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At least 307 records · Page 17

Understanding and eliminating artifact signals from diffusely scattered pump beam in measurements of rough samples by time-domain thermoreflectance (TDTR)

Time-domain thermoreflectance (TDTR) is a pump-probe technique frequently applied to measure the thermal transport properties of bulk materials, nanostructures, and interfaces. One of the limitations of TDTR is that it can only be employed to samples with a fairly smooth surface. For rough samples, artifact signals are collected when the pump beam in TDTR measurements is diffusely scattered by the rough surface into the photodetector, rendering the TDTR measurements invalid. In this paper, we systemically studied the factors affecting the artifact signals due to the pump beam leaked into the photodetector and thus established the origin of the artifact signals. We find that signals from the leaked pump beam are modulated by the probe beam due to the phase rotation induced in the photodetector by the illumination of the probe beam. As a result of the modulation, artifact signals due to the leaked pump beam are registered in TDTR measurements as the out-of-phase signals. We then developed a simple approach to eliminate the artifact signals due to the leaked pump beam. We verify our leak-pump correction approach by measuring the thermal conductivity of a rough InN sample, when the signals from the leaked pump beam are significant. We also discuss the advantages of our new method over the two-tint approach and its limitations. Our new approach enables measurements of the thermal conductivity of rough samples using TDTR.

46 INSTRUMENTATION RELATED TO NUCLEAR SCIENCE AND ↗

Effect of post annealing on spin accumulation and transport signals in Co{sub 2}FeSi/MgO/n{sup +}-Si on insulator devices

The post annealing temperature dependence of spin accumulation and transport signals in Co{sub 2}FeSi/MgO/n{sup +}-Si on insulator were investigated. The spin signals were detected using 3- and 4-terminal Hanle, 2-terminal local and 4-terminal nonlocal magnetoresistance measurements. The post annealing temperature (T{sub A}) dependence of the magnitude in 3-terminal narrow Hanle signals is nearly constant up to T{sub A} < 400°C, however a slight decrease above T{sub A} ≥ 400°C is observed. This behavior is consistent with the T{sub A} dependence of the magnitude of 4-terminal nonlocal magnetoresistance (MR) signals. The spin polarization estimated from the 3-terminal narrow Hanle signals and the magnitude of 2-terminal local MR signals show a slight improvement with increasing post annealing temperature with a peak at around 325°C and then start reducing slowly. The slight increase in the spin signal would be due to high spin polarization of Co{sub 2}FeSi as a result of structural ordering. The 2-terminal local MR signals do not vary significantly by annealing between as-deposited and T{sub A} = 400°C, indicating the robustness of our device. This result would be useful for future Si spintronics devices.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗

Investigating the mechanism of chloroplast singlet oxygen signaling in the Arabidopsis thaliana accelerated cell death 2 mutant

As sessile organisms, plants have evolved complex signaling mechanisms to sense stress and acclimate. This includes the use of reactive oxygen species (ROS) generated during dysfunctional photosynthesis to initiate signaling. One such ROS, singlet oxygen ( 1 O 2 ), can trigger retrograde signaling, chloroplast degradation, and programmed cell death. However, the signaling mechanisms are largely unknown. Several proteins (e.g. PUB4, OXI1, EX1) are proposed to play signaling roles across three Arabidopsis thaliana mutants that conditionally accumulate chloroplast 1 O 2 (fluorescent in blue light (flu), chlorina 1 (ch1), and plastid ferrochelatase 2 (fc2)). We previously demonstrated that these mutants reveal at least two chloroplast 1 O 2 signaling pathways (represented by flu and fc2/ch1). Here, we test if the 1 O 2 -accumulating lesion mimic mutant, accelerated cell death 2 (acd2), also utilizes these pathways. The pub4–6 allele delayed lesion formation in acd2 and restored photosynthetic efficiency and biomass. Conversely, an oxi1 mutation had no measurable effect on these phenotypes. acd2 mutants were not sensitive to excess light (EL) stress, yet pub4–6 and oxi1 both conferred EL tolerance within the acd2 background, suggesting that EL-induced 1 O 2 signaling pathways are independent from spontaneous lesion formation. Thus, 1 O 2 signaling in acd2 may represent a third (partially overlapping) pathway to control cellular degradation.

