Xiaotong Li, Minmin Hou, Su Jiang, Ian T. Cousins, Pengfei Li, Yali Shi, Yaqi Cai, Guibin Jiang
The occurrence of per- and polyfluoroalkyl substances (PFAS) in Antarctica has been previously reported; however, the mechanisms of their inland penetration and the interplay between their depositional histories and interhemispheric transport remain unclear. Here, PFAS in snow along a transect across East Antarctica (from Zhongshan Station to Dome A) and depositional records at Dome A were studied to elucidate the sources and transport of PFAS and to reconstruct the historical emission record. Our findings suggest that precursor degradation and sea spray aerosol are the main sources of PFAS and play a pivotal role in the regional and seasonal variability of PFAS accumulation. The half-century depositional records reveal connections between Antarctica and distant sources. We propose the hemispheric and interhemispheric transport of PFAS from source regions to Antarctica, where they are deposited.
{"title":"Atmospheric transport and deposition of PFAS in East Antarctica: Evidence from snow transect measurements and a multidecadal record","authors":"Xiaotong Li, Minmin Hou, Su Jiang, Ian T. Cousins, Pengfei Li, Yali Shi, Yaqi Cai, Guibin Jiang","doi":"10.1126/sciadv.adz4749","DOIUrl":"https://doi.org/10.1126/sciadv.adz4749","url":null,"abstract":"The occurrence of per- and polyfluoroalkyl substances (PFAS) in Antarctica has been previously reported; however, the mechanisms of their inland penetration and the interplay between their depositional histories and interhemispheric transport remain unclear. Here, PFAS in snow along a transect across East Antarctica (from Zhongshan Station to Dome A) and depositional records at Dome A were studied to elucidate the sources and transport of PFAS and to reconstruct the historical emission record. Our findings suggest that precursor degradation and sea spray aerosol are the main sources of PFAS and play a pivotal role in the regional and seasonal variability of PFAS accumulation. The half-century depositional records reveal connections between Antarctica and distant sources. We propose the hemispheric and interhemispheric transport of PFAS from source regions to Antarctica, where they are deposited.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"51 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Babak Bakhit, Xiao Xie, Simon M. Fairclough, Atif Jan, Ingemar Persson, Giuliana Di Martino, Bonan Zhu, Caterina Ducati, Quanxi Jia, Bilge Yildiz, Andrew J. Flewitt, Judith L. MacManus-Driscoll
The escalating energy consumption of existing artificial intelligence hardware has become a serious global issue that demands immediate action. Neuromorphic computing offers promises to drastically reduce this footprint. Here, we introduce multicomponent p-type Hf(Sr,Ti)O 2 thin films for energy-efficient, resistive switching–based neuromorphic devices. We demonstrate interfacial memristors with ultralow switching currents (≤~10 −8 A), exceptional cycle-to-cycle and device-to-device uniformities, and retention >10 5 s. They reveal hundreds of ultralow conductance levels with a modulation range of >50 (without reaching any saturation) and reproducibly satisfy unsupervised learning rules. This performance originates from incorporating a self-assembled p-n heterointerface between p-type Hf(Sr,Ti)O 2 and n-type TiO x N y , resulting in a fully depleted space-charge layer asymmetrically extended into Hf(Sr,Ti)O 2 , a large built-in potential, and extremely low saturation current density under reverse bias. Ultralow conductance modulation is controlled by tuning p-n heterointerface’s energy-barrier height through electro-ionic charge migration. This materials-engineering strategy addresses energy consumption and variability in existing memristors, opening a pathway toward energy-efficient neuromorphic computing systems.
