bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytokinin drives assembly of the phyllosphere microbiome and promotes disease resistance through structural and chemical cues
Authors: Gupta Rupali , Elkabetz Dorin , Leibman-Markus Meirav , Sayas Tali , Schneider Anat , Jami Elie , Kleiman Maya , Bar Maya 
Published: July 2021

Abstract
The plant hormone cytokinin (CK) is an important developmental regulator, promoting morphogenesis and delaying differentiation and senescence. From developmental processes, to growth, to stress tolerance, CKs are central in plant life. CKs are also known to mediate plant immunity and disease resistance, and several classes of microbes can also produce CKs, affecting the interaction with their plant hosts. While host species and genotype can be a driving force in shaping the plant microbiome, how plant developmental hormones such as CK can shape the microbiome is largely uninvestigated. Here, we examined the relationship between CK and the phyllosphere microbiome, finding that CK acts as a selective force in microbiome assembly, increasing richness, and promoting the presence of Firmicutes. CK-mediated immunity was found to partially depend on the microbial community, and bacilli isolated from previously described CK-rich plant genotypes, which overexpress a CK biosynthesis gene or have increased CK sensitivity, induced plant immunity, and promoted disease resistance. Using a biomimetic system, we investigated the relationship between the leaf microstructure, which is differentially patterned upon changes in CK content or signaling, and the growth of different phyllosphere microbes. We found that leaf structures derived from CK-rich plant genotypes support bacilli in the biomimetic system. CK was able to promote the growth, swarming, and biofilm formation of immunity inducing bacillus isolates in vitro. Overall, our results indicate that host genotype and hormonal profiles can act as a strong selective force in microbiome assembly, underlying differential immunity profiles, and pathogen resistance as a result.
PLEKHO2 inhibits TNFα-induced cell death by suppressing RIPK1 activation
Authors: Zhou Chenchen , Zhang Xueli , Yang Cuiping , He Yuan , Zhang Luo 
Published: July 2021

AbstractReceptor interaction protein kinase 1 (RIPK1) plays a diverse role in tumor necrosis factor α (TNFα) signalings. The ubiquitination of RIPK1 is essential for NF-κB activation, whereas its kinase activity promotes apoptosis and necroptosis. However, the mechanisms underlying have not been fully illuminated. Here we report that PH domain-containing family O member 2 (PLEKHO2) inhibits RIPK1-dependent cell death and is necessary for NF-κB activation in response to TNFα. Cells of PLKEHO2 deficiency are more susceptible to TNF-α induced apoptosis and necroptosis with increased RIPK1 activation, which is consistent with the observation that the susceptibility of PLEKHO2−/− cells is effectively prevented by treatment of RIPK1 kinase inhibitor. Moreover, PLEKHO2 deficient cells exhibit compromised RIPK1 ubiquitination and NF-κB activation in response to TNFα. Ultimately, PLEKHO2-deficient mice display greatly increased hepatotoxicity and lethality after TNFα-induced hepatitis. In summary, our study revealed that PLEKHO2 is a novel inhibitor of apoptosis and necroptosis, which plays a key role in regulating RIPK1 ubiquitination and activation
Melatonin inhibits triple-negative breast cancer progression through the Lnc049808-FUNDC1 pathway
Authors: Yang Anli , Peng Fu , Zhu Lewei , Li Xing , Ou Shunling , Huang Zhongying , Wu Song , Peng Cheng , Liu Peng , Kong Yanan 
Published: July 2021

AbstractMelatonin has been reported to have tumor-suppressive effects via comprehensive molecular mechanisms, and long non-coding RNAs (lncRNAs) may participate in this process. However, the mechanism by which melatonin affects the function of lncRNAs in triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, is still unknown. Therefore, we aimed to investigate the differentially expressed mRNAs and lncRNAs in melatonin-treated TNBC cells and the interaction mechanisms. Microarray analyses were performed to identify differentially expressed mRNAs and lncRNAs in TNBC cell lines after melatonin treatment. To explore the functions and underlying mechanisms of the mRNAs and lncRNAs candidates, a series of in vitro experiments were conducted, including CCK-8, Transwell, colony formation, luciferase reporter gene, and RNA immunoprecipitation (RIP) assays, and mouse xenograft models were established. We found that after melatonin treatment, FUNDC1 and lnc049808 downregulated in TNBC cell lines. Knockdown of FUNDC1 and lnc049808 inhibited TNBC cell proliferation, invasion, and metastasis. Moreover, lnc049808 and FUNDC1 acted as competing endogenous RNAs (ceRNAs) for binding to miR-101. These findings indicated that melatonin inhibited TNBC progression through the lnc049808-FUNDC1 pathway and melatonin could be used as a potential therapeutic agent for TNBC.
Recent advances in organic luminescent materials with narrowband emission
Authors: Ha Jung Min , Hur Seon Hyoung , Pathak Ambika , Jeong Ji-Eun , Woo Han Young 
Published: July 2021