59 BASIC BIOLOGICAL SCIENCES↗

Signal-Anticipation in Local Voltage Control in Distribution Systems

We consider the signal-anticipating behavior in local Volt/Var control for distribution systems. Such a behavior makes interaction among the nodes a game. We characterize Nash equilibrium of the game as the optimum of a global optimization problem and establish its asymptotic global stability. We also show that the signal-anticipating voltage control has less restrictive convergence condition than the signal-taking control. We then introduce the notion of price of signal-anticipation (PoSA) to characterize the impact of signal-anticipating control, and use the gap in cost between network equilibrium in the signal-taking control and Nash equilibrium in the signal-anticipating control as the metric for PoSA. We characterize how the PoSA scales with the size, topology, and heterogeneity of the distribution network for a few network settings. Our results show that the PoSA is upper bounded by a constant and the average PoSA per node will go to zero as the size of the network increases. This is desirable as it means that the PoSA will not be arbitrarily large, no matter what the size of the network is, and no mechanism is needed to mitigate the signal-anticipating behavior. We further carry out numerical experiments with a real-world distribution circuit to complement the theoretical analysis.

24 POWER TRANSMISSION AND DISTRIBUTION↗

MO-FG-BRA-02: A Feasibility Study of Integrating Breathing Audio Signal with Surface Surrogates for Respiratory Motion Management

Purpose: Tracking the surrogate placed on patient skin surface sometimes leads to problematic signals for certain patients, such as shallow breathers. This in turn impairs the 4D CT image quality and dosimetric accuracy. In this pilot study, we explored the feasibility of monitoring human breathing motion by integrating breathing sound signal with surface surrogates. Methods: The breathing sound signals were acquired though a microphone attached adjacently to volunteer’s nostrils, and breathing curve were analyzed using a low pass filter. Simultaneously, the Real-time Position Management™ (RPM) system from Varian were employed on a volunteer to monitor respiratory motion including both shallow and deep breath modes. The similar experiment was performed by using Calypso system, and three beacons taped on volunteer abdominal region to capture breath motion. The period of each breathing curves were calculated with autocorrelation functions. The coherence and consistency between breathing signals using different acquisition methods were examined. Results: Clear breathing patterns were revealed by the sound signal which was coherent with the signal obtained from both the RPM system and Calypso system. For shallow breathing, the periods of breathing cycle were 3.00±0.19 sec (sound) and 3.00±0.21 sec (RPM); For deep breathing, the periods were 3.49± 0.11 sec (sound) and 3.49±0.12 sec (RPM). Compared with 4.54±0.66 sec period recorded by the calypso system, the sound measured 4.64±0.54 sec. The additional signal from sound could be supplement to the surface monitoring, and provide new parameters to model the hysteresis lung motion. Conclusion: Our preliminary study shows that the breathing sound signal can provide a comparable way as the RPM system to evaluate the respiratory motion. It’s instantaneous and robust characteristics facilitate it possibly to be a either independently or as auxiliary methods to manage respiratory motion in radiotherapy.

60 APPLIED LIFE SCIENCES↗

Calcium and signal transduction in plants

Environmental and hormonal signals control diverse physiological processes in plants. The mechanisms by which plant cells perceive and transduce these signals are poorly understood. Understanding biochemical and molecular events involved in signal transduction pathways has become one of the most active areas of plant research. Research during the last 15 years has established that Ca2+ acts as a messenger in transducing external signals. The evidence in support of Ca2+ as a messenger is unequivocal and fulfills all the requirements of a messenger. The role of Ca2+ becomes even more important because it is the only messenger known so far in plants. Since our last review on the Ca2+ messenger system in 1987, there has been tremendous progress in elucidating various aspects of Ca(2+) -signaling pathways in plants. These include demonstration of signal-induced changes in cytosolic Ca2+, calmodulin and calmodulin-like proteins, identification of different Ca2+ channels, characterization of Ca(2+) -dependent protein kinases (CDPKs) both at the biochemical and molecular levels, evidence for the presence of calmodulin-dependent protein kinases, and increased evidence in support of the role of inositol phospholipids in the Ca(2+) -signaling system. Despite the progress in Ca2+ research in plants, it is still in its infancy and much more needs to be done to understand the precise mechanisms by which Ca2+ regulates a wide variety of physiological processes. The purpose of this review is to summarize some of these recent developments in Ca2+ research as it relates to signal transduction in plants.