现有人工智能硬件不断升级的能耗已经成为一个严重的全球性问题，需要立即采取行动。神经形态计算提供了大幅减少这种足迹的承诺。在这里，我们介绍了多组分p型Hf(Sr,Ti) o2薄膜，用于节能，电阻开关型神经形态器件。我们展示了具有超低开关电流（≤~10−8 A），出色的周期到周期和器件到器件均匀性以及保持时间为10.5 s的接口记忆电阻器。他们揭示了数百个超低电导水平，调制范围为>；50（没有达到任何饱和），并可重复地满足无监督学习规则。这种性能源于在p型Hf(Sr,Ti) o2和N型TiO x N y之间引入自组装的p-n异质界面，导致完全耗尽的空间电荷层不对称地扩展为Hf(Sr,Ti) o2，具有较大的内置电位，并且在反向偏压下具有极低的饱和电流密度。超低电导调制是通过电子-离子电荷迁移调节p-n异质界面的能垒高度来实现的。这种材料工程策略解决了现有忆阻器的能源消耗和可变性，为节能的神经形态计算系统开辟了一条道路。
{"title":"HfO 2 -based memristive synapses with asymmetrically extended p-n heterointerfaces for highly energy-efficient neuromorphic hardware","authors":"Babak Bakhit, Xiao Xie, Simon M. Fairclough, Atif Jan, Ingemar Persson, Giuliana Di Martino, Bonan Zhu, Caterina Ducati, Quanxi Jia, Bilge Yildiz, Andrew J. Flewitt, Judith L. MacManus-Driscoll","doi":"10.1126/sciadv.aec2324","DOIUrl":"https://doi.org/10.1126/sciadv.aec2324","url":null,"abstract":"The escalating energy consumption of existing artificial intelligence hardware has become a serious global issue that demands immediate action. Neuromorphic computing offers promises to drastically reduce this footprint. Here, we introduce multicomponent p-type Hf(Sr,Ti)O <jats:sub>2</jats:sub> thin films for energy-efficient, resistive switching–based neuromorphic devices. We demonstrate interfacial memristors with ultralow switching currents (≤~10 <jats:sup>−8</jats:sup> A), exceptional cycle-to-cycle and device-to-device uniformities, and retention >10 <jats:sup>5</jats:sup> s. They reveal hundreds of ultralow conductance levels with a modulation range of >50 (without reaching any saturation) and reproducibly satisfy unsupervised learning rules. This performance originates from incorporating a self-assembled p-n heterointerface between p-type Hf(Sr,Ti)O <jats:sub>2</jats:sub> and n-type TiO <jats:sub>x</jats:sub> N <jats:sub>y</jats:sub> , resulting in a fully depleted space-charge layer asymmetrically extended into Hf(Sr,Ti)O <jats:sub>2</jats:sub> , a large built-in potential, and extremely low saturation current density under reverse bias. Ultralow conductance modulation is controlled by tuning p-n heterointerface’s energy-barrier height through electro-ionic charge migration. This materials-engineering strategy addresses energy consumption and variability in existing memristors, opening a pathway toward energy-efficient neuromorphic computing systems.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"6 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paulina Podszywałow-Bartnicka, Morgan Shine, Jing Lin, Karla M. Neugebauer
Cellular stresses regulate transcriptional readthrough, whereby RNA polymerase II elongates past a gene’s polyadenylation cleavage site without RNA cleavage. Readthrough has been reported in several cancer types. Here, we use long-read sequencing of nascent RNA to quantify transcriptional readthrough in chronic myeloid leukemia (CML) cells and characterize early responses to the targeted therapeutic, imatinib. We show that the amount, length, and gene specificity of readthrough increase within 1 hour, before gene expression and alternative splicing alterations emerge. Notably, imatinib-dependent messenger RNA (mRNA) isoform changes involved “readthrough chimeras,” in which exons from an upstream gene are alternatively spliced to exons in a downstream gene. Altered mRNA isoforms and chimera levels were detected in imatinib-resistant K562 cells as well as cells of patients with CML. Thus, imatinib can provoke a cascade of early changes to transcription and splicing fidelity that may lead to longer-term adjustments in gene expression, cancer cell differentiation, and the development of therapy resistance.