AbstractThe International Telecommunication Union announced a new color gamut standard of broadcast service television (BT 2020) for ultra-high-definition TV in 2012. To satisfy the wide-color gamut standard of BT 2020, monochromatic red (R), green (G), and blue (B) emissions require a small full width at half-maximum, which is an important property for improving color purity. Although organic light-emitting diode (OLED) displays are currently one of the main types of display technologies, their broad emission via strong vibronic coupling between ground and excited states is a major hurdle to overcome in the development of next-generation wide-color gamut displays. Thus, the development of OLED emitters with narrowband R–G–B emissions is of great significance. In this review, the recent progress in the development of OLED materials with narrowband emission is summarized by grouping them into fluorescent, phosphorescent, and thermally activated delayed fluorescent emitters to reveal the correlation between molecular structures, optical properties, and device characteristics. We discuss rational molecular design strategies to achieve narrow photoluminescence and electroluminescence and the underlying mechanisms for controlling the emission bandwidth. Finally, the challenges in the realization of wide-color gamut OLED displays and the future prospects of such devices are discussed.
SARS-CoV-2 infection induces the dedifferentiation of multiciliated cells and impairs mucociliary clearance
Authors: Robinot Rémy , Hubert Mathieu , de Melo Guilherme Dias , Lazarini Françoise , Bruel Timothée , Smith Nikaïa , Levallois Sylvain , Larrous Florence , Fernandes Julien , Gellenoncourt Stacy , Rigaud Stéphane , Gorgette Olivier , Thouvenot Catherine , Trébeau Céline , Mallet Adeline , Duménil Guillaume , Gobaa Samy , Etournay Raphaël , Lledo Pierre-Marie , Lecuit Marc , Bourhy Hervé , Duffy Darragh , Michel Vincent , Schwartz Olivier , Chakrabarti Lisa A. 
Published: July 2021

AbstractUnderstanding how SARS-CoV-2 spreads within the respiratory tract is important to define the parameters controlling the severity of COVID-19. Here we examine the functional and structural consequences of SARS-CoV-2 infection in a reconstructed human bronchial epithelium model. SARS-CoV-2 replication causes a transient decrease in epithelial barrier function and disruption of tight junctions, though viral particle crossing remains limited. Rather, SARS-CoV-2 replication leads to a rapid loss of the ciliary layer, characterized at the ultrastructural level by axoneme loss and misorientation of remaining basal bodies. Downregulation of the master regulator of ciliogenesis Foxj1 occurs prior to extensive cilia loss, implicating this transcription factor in the dedifferentiation of ciliated cells. Motile cilia function is compromised by SARS-CoV-2 infection, as measured in a mucociliary clearance assay. Epithelial defense mechanisms, including basal cell mobilization and interferon-lambda induction, ramp up only after the initiation of cilia damage. Analysis of SARS-CoV-2 infection in Syrian hamsters further demonstrates the loss of motile cilia in vivo. This study identifies cilia damage as a pathogenic mechanism that could facilitate SARS-CoV-2 spread to the deeper lung parenchyma.
Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer
Authors: Prekovic Stefan , Schuurman Karianne , Mayayo-Peralta Isabel , Manjón Anna G. , Buijs Mark , Yavuz Selçuk , Wellenstein Max D. , Barrera Alejandro , Monkhorst Kim , Huber Anne , Morris Ben , Lieftink Cor , Chalkiadakis Theofilos , Alkan Ferhat , Silva Joana , Győrffy Balázs , Hoekman Liesbeth , van den Broek Bram , Teunissen Hans , Debets Donna O. , Severson Tesa , Jonkers Jos , Reddy Timothy , de Visser Karin E. , Faller William , Beijersbergen Roderick , Altelaar Maarten , de Wit Elzo , Medema Rene , Zwart Wilbert 
Published: July 2021