NASA Program Space Biology↗

Performance Assessment of LunaNet’s Augmented Forward Signal

LunaNet provides a common set of interoperable specifications for communication and position, navigation and time (PNT) services and interfaces soon to be implemented in lunar vicinity. The LunaNet Interoperability Specification (LNIS) provides the design for the GNSS-like Augmented Forward Signal (AFS), which enables orbiting and surface users in lunar space, such as Artemis, to estimate their position, velocity, and time. The specification of AFS defines two orthogonal signal components on a single carrier: the in-phase component (AFS-I), a lower-chip-rate data channel tailored for applications where low SWaP (Size, Weight, and Power) is critical (e.g., IoT devices or search and rescue), and the quadrature component (AFS-Q), a high-chip-rate data-less pilot signal for high-precision, robust lunar navigation and positioning applications. An initial description of AFS was provided in [1], with initial analysis results shown in [2] and [3] and the current signal in space description provided in [4]. As part of NASA's Lunar Communication Relay and Navigation Systems (LCRNS) project, this work expands upon the initial analysis results and proposes a new expanded set of AFS-Q spreading codes that exceed the cross-correlation and autocorrelation sidelobe performance of L1C and other GNSS signals, while providing additional expansion capabilities for future provider satellites. A set of 420 codes was selected from a Weil-based code derived from the prime number 10247, which is larger than the 10243 prime number used to derive Beidou’s B1C Weil sequences. Both the initial set of 210 codes and the expanded set of 420 codes are shown to provide the best cross-correlation of any 10230-chip satellite navigation codes. The performance is demonstrated for hierarchical sets of spreading codes optimized and organized in sets of 30 codes. The new codes were developed using an optimization approach and correlation methodology described in [5]. The work also compares LunaNet’s AFS to terrestrial GNSS signals in terms of acquisition, tracking, and data demodulation performance. Performance is evaluated for receivers that only track the 1.023 MCPS data channel spreading code for low SWaP IoT use cases, as well as for receivers that track both the 1.023 MCPS data channel and the 5.115 MCPS pilot channel spreading code for high-performance use cases. Performance is assessed in the presence of interference and thermal noise. The analysis is performed in terms of expected operating conditions on the lunar surface. Several unique flexibility aspects of the augmented forward signal are described, including the use of the Q channel’s secondary and tertiary codes to enable variable coherent integrations during acquisition. This is compared to GNSS signals such as L5/E5 and MBOC in terms of achievable processing gain for interference mitigation versus acquisition complexity. The work details acquisition and tracking techniques used to optimally acquire and track the primary, secondary, and tertiary codes on the Q channel, as well as acquisition of the I channel spreading code. Acquisition of the 8 ms Q channel spreading code is also compared to joint acquisition of the I and Q channel primary codes in noise and interference environments.

