A peroxiredoxin-P38 MAPK scaffold increases MAPK activity by MAP3K-independent mechanisms.

Peroxiredoxins (Prdxs) utilize reversibly oxidized cysteine residues to reduce peroxides and promote H2O2 signal transduction, including H2O2-induced activation of P38 MAPK. Prdxs form H2O2-induced disulfide complexes with many proteins, including multiple kinases involved in P38 MAPK signaling. Here, we show that a genetically encoded fusion between a Prdx and P38 MAPK is sufficient to hyperactivate the kinase in yeast and human cells by a mechanism that does not require the H2O2-sensing cysteine of the Prdx. We demonstrate that a P38-Prdx fusion protein compensates for loss of the yeast scaffold protein Mcs4 and MAP3K activity, driving yeast into mitosis. Based on our findings, we propose that the H2O2-induced formation of Prdx-MAPK disulfide complexes provides an alternative scaffold and signaling platform for MAPKK-MAPK signaling. The demonstration that formation of a complex with a Prdx is sufficient to modify the activity of a kinase has broad implications for peroxide-based signal transduction in eukaryotes.

Spatial IMA1 regulation restricts root iron acquisition on MAMP perception.

Iron is critical during host-microorganism interactions1-4. Restriction of available iron by the host during infection is an important defence strategy, described as nutritional immunity5. However, this poses a conundrum for externally facing, absorptive tissues such as the gut epithelium or the plant root epidermis that generate environments that favour iron bioavailability. For example, plant roots acquire iron mostly from the soil and, when iron deficient, increase iron availability through mechanisms that include rhizosphere acidification and secretion of iron chelators6-9. Yet, the elevated iron bioavailability would also be beneficial for the growth of bacteria that threaten plant health. Here we report that microorganism-associated molecular patterns such as flagellin lead to suppression of root iron acquisition through a localized degradation of the systemic iron-deficiency signalling peptide Iron Man 1 (IMA1) in Arabidopsis thaliana. This response is also elicited when bacteria enter root tissues, but not when they dwell on the outer root surface. IMA1 itself has a role in modulating immunity in root and shoot, affecting the levels of root colonization and the resistance to a bacterial foliar pathogen. Our findings reveal an adaptive molecular mechanism of nutritional immunity that affects iron bioavailability and uptake, as well as immune responses.

The future transistors.

The metal-oxide-semiconductor field-effect transistor (MOSFET), a core element of complementary metal-oxide-semiconductor (CMOS) technology, represents one of the most momentous inventions since the industrial revolution. Driven by the requirements for higher speed, energy efficiency and integration density of integrated-circuit products, in the past six decades the physical gate length of MOSFETs has been scaled to sub-20 nanometres. However, the downscaling of transistors while keeping the power consumption low is increasingly challenging, even for the state-of-the-art fin field-effect transistors. Here we present a comprehensive assessment of the existing and future CMOS technologies, and discuss the challenges and opportunities for the design of FETs with sub-10-nanometre gate length based on a hierarchical framework established for FET scaling. We focus our evaluation on identifying the most promising sub-10-nanometre-gate-length MOSFETs based on the knowledge derived from previous scaling efforts, as well as the research efforts needed to make the transistors relevant to future logic integrated-circuit products. We also detail our vision of beyond-MOSFET future transistors and potential innovation opportunities. We anticipate that innovations in transistor technologies will continue to have a central role in driving future materials, device physics and topology, heterogeneous vertical and lateral integration, and computing technologies.

TMK1-mediated auxin signalling regulates differential growth of the apical hook.

The plant hormone auxin has crucial roles in almost all aspects of plant growth and development. Concentrations of auxin vary across different tissues, mediating distinct developmental outcomes and contributing to the functional diversity of auxin. However, the mechanisms that underlie these activities are poorly understood. Here we identify an auxin signalling mechanism, which acts in parallel to the canonical auxin pathway based on the transport inhibitor response1 (TIR1) and other auxin receptor F-box (AFB) family proteins (TIR1/AFB receptors)1,2, that translates levels of cellular auxin to mediate differential growth during apical-hook development. This signalling mechanism operates at the concave side of the apical hook, and involves auxin-mediated C-terminal cleavage of transmembrane kinase 1 (TMK1). The cytosolic and nucleus-translocated C terminus of TMK1 specifically interacts with and phosphorylates two non-canonical transcriptional repressors of the auxin or indole-3-acetic acid (Aux/IAA) family (IAA32 and IAA34), thereby regulating ARF transcription factors. In contrast to the degradation of Aux/IAA transcriptional repressors in the canonical pathway, the newly identified mechanism stabilizes the non-canonical IAA32 and IAA34 transcriptional repressors to regulate gene expression and ultimately inhibit growth. The auxin-TMK1 signalling pathway originates at the cell surface, is triggered by high levels of auxin and shares a partially overlapping set of transcription factors with the TIR1/AFB signalling pathway. This allows distinct interpretations of different concentrations of cellular auxin, and thus enables this versatile signalling molecule to mediate complex developmental outcomes.