{"title":"Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib","authors":"Paulina Podszywałow-Bartnicka, Morgan Shine, Jing Lin, Karla M. Neugebauer","doi":"10.1126/sciadv.aea2475","DOIUrl":"https://doi.org/10.1126/sciadv.aea2475","url":null,"abstract":"Cellular stresses regulate transcriptional readthrough, whereby RNA polymerase II elongates past a gene’s polyadenylation cleavage site without RNA cleavage. Readthrough has been reported in several cancer types. Here, we use long-read sequencing of nascent RNA to quantify transcriptional readthrough in chronic myeloid leukemia (CML) cells and characterize early responses to the targeted therapeutic, imatinib. We show that the amount, length, and gene specificity of readthrough increase within 1 hour, before gene expression and alternative splicing alterations emerge. Notably, imatinib-dependent messenger RNA (mRNA) isoform changes involved “readthrough chimeras,” in which exons from an upstream gene are alternatively spliced to exons in a downstream gene. Altered mRNA isoforms and chimera levels were detected in imatinib-resistant K562 cells as well as cells of patients with CML. Thus, imatinib can provoke a cascade of early changes to transcription and splicing fidelity that may lead to longer-term adjustments in gene expression, cancer cell differentiation, and the development of therapy resistance.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"24 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Akram Abbasi, Alec McCall, Zhaowei Jiang, Brian W. LeBlanc, Anita Shukla
Wound infections are becoming increasingly difficult to treat due to rising antibiotic-resistant bacteria. β-Lactamase–producing bacteria are among the most common pathogens implicated in these infections. Here, we report a bacterial enzyme-responsive hydrogel formulated with a cephalosporin-derived, β-lactamase–cleavable crosslinker that undergoes selective degradation in the presence of bacterial β-lactamases. This degradation triggers the on-demand release of encapsulated ciprofloxacin-loaded liposomes, ensuring that antibiotic delivery occurs only at the site of infection. This selective degradation and release was demonstrated in both ex vivo and in vivo models of Pseudomonas aeruginosa wound infections. In a murine skin abrasion infection model, a single application of the hydrogel led to complete bacterial eradication and enhanced wound healing, outperforming a commercial silver-based hydrogel wound dressing. These responsive hydrogels did not induce ciprofloxacin resistance in non–β-lactamase–producing bacteria. These findings demonstrate that β-lactamase–responsive hydrogels provide a precise, infection-triggered antibiotic delivery platform that can improve the treatment of wound infections and mitigate antimicrobial resistance.
{"title":"Bacterial enzyme-responsive hydrogels for triggered delivery of antibiotics to infected wounds","authors":"Akram Abbasi, Alec McCall, Zhaowei Jiang, Brian W. LeBlanc, Anita Shukla","doi":"10.1126/sciadv.adz0786","DOIUrl":"https://doi.org/10.1126/sciadv.adz0786","url":null,"abstract":"Wound infections are becoming increasingly difficult to treat due to rising antibiotic-resistant bacteria. β-Lactamase–producing bacteria are among the most common pathogens implicated in these infections. Here, we report a bacterial enzyme-responsive hydrogel formulated with a cephalosporin-derived, β-lactamase–cleavable crosslinker that undergoes selective degradation in the presence of bacterial β-lactamases. This degradation triggers the on-demand release of encapsulated ciprofloxacin-loaded liposomes, ensuring that antibiotic delivery occurs only at the site of infection. This selective degradation and release was demonstrated in both ex vivo and in vivo models of <jats:italic toggle=\"yes\">Pseudomonas aeruginosa</jats:italic> wound infections. In a murine skin abrasion infection model, a single application of the hydrogel led to complete bacterial eradication and enhanced wound healing, outperforming a commercial silver-based hydrogel wound dressing. These responsive hydrogels did not induce ciprofloxacin resistance in non–β-lactamase–producing bacteria. These findings demonstrate that β-lactamase–responsive hydrogels provide a precise, infection-triggered antibiotic delivery platform that can improve the treatment of wound infections and mitigate antimicrobial resistance.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"146 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yun Hyeok Lee, Seung Won Moon, Min-Gyu Lee, Won Jun Song, Seong-Yu Choi, Gimin Sung, Yong Eun Cho, Junhyun Choi, Byung Ik Park, Younghoon Lee, Ho-Young Kim, Jeong-Yun Sun
Dielectric elastomer actuators (DEAs) are promising soft transducers capable of rapid and precise actuation. However, their conventional architecture for efficient actuation confines DEAs in predesigned operational modes, leading to limited applications. Here, we introduce a reconfigurable DEA system using phase-transitional ferrofluid (PTF) electrodes. PTF switches its states between solid and liquid, satisfying requirements for a reconfigurable electrode for DEAs. In the sol state, the stable and high magnetic responsiveness inspired by ferrofluid and the low viscosity achieved through plasticization collectively enable dynamic reconfiguration of the electrode. In the gel state, PTF ensures stable shape retention and exhibits reduced interfacial slip during DEA actuation. This reconfigurable nature greatly increases adaptability and ensures continuous operation even when electrodes undergo disconnection or dielectric failure. Moreover, the PTF electrodes can be retrieved and reused after actuation, demonstrating their excellent recyclability. The combination of mechanical compliance, magnetic reconfigurability, and material sustainability renders the PTF a versatile electrode strategy for next-generation reconfigurable electroactive systems.