LCRNS↗

Performance Assessment of LunaNet’s Augmented Forward Signal

LunaNet provides a common set of interoperable specifications for communication and position, navigation and time (PNT) services and interfaces soon to be implemented in lunar vicinity. The LunaNet Interoperability Specification (LNIS) provides the design for the GNSS-like Augmented Forward Signal (AFS), which enables orbiting and surface users in lunar space, such as Artemis, to estimate their position, velocity, and time. The specification of AFS defines two orthogonal signal components on a single carrier: the in-phase component (AFS-I), a lower-chip-rate data channel tailored for applications where low SWaP (Size, Weight, and Power) is critical (e.g., IoT devices or search and rescue), and the quadrature component (AFS-Q), a high-chip-rate data-less pilot signal for high-precision, robust lunar navigation and positioning applications. An initial description of AFS was provided in LNIS 2023, with initial analysis results shown in Dafesh 2024 and Dafesh 2025, and the current signal in space description provided in LNIS 2025. As part of NASA's Lunar Communication Relay and Navigation Systems (LCRNS) project, this work expands upon the initial analysis results and proposes a new expanded set of AFS-Q spreading codes that exceed the cross-correlation and autocorrelation sidelobe performance of L1C and other GNSS signals, while providing additional expansion capabilities for future service satellites. A set of 420 codes was selected from a Weil-based code derived from the prime number 10247, which is larger than the 10243 prime number used to derive BeiDou’s B1C Weil sequences. Both the initial set of 210 codes and the expanded set of 420 codes are shown to provide the best cross-correlation of any 10230-chip satellite navigation codes. The performance is demonstrated for hierarchical sets of spreading codes optimized and organized in sets of 30 codes. The work also compares LunaNet’s AFS to terrestrial GNSS signals in terms of acquisition, tracking, and data demodulation performance. Performance is evaluated for receivers that only track the 1.023 MCPS data channel spreading code for low SWaP IoT use cases, as well as for receivers that track both the 1.023 MCPS data channel and the 5.115 MCPS pilot channel spreading code for high-performance use cases. Performance is assessed in the presence of interference and thermal noise. The analysis is performed in terms of expected operating conditions on the lunar surface. Several unique flexibility aspects of the augmented forward signal are described, including the use of the Q channel’s secondary and tertiary codes to enable variable coherent integrations during acquisition. This is compared to GNSS signals such as L5/E5 and MBOC in terms of achievable processing gain for interference mitigation versus acquisition complexity. The work details acquisition and tracking techniques used to optimally acquire and track the primary, secondary, and tertiary codes on the Q channel, as well as acquisition of the I channel spreading code. Acquisition of the 8 ms, Q channel spreading code is also compared to joint acquisition of the I and Q channel primary codes in noise and interference environments

LCRNS↗

P44/WDR77 restricts the sensitivity of proliferating cells to TGFβ signaling

Highlights: • P44/WDR77 causes proliferating cells to become non-responsive to TGFβ signaling. • P44/WDR77 down-regulates TβRII and TβR2 expression. • P44/WDR77 down-regulated TGFβ signaling correlates with lung tumorigenesis. - Abstract: We previously reported that a novel WD-40 domain-containing protein, p44/WDR77, drives quiescent epithelial cells to re-enter the cell cycle and plays an essential role for growth of lung and prostate cancer cells. Transforming growth factor beta (TGFβ) signaling is important in the maintenance of non-transformed cells in the quiescent or slowly cycling stage. However, both non-transformed proliferating cells and human cancer cells are non-responsive to endogenous TGFβ signaling. The mechanism by which proliferating cells become refractory to TGFβ inhibition is not well established. Here, we found that silencing p44/WDR77 increased cellular sensitivity to TGFβ signaling and that this was inversely correlated with decreased cell proliferation. Smad2 or 3 phosphorylation, TGFβ-mediated transcription, and TGFβ2 and TGFβ receptor type II (TβRII) expression were dramatically induced by silencing of p44/WDR77. These data support the hypothesis that p44/WDR77 down-regulates the expression of the TGFβ ligand and its receptor, thereby leading to a cellular non-response to TGFβ signaling. Finally, we found that p44/WDR77 expression was correlated with cell proliferation and decreased TGFβ signaling during lung tumorigenesis. Together, these results suggest that p44/WDR77 expression causes the non-sensitivity of proliferating cells to TGFβ signaling, thereby contributing to cellular proliferation during lung tumorigenesis.

60 APPLIED LIFE SCIENCES↗

Lyn tyrosine kinase promotes silencing of ATM-dependent checkpoint signaling during recovery from DNA double-strand breaks

Highlights: • Inhibition of Src family kinases decreased γ-H2AX signal. • Inhibition of Src family increased ATM-dependent phosphorylation of Chk2 and Kap1. • shRNA-mediated knockdown of Lyn increased phosphorylation of Kap1 by ATM. • Ectopic expression of Src family kinase suppressed ATM-mediated Kap1 phosphorylation. • Src is involved in upstream signaling for inactivation of ATM signaling. - Abstract: DNA damage activates the DNA damage checkpoint and the DNA repair machinery. After initial activation of DNA damage responses, cells recover to their original states through completion of DNA repair and termination of checkpoint signaling. Currently, little is known about the process by which cells recover from the DNA damage checkpoint, a process called checkpoint recovery. Here, we show that Src family kinases promote inactivation of ataxia telangiectasia mutated (ATM)-dependent checkpoint signaling during recovery from DNA double-strand breaks. Inhibition of Src activity increased ATM-dependent phosphorylation of Chk2 and Kap1. Src inhibition increased ATM signaling both in G2 phase and during asynchronous growth. shRNA knockdown of Lyn increased ATM signaling. Src-dependent nuclear tyrosine phosphorylation suppressed ATM-mediated Kap1 phosphorylation. These results suggest that Src family kinases are involved in upstream signaling that leads to inactivation of the ATM-dependent DNA damage checkpoint.