Catalytic Enantioselective Hydroxylation of Tertiary Propargylic C(sp3)-H Bonds in Acyclic Systems: a Kinetic Resolution Study.

Direct site-selective and enantioselective oxyfunctionalization of C(sp3)-H bonds to form alcohols with a general scope, with predictable selectivities, and in preparatively useful yields represents a paradigm shift in the standard logic of synthetic organic chemistry. However, the knowledge of either enzymatic or nonenzymatic asymmetric hydroxylation of tertiary C-H bonds for enantioenriched tertiary alcohol synthesis is sorely lacking. Here, we report a practical manganese-catalyzed enantio-differentiating hydroxylation of tertiary propargylic C-H bonds in acyclic systems, producing a wide range of structurally diverse enantioenriched tertiary propargyl alcohols in high efficiency with extremely efficient chemo- and enantio-discrimination. Other features include the use of C-H substrates as the limiting reagent, noteworthy functional group compatibility, great synthetic utilities, and scalability. The findings serve as a blueprint for the development of metal-catalyzed asymmetric oxidation of challenging substrates.

Heparin Specifically Inhibits CRISPR/Cas12 Activation, Enabling Ultrasensitive Heparin Detection and Gene Editing Regulation.

Heparin is a highly sulfated linear glycosaminoglycan that is used as an anticoagulant to prevent and treat thrombotic diseases. Herein, we find that heparin specifically inhibits the activation of the Cas12 protein through the competitive binding of heparin and crRNA to Cas12. Studies illustrate that heparin's high molecular weight and strong negative charge are critical parameters for its inhibitory effect. This unexpected finding was engineered for the detection of heparin, affording a low detection limit of 0.36 ng/mL for fluorometric quantification. We further developed a rapid lateral flow-based system named HepaStrip (heparin strip), allowing heparin monitoring in clinical samples within 20 min. Finally, in vivo investigations revealed that heparin can regulate gene editing with the clusters of the regularly spaced short palindromic repeat (CRISPR)/Cas12 system in Escherichia coli. Heparin blocks the formation of Cas12-crRNA ribonucleoprotein, allowing the application of CRISPR for rapid and field-deployable detection of heparin and unleashing the potential use of heparin in future anti-CRISPR applications.

Loss of PTPRS elicits potent metastatic capability and resistance to temozolomide in glioblastoma.

Glioblastoma (GBM) is the most aggressive brain tumor type with worse clinical outcome due to the hallmarks of strong invasiveness, high rate of recurrence, and therapeutic resistance to temozolomide (TMZ), the first-line drug for GBM, representing a major challenge for successful GBM therapeutics. Understanding the underlying mechanisms that drive GBM progression will shed novel insight into therapeutic strategies. Receptor-type tyrosine-protein phosphatase S (PTPRS) is a frequently mutated gene in human cancers, including GBM. Its role in GBM has not yet been clarified. Here, inactivating PTPRS mutation or deficiency was frequently found in GBM, and deficiency in PTPRS significantly induced defects in the G2M checkpoint and limited GBM cells proliferation, leading to potent resistance to TMZ treatment in vitro and in vivo. Surprisingly, loss of PTPRS triggered an unexpected mesenchymal phenotype that markedly enhances the migratory capabilities of GBM cells through upregulating numerous matrix metalloproteinases via MAPK-MEK-ERK signaling. Therefore, this work provides a therapeutic window for precisely excluding PTPRS-mutated patients who do not respond to TMZ.

Clinically relevant plasma proteome for adiposity depots: evidence from systematic mendelian randomization and colocalization analyses.