{"title":"A reconfigurable dielectric elastomer actuator via phase-transitional ferrofluid enables sustainable operation","authors":"Yun Hyeok Lee, Seung Won Moon, Min-Gyu Lee, Won Jun Song, Seong-Yu Choi, Gimin Sung, Yong Eun Cho, Junhyun Choi, Byung Ik Park, Younghoon Lee, Ho-Young Kim, Jeong-Yun Sun","doi":"10.1126/sciadv.aeb7409","DOIUrl":"https://doi.org/10.1126/sciadv.aeb7409","url":null,"abstract":"Dielectric elastomer actuators (DEAs) are promising soft transducers capable of rapid and precise actuation. However, their conventional architecture for efficient actuation confines DEAs in predesigned operational modes, leading to limited applications. Here, we introduce a reconfigurable DEA system using phase-transitional ferrofluid (PTF) electrodes. PTF switches its states between solid and liquid, satisfying requirements for a reconfigurable electrode for DEAs. In the sol state, the stable and high magnetic responsiveness inspired by ferrofluid and the low viscosity achieved through plasticization collectively enable dynamic reconfiguration of the electrode. In the gel state, PTF ensures stable shape retention and exhibits reduced interfacial slip during DEA actuation. This reconfigurable nature greatly increases adaptability and ensures continuous operation even when electrodes undergo disconnection or dielectric failure. Moreover, the PTF electrodes can be retrieved and reused after actuation, demonstrating their excellent recyclability. The combination of mechanical compliance, magnetic reconfigurability, and material sustainability renders the PTF a versatile electrode strategy for next-generation reconfigurable electroactive systems.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"9 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wei Xie, Laura Wyckaert, Mike Vadi, Bruno Verstraeten, Tatyana Divert, Jef Haerinck, Riet De Rycke, Femke Baeke, Mohamed Lamkanfi, Geert Berx, Adam Wahida, Peter Vandenabeele
Aberrant intestinal epithelial cell (IEC) death is common in inflammatory bowel disease (IBD) and related animal models. While various cell death pathways contribute to disease, the dominant modalities and their regulatory mechanisms in intestinal inflammation remain ill defined. Using the DSS colitis model, we examined the contribution of apoptosis ( Casp3/7 Δ IEC ), necroptosis ( Mlkl Δ IEC ), pyroptosis ( Gsdme Δ IEC , Gsdmd −/− ) , and ferroptosis ( Gpx4i Δ IEC ) in IECs. Mice lacking caspase-3/7 in IECs showed worsened colitis, higher mortality, and impaired regeneration, not seen in the other transgenic mice. Caspase-3/7 deficiency in IECs hindered stem cell proliferation and increased inflammatory cell death, disrupting barrier integrity and delaying recovery. Despite heightened inflammation, Casp3/7 Δ IEC mice had reduced tumor formation in the AOM/DSS-induced colorectal cancer model. These findings highlight a protective role for caspase-3/7 in controlling inflammation and tissue regeneration, while promoting tumorigenesis following intestinal injury, and suggest modulation of caspase-3/7 as a promising therapeutic strategy in IBD and colorectal cancer.