60 APPLIED LIFE SCIENCES↗

Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation

Brain microvascular endothelial cells (BMECs) play vital roles in cerebral ischemia, during which many signal pathways mediate BMECs apoptosis. In this study, we explored the potential role of Wnt3α/β-catenin signal in BMECs apoptosis induced by ischemia. Here, we found that oxygen-glucose deprivation (OGD) could induce apoptosis of BMECs with Wnt3a mRNA expression decrease. Meanwhile, activation Wnt3a/β-catenin signal with exogenous Wnt3α protein (100 ng/ml) or Lithium Chloride (LiCl, 4 mM) decreased significantly apoptosis of BMECs induced by OGD with increasing expression of Bcl-2 in the whole cell and β-catenin in the nucleus. But, inhibition Wnt3a/β-catenin signal with DKK1 (100 ng/ml) or 2.4-diamino quinazoline (DQ, 0.2 μM) increased apoptosis of BMECs with decreasing expression of Bcl-2. These results suggest that activation Wnt3α/β-catenin signal attenuate apoptosis of BMECs induced by ischemia. - Highlights: • OGD induced BMECs apoptosis with Wnt3a mRNA expression decrease. • Activation Wnt signal reduced BMECs apoptosis with increasing Bcl-2 and β-catenin. • Inhibition Wnt signal increased BMECs apoptosis with decreasing Bcl-2. • Wnt3α/β-catenin signal attenuates apoptosis of BMECs induced by ischemia.

60 APPLIED LIFE SCIENCES↗

Inhibition of tissue factor signaling in breast tumour xenografts induces widespread changes in the microRNA expression profile

Highlights: • Clotting protein, tissue factor (TF) mediates intracellular signalling in cancer. • Selective inhibition of TF signalling exerts potent anticancer effect in mice. • Inhibition of TF signalling changes the tumour miR expression profile in vivo. • MiRs altered by blockade of TF signalling share common biological pathways. Tissue factor (TF) is a transmembrane receptor for coagulation factor VII/VIIa and is frequently overexpressed by cancer cells. The TF/VIIa complex acts as the main initiator of the clotting cascade in blood and a trigger of intracellular signaling that changes gene expression and the cellular phenotype. However, pathways mediating these changes are still poorly characterized and especially the impact of TF signals on regulatory microRNA (miR) networks in cancer remains unknown. We show that the monoclonal antibody that selectively neutralises the signaling (but not coagulant) function of human TF (CNTO 2559) inhibits progression of MDA-MB-231 breast cancer xenografts in mice and prolongs animal survival. CNTO 2559 blocks FVIIa-induced expression of interleukin 8 (IL-8) by cancer cells without impacting factor Xa (FXa) generation. Notably, acute exposure of MDA-MB-231 tumour xenografts to CNTO 2559 systemic injections triggers wide spread changes in the tumour miR profile including alterations in 75 miRs (55 downregulated) and impacting several miR-regulated and cancer-related pathways. These results suggest that TF signaling in the tumour microenvironment may provoke vast changes in the miR profile of cancer cells, affect disease biology, and reflect tumour interaction with the coagulation system, thereby presenting itself as a possible biomarker.