BACKGROUND: The accumulation of visceral and ectopic fat comprise a major cause of cardiometabolic diseases. However, novel drug targets for reducing unnecessary visceral and ectopic fat are still limited. Our study aims to provide a comprehensive investigation of the causal effects of the plasma proteome on visceral and ectopic fat using Mendelian randomization (MR) approach. METHODS: We performed two-sample MR analyses based on five large genome-wide association study (GWAS) summary statistics of 2656 plasma proteins, to screen for causal associations of these proteins with traits of visceral and ectopic fat in over 30,000 participants of European ancestry, as well as to assess mediation effects by risk factors of outcomes. The colocalization analysis was conducted to examine whether the identified proteins and outcomes shared casual variants. RESULTS: Genetically predicted levels of 14 circulating proteins were associated with visceral and ectopic fat (P < 4.99 × 10- 5, at a Bonferroni-corrected threshold). Colocalization analysis prioritized ten protein targets that showed effect on outcomes, including FST, SIRT2, DNAJB9, IL6R, CTSA, RGMB, PNLIPRP1, FLT4, PPY and IL6ST. MR analyses revealed seven risk factors for visceral and ectopic fat (P < 0.0024). Furthermore, the associations of CTSA, DNAJB9 and IGFBP1 with primary outcomes were mediated by HDL-C and SHBG. Sensitivity analyses showed little evidence of pleiotropy. CONCLUSIONS: Our study identified candidate proteins showing putative causal effects as potential therapeutic targets for visceral and ectopic fat accumulation and outlined causal pathways for further prevention of downstream cardiometabolic diseases.

Repair of Limb Ischemia Is Dependent on Hematopoietic Stem Cell Specific-SHP-1 Regulation of TGF-ß1.

BACKGROUND: Hematopoietic stem cell (HSC) therapy has shown promise for tissue regeneration after ischemia. Therefore, there is a need to understand mechanisms underlying endogenous HSCs activation in response to ischemic stress and coordination of angiogenesis and repair. SHP-1 plays important roles in HSC quiescence and differentiation by regulation of TGF-ß1 signaling. TGF-ß1 promotes angiogenesis by stimulating stem cells to secrete growth factors to initiate the formation of blood vessels and later aid in their maturation. We propose that SHP-1 responds to ischemia stress in HSC and progenitor cells (HSPC) via regulation of TGF-ß1. METHODS: A mouse hind limb ischemia model was used. Local blood perfusion in the limbs was determined using laser doppler perfusion imaging. The number of positive blood vessels per square millimeter, as well as blood vessel diameter (µm) and area (µm2), were calculated. Hematopoietic cells were analyzed using flow cytometry. The bone marrow transplantation assay was performed to measure HSC reconstitution. RESULTS: After femoral artery ligation, TGF-ß1 was initially decreased in the bone marrow by day 3 of ischemia, followed by an increase on day 7. This pattern was opposite to that in the peripheral blood, which is concordant with the response of HSC to ischemic stress. In contrast, SHP-1 deficiency in HSC is associated with irreversible activation of HSPCs in the bone marrow and increased circulating HSPCs in peripheral blood following limb ischemia. In addition, there was augmented auto-induction of TGF-ß1 and sustained inactivation of SHP-1-Smad2 signaling, which impacted TGF-ß1 expression in HSPCs in circulation. Importantly, restoration of normal T GF-ß1 oscillations helped in the recovery of limb repair and function. CONCLUSIONS: HSPC-SHP-1-mediated regulation of TGF-ß1 in both bone marrow and peripheral blood is required for a normal response to ischemic stress.

Regulatory roles of miRNA-530 in the post-transcriptional regulation of NF-κB signaling pathway through targeted modulation of IκBα in Sebastesschlegelii.

MicroRNAs (miRNAs) are a crucial type of non-coding RNAs involved in post-transcriptional regulation. The playing essential regulatory roles in the NF-κB signaling pathway and modulate the host immune response to diverse pathogens by targeting IκBα. However, the regulatory mechanism of miRNAs in relation with IκBα in Sebastes schlegelii remains unclear. In our study, we identified two copies of IkBα gene in black rockfish (Sebastes schlegelii), namely IkBα1 and IkBα2. Moreover, we have discovered that miRNA-530 can activate the NF-κB signaling pathway by inhibiting the expression of IκBα, thereby inducing the inflammatory response. This project comprehensively investigated the interactive regulatory roles of miRNA-530 in the NF-κB signaling pathway at both cellular and in vivo levels, while also elucidating the regulatory relationships between miRNA-530 and IκBα. In conclusion, our research confirmed that miRNA-530 can target the 3'UTR region of IκBα, resulting in a decrease in the expression of IκBα at the post-transcriptional level and inhibiting its translation. The findings contribute to the understanding of the regulatory network of non-coding RNA in teleosts and its subsequent regulation of the NF-κB signaling pathway by miRNAs.