{"title":"Caspase-3/7 deficiency results in enhanced intestinal inflammation and reduced tumorigenesis","authors":"Wei Xie, Laura Wyckaert, Mike Vadi, Bruno Verstraeten, Tatyana Divert, Jef Haerinck, Riet De Rycke, Femke Baeke, Mohamed Lamkanfi, Geert Berx, Adam Wahida, Peter Vandenabeele","doi":"10.1126/sciadv.adz5906","DOIUrl":"https://doi.org/10.1126/sciadv.adz5906","url":null,"abstract":"Aberrant intestinal epithelial cell (IEC) death is common in inflammatory bowel disease (IBD) and related animal models. While various cell death pathways contribute to disease, the dominant modalities and their regulatory mechanisms in intestinal inflammation remain ill defined. Using the DSS colitis model, we examined the contribution of apoptosis ( <jats:italic toggle=\"yes\">Casp3/7</jats:italic> <jats:sup> Δ <jats:italic toggle=\"yes\">IEC</jats:italic> </jats:sup> ), necroptosis ( <jats:italic toggle=\"yes\">Mlkl</jats:italic> <jats:sup> Δ <jats:italic toggle=\"yes\">IEC</jats:italic> </jats:sup> ), pyroptosis ( <jats:italic toggle=\"yes\">Gsdme</jats:italic> <jats:sup> Δ <jats:italic toggle=\"yes\">IEC</jats:italic> </jats:sup> , <jats:italic toggle=\"yes\"> Gsdmd <jats:sup>−/−</jats:sup> ) </jats:italic> , and ferroptosis ( <jats:italic toggle=\"yes\">Gpx4</jats:italic> <jats:sup> <jats:italic toggle=\"yes\">i</jats:italic> Δ <jats:italic toggle=\"yes\">IEC</jats:italic> </jats:sup> ) in IECs. Mice lacking caspase-3/7 in IECs showed worsened colitis, higher mortality, and impaired regeneration, not seen in the other transgenic mice. Caspase-3/7 deficiency in IECs hindered stem cell proliferation and increased inflammatory cell death, disrupting barrier integrity and delaying recovery. Despite heightened inflammation, <jats:italic toggle=\"yes\">Casp3/7</jats:italic> <jats:sup> Δ <jats:italic toggle=\"yes\">IEC</jats:italic> </jats:sup> mice had reduced tumor formation in the AOM/DSS-induced colorectal cancer model. These findings highlight a protective role for caspase-3/7 in controlling inflammation and tissue regeneration, while promoting tumorigenesis following intestinal injury, and suggest modulation of caspase-3/7 as a promising therapeutic strategy in IBD and colorectal cancer.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"16 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kyle R. Barrie, Sarah Körber, Ingrid Billault-Chaumartin, Malgorzata Boczkowska, Peter J. Carman, Omar El Hamoui, Johan Peränen, Guillaume Romet-Lemonne, Antoine Jégou, Pekka Lappalainen, Roberto Dominguez
Capping protein (CP) regulates actin-based motility by blocking monomer exchange at the filament barbed end. Several proteins, including CARMIL, bind CP and allosterically weaken its affinity for the barbed end. CARMIL comprises pleckstrin homology (PH), leucine-rich repeat (LRR), helical dimerization (HD), CP-binding region (CBR), and proline-rich (PR) domains, but their roles in CP regulation remain unclear. We show that CARMIL1 is partially autoinhibited, with CBR (CARMIL1 961–1046 ) displaying greater uncapping activity than CARMIL1 1–1046 . A structure of CP-bound CARMIL1 1–1046 reveals a dimeric assembly, with PH-LRR on a plane flanked by HD and CBR-bound CP. A motif connecting HD to CBR-CP, the “antenna,” binds at the dimer LRR-LRR interface. An antenna mutant disrupting this interaction partially relieves autoinhibition in vitro. In CARMIL1 knockout cells, expression of the antenna mutant increases cell area, while deleting the myosin-I–binding PR domain induces membrane spikes. The results inform mechanisms of CARMIL dimerization, autoinhibition, and coordination of CP and myosin-I activities in cells.