AbstractThe glucocorticoid receptor (GR) regulates gene expression, governing aspects of homeostasis, but is also involved in cancer. Pharmacological GR activation is frequently used to alleviate therapy-related side-effects. While prior studies have shown GR activation might also have anti-proliferative action on tumours, the underpinnings of glucocorticoid action and its direct effectors in non-lymphoid solid cancers remain elusive. Here, we study the mechanisms of glucocorticoid response, focusing on lung cancer. We show that GR activation induces reversible cancer cell dormancy characterised by anticancer drug tolerance, and activation of growth factor survival signalling accompanied by vulnerability to inhibitors. GR-induced dormancy is dependent on a single GR-target gene,CDKN1C, regulated through chromatin looping of a GR-occupied upstream distal enhancer in a SWI/SNF-dependent fashion. These insights illustrate the importance of GR signalling in non-lymphoid solid cancer biology, particularly in lung cancer, and warrant caution for use of glucocorticoids in treatment of anticancer therapy related side-effects.
A small molecule that induces translational readthrough of CFTR nonsense mutations by eRF1 depletion
Authors: Sharma Jyoti , Du Ming , Wong Eric , Mutyam Venkateshwar , Li Yao , Chen Jianguo , Wangen Jamie , Thrasher Kari , Fu Lianwu , Peng Ning , Tang Liping , Liu Kaimao , Mathew Bini , Bostwick Robert J. , Augelli-Szafran Corinne E. , Bihler Hermann , Liang Feng , Mahiou Jerome , Saltz Josef , Rab Andras , Hong Jeong , Sorscher Eric J. , Mendenhall Eric M. , Coppola Candice J. , Keeling Kim M. , Green Rachel , Mense Martin , Suto Mark J. , Rowe Steven M. , Bedwell David M. 
Published: July 2021

AbstractPremature termination codons (PTCs) prevent translation of a full-length protein and trigger nonsense-mediated mRNA decay (NMD). Nonsense suppression (also termed readthrough) therapy restores protein function by selectively suppressing translation termination at PTCs. Poor efficacy of current readthrough agents prompted us to search for better compounds. An NMD-sensitive NanoLuc readthrough reporter was used to screen 771,345 compounds. Among the 180 compounds identified with readthrough activity, SRI-37240 and its more potent derivative SRI-41315, induce a prolonged pause at stop codons and suppress PTCs associated with cystic fibrosis in immortalized and primary human bronchial epithelial cells, restoring CFTR expression and function. SRI-41315 suppresses PTCs by reducing the abundance of the termination factor eRF1. SRI-41315 also potentiates aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity. Combining readthrough agents that target distinct components of the translation machinery is a promising treatment strategy for diseases caused by PTCs.
Near-field thermophotovoltaics for efficient heat to electricity conversion at high power density
Authors: Mittapally Rohith , Lee Byungjun , Zhu Linxiao , Reihani Amin , Lim Ju Won , Fan Dejiu , Forrest Stephen R. , Reddy Pramod , Meyhofer Edgar 
Published: July 2021

AbstractThermophotovoltaic approaches that take advantage of near-field evanescent modes are being actively explored due to their potential for high-power density and high-efficiency energy conversion. However, progress towards functional near-field thermophotovoltaic devices has been limited by challenges in creating thermally robust planar emitters and photovoltaic cells designed for near-field thermal radiation. Here, we demonstrate record power densities of ~5 kW/m2 at an efficiency of 6.8%, where the efficiency of the system is defined as the ratio of the electrical power output of the PV cell to the radiative heat transfer from the emitter to the PV cell. This was accomplished by developing novel emitter devices that can sustain temperatures as high as 1270 K and positioning them into the near-field (<100 nm) of custom-fabricated InGaAs-based thin film photovoltaic cells. In addition to demonstrating efficient heat-to-electricity conversion at high power density, we report the performance of thermophotovoltaic devices across a range of emitter temperatures (~800 K–1270 K) and gap sizes (70 nm–7 µm). The methods and insights achieved in this work represent a critical step towards understanding the fundamental principles of harvesting thermal energy in the near-field.
Diffusion controls the ventilation of a Pacific Shadow Zone above abyssal overturning
Authors: Holzer Mark , DeVries Tim , de Lavergne Casimir 
Published: July 2021