Intraspecific alternative phenotypes contribute to variation in species' strategies for growth.

Ecologists have historically sought to identify the mechanisms underlying the maintenance of local species diversity. High-dimensional trait-based relationships, such as alternative phenotypes, have been hypothesized as important for maintaining species diversity such that phenotypically dissimilar individuals compete less for resources but have similar performance in a given environment. The presence of alternative phenotypes has primarily been investigated at the community level, despite the importance of intraspecific variation to diversity maintenance. The aims of this research are to (1) determine the presence or absence of intraspecific alternative phenotypes in three species of tropical tree seedlings, (2) investigate if these different species use the same alternative phenotypes for growth success, and (3) evaluate how findings align with species co-occurrence patterns. We model species-specific relative growth rate with individual-level measurements of leaf mass per area (LMA) and root mass fraction (RMF), environmental data, and their interactions. We find that two of the three species have intraspecific alternative phenotypes, with individuals within species having different functional forms leading to similar growth. Interestingly, individuals within these species use the same trait combinations, high LMA × low RMF and low LMA × high RMF, in high soil nutrient environments to acquire resources for higher growth. This similarity among species in intraspecific alternative phenotypes and variables that contribute most to growth may lead to their negative spatial co-occurrence. Overall, we find that multiple traits or interactions between traits and the environment drive species-specific strategies for growth, but that individuals within species leverage this multi-dimensionality in different ways for growth success.

Integrated multi-omics approach revealed cellular senescence landscape.

Cellular senescence is a complex multifactorial biological phenomenon that plays essential roles in aging, and aging-related diseases. During this process, the senescent cells undergo gene expression altering and chromatin structure remodeling. However, studies on the epigenetic landscape of senescence using integrated multi-omics approaches are limited. In this research, we performed ATAC-seq, RNA-seq and ChIP-seq on different senescent types to reveal the landscape of senescence and identify the prime regulatory elements. We also obtained 34 key genes and deduced that NAT1, PBX1 and RRM2, which interacted with each other, could be the potential markers of aging and aging-related diseases. In summary, our work provides the landscape to study accessibility dynamics and transcriptional regulations in cellular senescence. The application of this technique in different types of senescence allows us to identify the regulatory elements responsible for the substantial regulation of transcription, providing the insights into molecular mechanisms of senescence.

Preparation of (S)-epichlorohydrin using a novel halohydrin dehalogenase by selective conformation adjustment.

Chiral epichlorohydrin (ECH) is an attractive intermediate for chiral pharmaceuticals and chemicals preparation. The asymmetric synthesis of chiral ECH using 1,3-dicholoro-2-propanol (1,3-DCP) catalyzed by a haloalcohol dehalogenase (HHDH) was considered as a feasible approach. However, the reverse ring opening reaction caused low optical purity of chiral ECH, thus severely restricts the industrial application of HHDHs. In the present study, a novel selective conformation adjustment strategy was developed with an engineered HheCPS to regulate the kinetic parameters of the forward and reverse reactions, based on site saturation mutation and molecular simulation analysis. The HheCPS mutant E85P was constructed with a markable change in the conformation of (S)-ECH in the substrate pocket and a slight impact on the interaction between 1,3-DCP and the enzyme, which resulted in the kinetic deceleration of the reverse reactions. Compared with HheCPS, the catalytic efficiency (kcat(S)-ECH/Km(S)-ECH) of the reversed reaction dropped to 0.23-fold (from 0.13 to 0.03 mM-1 s-1), while the catalytic efficiency (kcat(1,3-DCP)/Km(1,3-DCP)) of the forward reaction only reduced from 0.83 to 0.71 mM-1 s-1. With 40 mM 1,3-DCP as substrate, HheCPS E85P catalyzed the synthesis of (S)-ECH with the yield up to 55.35% and the e.e. increased from 92.54 to >99%. Our work provided an effective approach for understanding the stereoselective catalytic mechanism as well as the green manufacturing of chiral epoxides.