60 APPLIED LIFE SCIENCES↗

The role of N-terminal segment and membrane association in MyD88-mediated signaling

Highlights: • 21 AA MYD88 deletion mutant fails to support MyD88-mediated signaling. • WT MyD88 and 21 AA NTD peptide bind to the phosphatidic acid (PA). • Anchoring of MyD88 to cell membrane and addition of PA augments cell signaling. MyD88 is a central signaling mediator of innate immunity, composed of the N-terminal death (DD) and C-terminal Toll/interleukin-1 receptor (TIR) domain linked by an intermediary (INT) domain. We showed that the N-terminal domain (NTD), composed of apparently unstructured 21 amino-acid residues, is involved in localization and clustering of MyD88 and is required for the efficient signaling, since the deletion mutant is unable to reconstitute MyD88-dependent signaling. Furthermore, we found that the NTD peptide interacts with phosphatidic acid, which potentiates MyD88-mediated signaling through TLRs. Propranolol and expression of lysophosphatidyl acid acyltransferase 1, which increase the level of phosphatidic acid augment cell activation via MyD88. Moreover, anchoring of MyD88 to the cell membrane augments signaling supporting the importance of membrane localization in MyD88-mediated signaling.

60 APPLIED LIFE SCIENCES↗

Molecular mechanism of biased signaling at the kappa opioid receptor

The κ-opioid receptor (KOR) has emerged as an attractive drug target for pain management without addiction, and biased signaling through particular pathways of KOR may be key to maintaining this benefit while minimizing side-effect liabilities. As for most G protein-coupled receptors (GPCRs), however, the molecular mechanisms of ligand-specific signaling at KOR have remained unclear. To better understand the molecular determinants of KOR signaling bias, we apply structure determination, atomic-level molecular dynamics (MD) simulations, and functional assays. We determine a crystal structure of KOR bound to the G protein-biased agonist nalfurafine, the first approved KOR-targeting drug. We also identify an arrestin-biased KOR agonist, WMS-X600. Using MD simulations of KOR bound to nalfurafine, WMS-X600, and a balanced agonist U50,488, we identify three active-state receptor conformations, including one that appears to favor arrestin signaling over G protein signaling and another that appears to favor G protein signaling over arrestin signaling. These results, combined with mutagenesis validation, provide a molecular explanation of how agonists achieve biased signaling at KOR.

59 BASIC BIOLOGICAL SCIENCES↗

Investigation of defects in In–Ga–Zn oxide thin film using electron spin resonance signals

In–Ga–Zn oxide (IGZO) is a next-generation semiconductor material seen as an alternative to silicon. Despite the importance of the controllability of characteristics and the reliability of devices, defects in IGZO have not been fully understood. We investigated defects in IGZO thin films using electron spin resonance (ESR) spectroscopy. In as-sputtered IGZO thin films, we observed an ESR signal which had a g-value of g = 2.010, and the signal was found to disappear under thermal treatment. Annealing in a reductive atmosphere, such as N{sub 2} atmosphere, generated an ESR signal with g = 1.932 in IGZO thin films. The temperature dependence of the latter signal suggests that the signal is induced by delocalized unpaired electrons (i.e., conduction electrons). In fact, a comparison between the conductivity and ESR signal intensity revealed that the signal's intensity is related to the number of conduction electrons in the IGZO thin film. The signal's intensity did not increase with oxygen vacancy alone but also with increases in both oxygen vacancy and hydrogen concentration. In addition, first-principle calculation suggests that the conduction electrons in IGZO may be generated by defects that occur when hydrogen atoms are inserted into oxygen vacancies.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗

Stacked CMB lensing and ISW signals around superstructures in the DESI Legacy Survey

The imprints of large-scale structures on the Cosmic Microwave Background (CMB) can be studied via the CMB lensing and Integrated Sachs–Wolfe (ISW) signals. In particular, the stacked ISW signal around supervoids has been claimed in several works to be anomalously high. In this study, we find cluster and void superstructures using four tomographic redshift bins with 0 < z < 0.8 from the DESI Legacy Survey and measure the stacked CMB lensing and ISW signals around them. To compare our measurements with ΛCDM model predictions, we construct a mock catalogue with matched galaxy number density and bias and apply the same photo-z uncertainty as the data. The consistency between the mock and the data is verified via the stacked galaxy density profiles around the superstructures and their quantity. The corresponding lensing convergence and ISW maps are then constructed and compared. The stacked lensing signal agrees with data well except at the highest redshift bin in density peaks, where the mock prediction is significantly higher, by approximately a factor of 1.3. The stacked ISW signal is generally consistent with the mock prediction. We do not obtain a significant signal from voids, A ISW = -0.10 ± 0.69, and the signal from clusters, A ISW = 1.52 ± 0.72, is at best weakly detected. However, these results are strongly inconsistent with previous claims of ISW signals at many times the level of the ΛCDM prediction. We discuss the comparison of our results with past work in this area and investigate possible explanations for this discrepancy.

