-mediated anaplerosis facilitated by asparagine synthetase (ASNS). Nutrient deprivation causes cilia elongation, mediated by reduced mitochondrial function, ATP availability and AMPK activation independently of mTORC1. Of note, glutamine removal and replenishment is necessary and sufficient to induce ciliary elongation or retraction, respectively, under nutrient stress conditions both in vivo and in vitro by restoring mitochondrial anaplerosis via ASNS-dependent glutamate generation. Ift88-mutant cells lacking cilia show reduced glutamine-dependent mitochondrial anaplerosis during metabolic stress, due to reduced expression and activity of ASNS at the base of cilia. Our data indicate a role for cilia in responding to, and possibly sensing, cellular glutamine levels via ASNS during metabolic stress.

Although accumulating evidence has highlighted the molecular mechanisms by which hTERT promotes tumour cell invasion and metastasis, the molecular mechanisms of the properties enabling hTERT to contribute to invasion and metastasis have not been clearly illustrated. Here, we report that hTERT promotes gastric cancer invasion and metastasis by recruiting p50 to synergistically inhibit PLEKHA7 expression. We observed that the expression of PLEKHA7 in gastric cancer was significantly negatively associated with the TNM stage and lymphatic metastasis and that decreased PLEKHA7 expression dramatically increased invasion and metastasis in gastric cancer cells. Further mechanistic research showed that hTERT directly regulates PLEKHA7 expression by binding p50 and recruiting the hTERT/p50 complex to the PLEKHA7 promoter. Increased hTERT dramatically decreased PLEKHA7 expression and promoted invasion and metastasis in gastric cancer cells. The hTERT-mediated invasion/metastasis properties at least partially depended on PLEKHA7. Our work uncovers a novel molecular mechanism underlying invasion/metastasis in gastric cancer orchestrated by hTERT and p50.

Mangrove species are undergoing environmental changes from nutrient-poor to enrichment due to the large input of external nutrients. The potential difference in adaptive strategies between the slow- and fast-growing species may lead to great changes in species interaction and ecosystem stability. This study aims to test whether the slow-growing species Aegiceras corniculatum (L.) Blanco and Kandelia obovata Sheue, Liu & Yong sp. nov. are distinctly different from Laguncularia racemosa (L.) Gaertn. f. in response to soil nutrient enrichment. With the increase of soil nutrients, L. racemosa shifted from more conservative to more acquisitive strategy, which might be attributed to the increases in specific leaf area, nutrient resorption efficiency and photosynthesis capacity (indicated by the increase of leaf δ13C and unchanged leaf succulence), as well as the relocation of photosynthetic products (indicated by the shift towards fast-growing at the cost of constructive and defense compounds). In contrast, A. corniculatum and K. obovata maintained conservative strategies at any soil nutrient levels with only a slight increase in growth. These findings implied that L. racemosa will be more competitive over the other species in nutrient-rich soils.

Systemic inflammation plays an important role in cancer cachexia. However, among the systemic inflammatory biomarkers, it is unclear which has optimal prognostic value for cancer cachexia.The Kaplan-Meier method was used and the log-rank analysis was performed to estimate survival differences between groups. Cox proportional hazard regression analyses were conducted to assess independent risk factors for all-cause mortality.The C-reactive protein-to-albumin ratio (CAR) was the optimal prognostic assessment tool for patients with cancer cachexia, with 1-, 3-, and 5-year predictive powers of 0.650, 0.658, and 0.605, respectively. Patients with a high CAR had significantly lower survival rates than those with a low CAR. Moreover, CAR can differentiate the prognoses of patients with the same pathological stage. Cox proportional risk regression analyses showed that a high CAR was an independent risk factor for cancer cachexia. For every standard deviation increase in CAR, the risk of poor prognosis for patients with cancer cachexia was increased by 20% (hazard ratio = 1.200, 95% confidence interval = 1.132-1.273, P 0.001).CAR is an effective representative of systemic inflammation and a powerful factor for predicting the life function and clinical outcome of patients with cancer cachexia.

Copper-based catalyst is uniquely positioned to catalyze the hydrocarbon formations through electrochemical CO2 reduction. The catalyst design freedom is limited for alloying copper with H-affinitive elements represented by platinum group metals because the latter would easily drive the hydrogen evolution reaction to override CO2 reduction. We report an adept design of anchoring atomically dispersed platinum group metal species on both polycrystalline and shape-controlled Cu catalysts, which now promote targeted CO2 reduction reaction while frustrating the undesired hydrogen evolution reaction. Notably, alloys with similar metal formulations but comprising small platinum or palladium clusters would fail this objective. With an appreciable amount of CO-Pd1 moieties on copper surfaces, facile CO* hydrogenation to CHO* or CO-CHO* coupling is now viable as one of the main pathways on Cu(111) or Cu(100) to selectively produce CH4 or C2H4 through Pd-Cu dual-site pathways. The work broadens copper alloying choices for CO2 reduction in aqueous phases.

Manipulating spin polarization orientation is challenging but crucial for field-free spintronic devices. Although such manipulation has been demonstrated in a limited number of antiferromagnetic metal-based systems, the inevitable shunting effects from the metallic layer can reduce the overall device efficiency. In this study, we propose an antiferromagnetic insulator-based heterostructure NiO/Ta/Pt/Co/Pt for such spin polarization control without any shunting effect in the antiferromagnetic layer. We show that zero-field magnetization switching can be realized and is related to the out-of-plane component of spin polarization modulated by the NiO/Pt interface. The zero-field magnetization switching ratio can be effectively tuned by the substrates, in which the easy axis of NiO can be manipulated by the tensile or compressive strain from the substrates. Our work demonstrates that the insulating antiferromagnet based heterostructure is a promising platform to enhance the spin-orbital torque efficiency and achieve field-free magnetization switching, thus opening an avenue towards energy-efficient spintronic devices.