Association of spinal-pelvic parameters with recurrence of lumbar disc herniation after endoscopic surgery: a retrospective case-control study.

PURPOSE: This study aimed to investigate the relationship between spinal-pelvic parameters and recurrence of lumbar disc herniation (rLDH) after percutaneous endoscopic lumbar discectomy (PELD) through a retrospective case-control study. METHODS: Patients who underwent PELD for single-segment LDH at our hospital were included in this study. The relationship between sagittal balance parameters of the spine and recurrence was analysed through correlation analysis, and ROC curves were plotted. The baseline characteristics, sagittal balance parameters of the spine and radiological parameters of the case and control groups were compared, and the relationship between sagittal balance parameters of the spine and recurrence of rLDH after PELD was determined through univariate and multivariate logistic regression analysis. RESULTS: Correlation analysis showed that PI and ∆PI-LL were negatively correlated with grouping (r = -0.090 and -0.120, respectively, P = 0.001 and 0.038). ROC curve analysis showed that the area under the curve (ROC-AUC) for predicting rLDH based on PI was 0.65 (CI95% = 0.598, 0.720), with a cut-off of 50.26°. The ROC-AUC for predicting rLDH based on ∆PI-LL was 0.56 (CI95% = 0.503, 0.634), with a cut-off of 28.21°. Multivariate logistic regression analysis showed that smoking status (OR = 2.667, P = 0.008), PI ≤ 50.26 (OR = 2.161, P = 0.009), ∆PI-LL ≤ 28.21 (OR = 3.185, P = 0.001) and presence of Modic changes (OR = 4.218, P = 0.001) were independent risk factors, while high DH (OR = 0.788, P = 0.001) was a protective factor. CONCLUSION: PI < 50.26 and ∆PI-LL < 28.21 were risk factors for recurrence of lumbar disc herniation after spinal endoscopic surgery and had some predictive value for post-operative recurrence.

Effect of magnetized water irrigation on Cd subcellular allocation and chemical forms in leaves of Festuca arundinacea during phytoremediation.

The application of an external magnetic field has been shown to improve the Cd phytoremediation efficiency of F. arundinacea by leaf harvesting. However, the influencing mechanisms of the promoting effect have not yet been revealed. This study evaluated variations in the Cd subcellular allocation and fractions in various F. arundinacea leaves, with or without magnetized water irrigation. Over 50 % of the metal were sequestered within the cell wall in all tissues under all treatments, indicating that cell wall binding was a critical detoxification pathway for Cd. After magnetized water treatment, the metal stored in the cytoplasm of roots raised from 33.1 % to 45.3 %, and the quantity of soluble Cd in plant roots enhanced from 53.4 % to 59.0 %. The findings suggested that magnetized water mobilized Cd in the roots, and thus drove it into the leaves. In addition, the proportion of Cd in the organelles, and the concentration of ethanol-extracted Cd in emerging leaves, decreased by 13.0 % and 47.1 %, respectively, after magnetized water treatment. These results explained why an external field improved the phytoextraction effect of the plant through leaf harvesting.

Effects of magnetic field on cd subcellular distribution and chemical speciation in Noccaea caerulescens.

Implementing an external magnetic field of suitable strength has been reported to increase Cd uptake by Noccaea caerulescence. However, only a few mechanisms promoting this efficiency have been reported. A series of culture experiments was conducted to explore how Cd subcellular distribution and speciation vary within the tissue of N. caerulescens when subjected to external magnetic fields of different intensities. Without a magnetic field, over 80% of the Cd was deposited in the cell wall and cytoplasm, indicating that cell wall retention and cytoplasm isolation are significant mechanisms for the detoxification of Cd. An external magnetic field (120 mT) increased the Cd concentrations deposited in the cytoplasm and water-soluble inorganic Cd in the roots, increasing the cell wall-bound Cd and undissolved Cd phosphate in the shoots. Meanwhile, the magnetic field increased carbonic anhydrase activity in plant shoots, except at 400 mT. These results indicated that an external field can elevate the Cd decontamination capacity of N. caerulescens by changing the subcellular compartmentalization and speciation of Cd in different tissues.

External validation of the prediction model of intradialytic hypotension: a multicenter prospective cohort study.