79 ASTRONOMY AND ASTROPHYSICS↗

A maize semi-dwarf mutant reveals a GRAS transcription factor involved in brassinosteroid signaling

Brassinosteroids (BR) and gibberellins (GA) regulate plant height and leaf angle in maize (Zea mays). Mutants with defects in BR or GA biosynthesis or signaling identify components of these pathways and enhance our knowledge about plant growth and development. In this study, we characterized three recessive mutant alleles of GRAS transcription factor 42 (gras42) in maize, a GRAS transcription factor gene orthologous to the DWARF AND LOW TILLERING (DLT) gene of rice (Oryza sativa). These maize mutants exhibited semi-dwarf stature, shorter and wider leaves, and more upright leaf angle. Transcriptome analysis revealed a role for GRAS42 as a determinant of BR signaling. Analysis of the expression consequences from loss of GRAS42 in the gras42-mu1021149 mutant indicated a weak loss of BR signaling in the mutant, consistent with its previously demonstrated role in BR signaling in rice. Loss of BR signaling was also evident by the enhancement of weak BR biosynthetic mutant alleles in double mutants of nana plant1-1 and gras42-mu1021149. The gras42-mu1021149 mutant had little effect on GA-regulated gene expression, suggesting that GRAS42 is not a regulator of core GA signaling genes in maize. Single-cell expression data identified gras42 expressed among cells in the G2/M phase of the cell cycle consistent with its previously demonstrated role in cell cycle gene expression in Arabidopsis (Arabidopsis thaliana). Cis-acting natural variation controlling GRAS42 transcript accumulation was identified by expression genome-wide association study (eGWAS) in maize. Our results demonstrate a conserved role for GRAS42/SCARECROW-LIKE 28 (SCL28)/DLT in BR signaling, clarify the role of this gene in GA signaling, and suggest mechanisms of tillering and leaf angle control by BR.

54 ENVIRONMENTAL SCIENCES↗

Bio‐Imaging quorum sensing signal molecules in a soil‐mimic gel

Rhizosphere, the narrow region surrounding plant roots directly influenced by root exudates and the root associated microbiome, plays an important role in plant productivity and the rhizosphere is well known for stimulating microbial metabolic activities. How microbial communities interact to form stable, metabolically interconnected functional communities is an area of intense interest. The question remains on how microbially produced secreted molecules that function as intercellular communication signals shape the structure and function of microbial communities. Our goal is to detect and quantify signal molecules produced by microbes or plants in the root‐soil environment, spatially and temporarily. As a proof‐of‐concept, we are imaging diffusible extracellular microbial metabolites involved in a bacteria‐bacteria communication process called quorum‐sensing. Quorum‐sensing relies on the accumulation of high concentrations of signal molecules in the environment to control bacterial gene expression, influencing rhizosphere colonization and plant health. Local concentration of quorum sensing molecules are determined using aptamer based sensors. Aptamers that can specifically bind the desired signal molecules are selected through SELEX and immobilized on the surface of nano‐porous membranes. Binding of the signal molecules and aptamer covered surface results in changes in surface charge distribution and steric hinderance and thus modifying the transmembrane ionic transport. Changes in transmembrane impedance can be measured through electrochemical impedance spectroscopy methods to monitor local concentrations of signal molecules. Sensor responses were determined for different concentrations of signal molecules and results showed detection of C4‐HSL in a soil‐mimic solution with K D of 10 nM. We demonstrate that the quorum‐sensing signal molecule C4‐homoserine lactone and (C4‐HSL) can rapidly diffuse in a soil‐mimic gel, providing evidence for our use of a soil‐mimic for further aptasensor development and validation. The sensors were then inserted into soil mimic gel for monitoring C4‐HSL diffusion and the resulted impedance changes were used to determine the C4‐HSL concentration at different positions in the gel. Measurements of local C4‐HSL concentrations variation and numerical solution of diffusion equation were used to create 4D images of C4‐HSL molecule diffusion in the soil‐mimic gel.

Jiang, Nianyu↗