AbstractMid-depth North Pacific waters are rich in nutrients and respired carbon accumulated over centuries. The rates and pathways with which these waters exchange with the surface ocean are uncertain, with divergent paradigms of the Pacific overturning: one envisions bottom waters upwelling to 1.5 km depth; the other confines overturning beneath a mid-depth Pacific shadow zone (PSZ) shielded from mean advection. Here global inverse modelling reveals a PSZ where mean ages exceed 1400 years with overturning beneath. The PSZ is supplied primarily by Antarctic and North-Atlantic ventilated waters diffusing from below and from the south. Half of PSZ waters re-surface in the Southern Ocean, a quarter in the subarctic Pacific. The abyssal North Pacific, despite strong overturning, has mean re-surfacing times also exceeding 1400 years because of diffusion into the overlying PSZ. These results imply that diffusive transports – distinct from overturning transports – are a leading control on Pacific nutrient and carbon storage.
Interplay and cooperation between SREBF1 and master transcription factors regulate lipid metabolism and tumor-promoting pathways in squamous cancer
Authors: Li Li-Yan , Yang Qian , Jiang Yan-Yi , Yang Wei , Jiang Yuan , Li Xiang , Hazawa Masaharu , Zhou Bo , Huang Guo-Wei , Xu Xiu-E , Gery Sigal , Zhang Ying , Ding Ling-Wen , Ho Allen S. , Zumsteg Zachary S. , Wang Ming-Rong , Fullwood Melissa J. , Freedland Stephen J. , Meltzer Stephen J. , Xu Li-Yan , Li En-Min , Koeffler H. Phillip , Lin De-Chen 
Published: July 2021

AbstractSquamous cell carcinomas (SCCs) comprise one of the most common histologic types of human cancer. Transcriptional dysregulation of SCC cells is orchestrated by tumor protein p63 (TP63), a master transcription factor (TF) and a well-researched SCC-specific oncogene. In the present study, both Gene Set Enrichment Analysis (GSEA) of SCC patient samples and in vitro loss-of-function assays establish fatty-acid metabolism as a key pathway downstream of TP63. Further studies identify sterol regulatory element binding transcription factor 1 (SREBF1) as a central mediator linking TP63 with fatty-acid metabolism, which regulates the biosynthesis of fatty-acids, sphingolipids (SL), and glycerophospholipids (GPL), as revealed by liquid chromatography tandem mass spectrometry (LC-MS/MS)-based lipidomics. Moreover, a feedback co-regulatory loop consisting of SREBF1/TP63/Kruppel like factor 5 (KLF5) is identified, which promotes overexpression of all three TFs in SCCs. Downstream of SREBF1, a non-canonical, SCC-specific function is elucidated: SREBF1 cooperates with TP63/KLF5 to regulate hundreds of cis-regulatory elements across the SCC epigenome, which converge on activating cancer-promoting pathways. Indeed, SREBF1 is essential for SCC viability and migration, and its overexpression is associated with poor survival in SCC patients. Taken together, these data shed light on mechanisms of transcriptional dysregulation in cancer, identify specific epigenetic regulators of lipid metabolism, and uncover SREBF1 as a potential therapeutic target and prognostic marker in SCC.
Si-C is a method for inferring super-resolution intact genome structure from single-cell Hi-C data
Authors: Meng Luming , Wang Chenxi , Shi Yi , Luo Qiong 
Published: July 2021

AbstractThere is a strong demand for methods that can efficiently reconstruct valid super-resolution intact genome 3D structures from sparse and noise single-cell Hi-C data. Here, we develop Single-Cell Chromosome Conformation Calculator (Si-C) within the Bayesian theory framework and apply this approach to reconstruct intact genome 3D structures from single-cell Hi-C data of eight G1-phase haploid mouse ES cells. The inferred 100-kb and 10-kb structures consistently reproduce the known conserved features of chromatin organization revealed by independent imaging experiments. The analysis of the 10-kb resolution 3D structures reveals cell-to-cell varying domain structures in individual cells and hyperfine structures in domains, such as loops. An average of 0.2 contact reads per divided bin is sufficient for Si-C to obtain reliable structures. The valid super-resolution structures constructed by Si-C demonstrate the potential for visualizing and investigating interactions between all chromatin loci at the genome scale in individual cells.
Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage
Authors: Wu Xiao , Wang Bin 
Published: July 2021