OBJECTIVE: Intradialytic hypotension (IDH) is a common and serious complication in patients with Maintenance Hemodialysis (MHD). The purpose of this study is to externally verify three IDH risk prediction models recently developed by Ma et al. and recalibrate, update and present the optimal model to improve the accuracy and applicability of the model in clinical environment. METHODS: A multicenter prospective cohort study of patients from 11 hemodialysis centers in Sichuan Province, China, was conducted using convenience sampling from March 2022 to July 2022, with a follow-up period of 1 month. Model performance was assessed by: (1) Discrimination: Evaluated through the computation of the Area Under Curve (AUC) and its corresponding 95% confidence intervals. (2) Calibration: scrutinized through visual inspection of the calibration plot and utilization of the Brier score. (3) The incremental value of risk prediction and the utility of updating the model were gauged using NRI (Net Reclassification Improvement) and IDI (Integrated Discrimination Improvement). Decision Curve Analysis (DCA) was employed to evaluate the clinical benefit of updating the model. RESULTS: The final cohort comprised 2235 individuals undergoing maintenance hemodialysis, exhibiting a 14.6% occurrence rate of IDH. The externally validated Area Under the Curve (AUC) values for the three original prediction models were 0.746 (95% CI: 0.718 to 0.775), 0.709 (95% CI: 0.679 to 0.739), and 0.735 (95% CI: 0.706 to 0.764) respectively. Conversely, the AUC value for the recalibrated and updated columnar plot model reached 0.817 (95% CI: 0.791 to 0.842), accompanied by a Brier score of 0.081. Furthermore, Decision Curve Analysis (DCA) exhibited a net benefit within the threshold probability range of 15.2% to 87.1%. CONCLUSION: Externally validated, recalibrated, updated, and presented IDH prediction models may serve as a valuable instrument for evaluating IDH risk in clinical practice. Furthermore, they hold the potential to guide clinical providers in discerning individuals at risk and facilitating judicious clinical intervention decisions.

A nomogram prediction model for mild cognitive impairment in non-dialysis outpatient patients with chronic kidney disease.

BACKGROUND: The high prevalence of mild cognitive impairment (MCI) in non-dialysis individuals with chronic kidney disease (CKD) impacts their prognosis and quality of life. OBJECTIVE: This study aims to investigate the variables associated with MCI in non-dialysis outpatient patients with CKD and to construct and verify a nomogram prediction model. METHODS: 416 participants selected from two hospitals in Chengdu, between January 2023 and June 2023. They were categorized into two groups: the MCI group (n = 210) and the non-MCI (n = 206). Univariate and multivariate binary logistic regression analyses were employed to identify independent influences (candidate predictor variables). Subsequently, regression models was constructed, and a nomogram was drawn. The restricted cubic spline diagram was drawn to further analyze the relationship between the continuous numerical variables and MCI. Internally validated using a bootstrap resampling procedure. RESULTS: Among 416 patients, 210 (50.9%) had MCI. Logistic regression analysis revealed that age, educational level, occupational status, use of smartphones, sleep disorder, and hemoglobin were independent influencing factors of MCI (all p<.05). The model's area under the curve was 0.926,95% CI (0.902, 0.951), which was a good discriminatory measure; the Calibration curve, the Hosmer-Lemeshow test, and the Clinical Decision Curve suggested that the model had good calibration and clinical benefit. Internal validation results showed the consistency index was 0.926, 95%CI (0.925, 0.927). CONCLUSION: The nomogram prediction model demonstrates good performance and can be used for early screening and prediction of MCI in non-dialysis patients with CKD. It provides valuable reference for medical staff to formulate corresponding intervention strategies.

Microwave Flow Cytometric Detection and Differentiation of Escherichia coli.

Label-free measurement and analysis of single bacterial cells are essential for food safety monitoring and microbial disease diagnosis. We report a microwave flow cytometric sensor with a microstrip sensing device with reduced channel height for bacterial cell measurement. Escherichia coli B and Escherichia coli K-12 were measured with the sensor at frequencies between 500 MHz and 8 GHz. The results show microwave properties of E. coli cells are frequency-dependent. A LightGBM model was developed to classify cell types at a high accuracy of 0.96 at 1 GHz. Thus, the sensor provides a promising label-free method to rapidly detect and differentiate bacterial cells. Nevertheless, the method needs to be further developed by comprehensively measuring different types of cells and demonstrating accurate cell classification with improved machine-learning techniques.