{"title":"Mechanisms of CARMIL dimerization, autoinhibition, and capping protein binding","authors":"Kyle R. Barrie, Sarah Körber, Ingrid Billault-Chaumartin, Malgorzata Boczkowska, Peter J. Carman, Omar El Hamoui, Johan Peränen, Guillaume Romet-Lemonne, Antoine Jégou, Pekka Lappalainen, Roberto Dominguez","doi":"10.1126/sciadv.aeb4543","DOIUrl":"https://doi.org/10.1126/sciadv.aeb4543","url":null,"abstract":"Capping protein (CP) regulates actin-based motility by blocking monomer exchange at the filament barbed end. Several proteins, including CARMIL, bind CP and allosterically weaken its affinity for the barbed end. CARMIL comprises pleckstrin homology (PH), leucine-rich repeat (LRR), helical dimerization (HD), CP-binding region (CBR), and proline-rich (PR) domains, but their roles in CP regulation remain unclear. We show that CARMIL1 is partially autoinhibited, with CBR (CARMIL1 <jats:sub>961–1046</jats:sub> ) displaying greater uncapping activity than CARMIL1 <jats:sub>1–1046</jats:sub> . A structure of CP-bound CARMIL1 <jats:sub>1–1046</jats:sub> reveals a dimeric assembly, with PH-LRR on a plane flanked by HD and CBR-bound CP. A motif connecting HD to CBR-CP, the “antenna,” binds at the dimer LRR-LRR interface. An antenna mutant disrupting this interaction partially relieves autoinhibition in vitro. In CARMIL1 knockout cells, expression of the antenna mutant increases cell area, while deleting the myosin-I–binding PR domain induces membrane spikes. The results inform mechanisms of CARMIL dimerization, autoinhibition, and coordination of CP and myosin-I activities in cells.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Spin-phonon interactions are known to drive magnetic relaxation in solid-state systems but are generally overlooked as a contribution to spin decoherence through dephasing. Here, we extend quantum master equations to account for coherence terms and describe the full effect of up to two-phonon processes on spin dynamics. We implement this method fully ab initio for a molecule with large magnetization blocking temperature and show that, although strong axial magnetic anisotropy ensures slow magnetic relaxation approaching seconds at 77 kelvins, the superposition of Kramers doublets is coherent for less than 10 nanoseconds due to a two-phonon pure dephasing mechanism. This process, in principle, applies to any quantum system interacting with a thermal bath of phonons, advancing our understanding of quantum decoherence in solid-state systems.
{"title":"A unified ab initio theory of spin-phonon relaxation and decoherence uncovers fast dephasing in magnetic molecules","authors":"Alessandro Lunghi","doi":"10.1126/sciadv.aeb3868","DOIUrl":"https://doi.org/10.1126/sciadv.aeb3868","url":null,"abstract":"Spin-phonon interactions are known to drive magnetic relaxation in solid-state systems but are generally overlooked as a contribution to spin decoherence through dephasing. Here, we extend quantum master equations to account for coherence terms and describe the full effect of up to two-phonon processes on spin dynamics. We implement this method fully ab initio for a molecule with large magnetization blocking temperature and show that, although strong axial magnetic anisotropy ensures slow magnetic relaxation approaching seconds at 77 kelvins, the superposition of Kramers doublets is coherent for less than 10 nanoseconds due to a two-phonon pure dephasing mechanism. This process, in principle, applies to any quantum system interacting with a thermal bath of phonons, advancing our understanding of quantum decoherence in solid-state systems.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"13 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The superconductor-insulator transition in two-dimensional (2D) systems has been extensively studied as a typical example of quantum phase transition. Recent investigations of highly conductive 2D systems have revealed an intervening metallic regime, in which the electrical resistivity saturates at the limit of zero temperature. The nature and origin of this metallicity remain debated, partly because of the lack of microscopic understanding. In this study, using scanning tunneling spectroscopy, we investigate the metallic state and other phases observed in crystalline Pb monoatomic-layer superconductors formed on vicinal semiconducting substrates. Our spectroscopic images reveal stable and isolated vortices in the metallic regime, distinct from delocalized or liquidized vortices. These findings suggest that the saturated resistance in the metallic state arises from the pinning-free vortex motion driven by the finite current applied for the transport measurements. Our disorder-controlled microscopic experiments provide new insights into the fluctuation-induced phases of ultrathin crystalline 2D superconductors.