AbstractAlthough homologous recombination (HR) is indicated as a high-fidelity repair mechanism, break-induced replication (BIR), a subtype of HR, is a mutagenic mechanism that leads to chromosome rearrangements. It remains poorly understood how cells suppress mutagenic BIR. Trapping of Topoisomerase 1 by camptothecin (CPT) in a cleavage complex on the DNA can be transformed into single-ended double-strand breaks (seDSBs) upon DNA replication or colliding with transcriptional machinery. Here, we demonstrate a role of Abraxas in limiting seDSBs undergoing BIR-dependent mitotic DNA synthesis. Through counteracting K63-linked ubiquitin modification, Abraxas restricts SLX4/Mus81 recruitment to CPT damage sites for cleavage and subsequent resection processed by MRE11 endonuclease, CtIP, and DNA2/BLM. Uncontrolled SLX4/MUS81 loading and excessive end resection due to Abraxas-deficiency leads to increased mitotic DNA synthesis via RAD52- and POLD3- dependent, RAD51-independent BIR and extensive chromosome aberrations. Our work implicates Abraxas/BRCA1-A complex as a critical regulator that restrains BIR for protection of genome stability.
GazeBase, a large-scale, multi-stimulus, longitudinal eye movement dataset
Authors: Griffith Henry , Lohr Dillon , Abdulin Evgeny , Komogortsev Oleg 
Published: July 2021

AbstractThis manuscript presents GazeBase, a large-scale longitudinal dataset containing 12,334 monocular eye-movement recordings captured from 322 college-aged participants. Participants completed a battery of seven tasks in two contiguous sessions during each round of recording, including a – (1) fixation task, (2) horizontal saccade task, (3) random oblique saccade task, (4) reading task, (5/6) free viewing of cinematic video task, and (7) gaze-driven gaming task. Nine rounds of recording were conducted over a 37 month period, with participants in each subsequent round recruited exclusively from prior rounds. All data was collected using an EyeLink 1000 eye tracker at a 1,000 Hz sampling rate, with a calibration and validation protocol performed before each task to ensure data quality. Due to its large number of participants and longitudinal nature, GazeBase is well suited for exploring research hypotheses in eye movement biometrics, along with other applications applying machine learning to eye movement signal analysis. Classification labels produced by the instrument’s real-time parser are provided for a subset of GazeBase, along with pupil area.
A database of submarine landslides offshore West and Southwest Iberia
Authors: Gamboa Davide , Omira Rachid , Terrinha Pedro 
Published: July 2021

AbstractSubmarine landslides are major geohazards occurring on distinct seabed domains ranging from shallow coastal areas to the deeper points of the ocean. The nature and relief of the seabed are key factors influencing the location and size of submarine landslides. Efforts have recently been made to compile databases of submarine landslide distribution and morphometry, a crucial task to assess submarine geohazards. The MAGICLAND (Marine Geo-hazards Induced by underwater Landslides in the SW Iberian Margin) database here presented contributed to that assessment offshore Portugal. Based on EMODnet bathymetric DEMs and GIS analysis, the morphometric properties of 1552 submarine landslides were analysed and wealth of 40 parameters was obtained. This dataset is now made available for the free use and benefit of the international marine community. Further contributions or analysis based on, and complementing the MAGICLAND database will be welcome.
Clinical characteristics of optic neuritis phenotypes in a 3-year follow-up Chinese cohort
Authors: Feng Chaoyi , Chen Qian , Zhao Guixian , Li Zhenxin , Chen Weimin , Sha Yan , Sun Xinghuai , Wang Min , Tian Guohong 
Published: July 2021

AbstractTo evaluate the clinical characteristics of optic neuritis (ON) with different phenotypes. This prospective study recruited patients with new-onset ON between January 2015 and March 2017 who were followed-up for 3 years. They were divided into the myelin oligodendrocyte glycoprotein-seropositive (MOG-ON), aquaporin-4-seropositive (AQP4-ON), and double-seronegative (seronegative-ON) groups, and their clinical characteristics and imaging findings were evaluated and compared. Two-hundred-eighty patients (405 eyes) were included (MOG-ON: n = 57, 20.4%; AQP4-ON: n = 98, 35.0%; seronegative-ON: n = 125, 44.6%). The proportion of eyes with best-corrected visual acuity > 20/25 at the 3-year follow-up was similar between the MOG-ON and seronegative-ON groups; the proportion in both groups was higher than that in the AQP4-ON group (p < 0.001). Relapse rates were higher in the MOG-ON and AQP4-ON groups than in the seronegative-ON group (p < 0.001). Average retinal nerve fiber layer (RNFL) thickness at 3 years was similar between the MOG-ON and AQP4-ON groups (63.41 ± 13.39 and 59.40 ± 11.46 μm, p = 0.476) but both were thinner than the seronegative-ON group (74.06 ± 11.14 μm, p < 0.001). Macular ganglion cell-inner plexiform layer (GCIPL) revealed the same pattern. Despite RNFL and GCIPL thinning, the MOG-ON group’s outcome was as favorable as that of the seronegative-ON group, whereas the AQP4-ON group showed unsatisfactory results.