{"title":"Stable vortices in the anomalous metallic state observed on monoatomic-layer superconductors","authors":"Yudai Sato, Masahiro Haze, Ryohei Nemoto, Wenxuan Qian, Shunsuke Yoshizawa, Takashi Uchihashi, Yukio Hasegawa","doi":"10.1126/sciadv.adu9610","DOIUrl":"https://doi.org/10.1126/sciadv.adu9610","url":null,"abstract":"The superconductor-insulator transition in two-dimensional (2D) systems has been extensively studied as a typical example of quantum phase transition. Recent investigations of highly conductive 2D systems have revealed an intervening metallic regime, in which the electrical resistivity saturates at the limit of zero temperature. The nature and origin of this metallicity remain debated, partly because of the lack of microscopic understanding. In this study, using scanning tunneling spectroscopy, we investigate the metallic state and other phases observed in crystalline Pb monoatomic-layer superconductors formed on vicinal semiconducting substrates. Our spectroscopic images reveal stable and isolated vortices in the metallic regime, distinct from delocalized or liquidized vortices. These findings suggest that the saturated resistance in the metallic state arises from the pinning-free vortex motion driven by the finite current applied for the transport measurements. Our disorder-controlled microscopic experiments provide new insights into the fluctuation-induced phases of ultrathin crystalline 2D superconductors.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"10 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microRNAs are ~22-nucleotide RNAs processed from primary transcripts and exported from the nucleus to repress gene expression by base-pairing to mRNAs. Unexpectedly, we find that the highest levels of RNA polymerase II (Pol II) at human microRNA genes are within the ribosomal gene repeat arrays (rDNAs). Alignment of public nascent transcript data to the hs1 human genome assembly reveals a 50-nucleotide transcript for both miR-1275 and miR-6724, which exits from the nucleus with exceptional rapidity. We show that the miR-1275/miR-6724 transcription unit is closely flanked by CCCTC-binding factor (CTCF) within a <400-bp span of the rDNA spacer promoter. miR-1275/miR-6724 and microRNA precursors expressed from the 5′ external transcribed spacer (5′ETS) are exported independently of known RNA processing activities and are detected in exosomes and as circulating cancer biomarkers. We propose that the rDNA spacer promoter and 5′ETS microRNA genes have evolved for general regulatory functions in recipient cells.
{"title":"Superabundant microRNAs are transcribed from human rDNA spacer promoters insulated by CTCF","authors":"Steven Henikoff, Jorja G. Henikoff","doi":"10.1126/sciadv.aec1451","DOIUrl":"https://doi.org/10.1126/sciadv.aec1451","url":null,"abstract":"microRNAs are ~22-nucleotide RNAs processed from primary transcripts and exported from the nucleus to repress gene expression by base-pairing to mRNAs. Unexpectedly, we find that the highest levels of RNA polymerase II (Pol II) at human microRNA genes are within the ribosomal gene repeat arrays (rDNAs). Alignment of public nascent transcript data to the hs1 human genome assembly reveals a 50-nucleotide transcript for both miR-1275 and miR-6724, which exits from the nucleus with exceptional rapidity. We show that the miR-1275/miR-6724 transcription unit is closely flanked by CCCTC-binding factor (CTCF) within a <400-bp span of the rDNA spacer promoter. miR-1275/miR-6724 and microRNA precursors expressed from the 5′ external transcribed spacer (5′ETS) are exported independently of known RNA processing activities and are detected in exosomes and as circulating cancer biomarkers. We propose that the rDNA spacer promoter and 5′ETS microRNA genes have evolved for general regulatory functions in recipient cells.","PeriodicalId":21609,"journal":{"name":"Science Advances","volume":"12 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147489736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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