Albert Batushansky

Biological strategies for manipulating light have revealed new concepts in light scattering, inspiring the design of sustainable photonic materials. While iridescent optical systems have been extensively studied, many applications require noniridescent structural colors which are much more difficult to achieve. Photonic glasses, comprising randomly arranged dielectric spheres, offer a promising solution toward such structural colors. However, their intrinsic disorder and particle size polydispersity typically lead to poor color saturation. Here, we identify two strategies employed by certain damselflies to generate unexpectedly vivid, tunable angle-independent colors from a photonic glass. First, doping of transparent pteridine nanospheres with yellow pigments strengthens blue–green reflectance resonances by simultaneously absorbing off-resonant wavelengths and enhancing the refractive-index near the reflectance band. Second, the refractive index of the nanospheres is modulated, via changes in crystallinity, to be almost exactly inversely correlated with nanosphere size. Thus, variations in nanosphere size, that ordinarily broaden reflectance resonances, resulting in poor color saturation, are compensated for by a correlated change in their refractive index. This ensures that even in a polydisperse ensemble, a consistent Mie scattering size parameter is maintained, strengthening short-range correlations and Mie scattering resonances. Finally, we show how damselflies tune these structural colors during maturation by precisely modulating the average size of the nanospheres, which arises naturally during the development of the pigment cells due to the densification and crystallization of the nanospheres. These findings reveal design strategies for overcoming limitations in the saturation of disordered photonic systems.

Acquiring new cellular states entails metabolic reprogramming driven by changes in the expression of cytosolic and mitochondrial metabolic enzymes. Most mitochondrial proteins are synthesized in the cytosol and imported into the mitochondria in a linear form, after which they are folded by a network of mitochondrial chaperones and co-chaperones. Which mitochondrial protein is dependent upon which chaperone for its folding is largely unknown. HSPD1/HSPE1 (HSP60/HSP10) are evolutionarily conserved mammalian homologues of the bacterial proteins GroEL/GroES, forming a chamber-and-lid chaperonin to facilitate the folding of client proteins. We used gene knockdown and SILAC-based proteomics to identify HSPD1 client proteins. We found that HSPD1 supports the expression of Methylenetetrahydrofolate Dehydrogenase 2 (MTHFD2), a key essential protein in the mitochondrial one-carbon (1C) pathway, in cells and tumors, and directly folds MTHFD2, independently of its co-chaperone HSPE1. HSPD1 interacts with MTHFD2 in mitochondria, and MTHFD2 is degraded by LONP1 in HSPD1 knockdown cells. Consequently, we observed reduced nucleotide and S-adenosylmethionine (SAM) levels in HSPD1 knockdown and found minimal overlap in the transcriptional and metabolic cellular responses to HSPD1 vs. HSPE1 depletion. In C. elegans, knockout of HSP60 triggers the mitochondrial stress response in the gut, while HSP10 knockout triggers the mitochondrial stress response in muscle tissue. Our data support that HSPD1 is an MTHFD2 chaperone and that, in addition to working together, HSPD1 and HSPE1 have distinct biological functions.

Biology’s strategies for manipulating light offer rich inspiration for the design of sustainable replacements to conventional pigments in paints, coatings, and displays. For these applications, where angle-independent color is required, photonic glasses, composed of random arrangements of dielectric spheres, offer a promising solution. However, their intrinsic disorder, particularly from particle polydispersity, fundamentally limits their color saturation and practical utility. In contrast, insects like damselflies and dragonflies exhibit surprisingly vivid, non-iridescent structural colors, despite relying on disordered photonic structures. Here, we show how damselflies combine compositional and structural dispersion to overcome color saturation limits of photonic glasses. Firstly, doping transparent particles with yellow pigments dramatically enhances blue-green structural resonances by the coupled effects of narrowband absorption and refractive index (material) dispersion. Secondly, the refractive index of the nanospheres varies with their size and crystallinity. This gives rise to a ‘structural dispersion’ which maintains consistent optical path lengths in polydisperse assemblies, preserving high color purity. Finally, we show how damselflies tune their structural colors during maturation by precisely modulating the size of the nanospheres. Remarkably, the tuning of particle size, refractive index and pigment loading, arises naturally during the development of the pigment cells – where the pteridine nanospheres undergo a process of densification, crystallization and metabolic maturation.

Sediments are key players in the optimum functioning of ecosystems; however, they also represent the largest known repository of harmful contaminants. The vast variety of these sediment-associated contaminants may exert harmful effects on marine communities and can impair ecosystem functioning. Whole-cell biosensors are a rapid and biologically relevant tool for assessing environmental toxicity. Therefore, in this study, we developed a bioassay-based toxicity measurement system using genetically modified bacteria to create a whole-cell optical biosensor. Briefly, reporter bacteria were integrated and immobilized using a calcium alginate matrix on fiber-optic tips connected to a photon counter placed inside a light-proof, portable case. The calcium alginate matrix acts as a semi-permeable membrane that protects the reporter-encapsulated optical fiber tips and allows the inward passage of toxicant(s) to induce a dose-dependent response in the bioreporter. The samples were tested by directly submerging the fiber tip with immobilized bacteria into vials containing either water or suspended sediment samples, and the subsequent bioluminescent responses were acquired. In addition to bioavailable sediment toxicity assessments, conventional chemical methods, such as liquid chromatography–mass spectroscopy (LC-MS) and inductively coupled plasma optical emission spectroscopy (ICP-OES), were used for comprehensive evaluation. The results demonstrated the efficacy of the biosensor in detecting various toxicity levels corresponding to identified contaminants, highlighting its potential integration into environmental monitoring frameworks for enhanced sediment and water quality assessments. Despite its utility, this study notes the system’s operational challenges in field conditions, recommending future enhancements for improved portability and usability in remote locations.

Sediments are key players in the optimum functioning of ecosystems; however, they also represent the largest known repository of harmful contaminants. The vast variety of these sediment-associated contaminants may exert harmful effects on marine communities and can impair ecosystem functioning. Whole-cell biosensors are a rapid and one of the biologically relevant tools for assessing environmental toxicity. Therefore, in this study, we aimed to develop a bioassay-based toxicity measurement system using genetically modified bacteria to create a whole-cell optical biosensor. Briefly, reporter bacteria are integrated and immobilized using a calcium-alginate matrix on fiber-optic tips connected to a photon counter placed inside a light-proof, portable case. The calcium alginate matrix acts as a semi-permeable membrane that protects the reporter-encapsulated optical fiber tips and allows the inward passage of the toxicant(s) to induce a dose-dependent response in the bioreporter. Samples were tested by directly submerging the fiber tip with immobilized bacteria into vials containing either water or suspended sediment samples and the subsequent bioluminescent responses acquired. In addition to bioavailable sediment toxicity assessments, conventional chemical methods – liquid chromatography-mass spectroscopy (LC-MS), inductively coupled plasma optical emission spectroscopy (ICP-OES) for comprehensive evaluation were likewise used. Results demonstrated the biosensor's efficacy in detecting various toxicity levels corresponding to identified contaminants, showcasing its potential integration into environmental monitoring frameworks for enhanced sediment and water quality assessments. Despite its utility, the study notes the system's operational challenges in field conditions, recommending future enhancements for improved portability and usability in remote locations.

Wheat is a staple crop and one of the most widely consumed grains globally. Wheat yields can experience significant losses due to the damaging effects of herbivore infestation. However, little is known about the effect aphids have on the natural diurnal rhythms in plants. Our time-series transcriptomics and metabolomics study reveal intriguing molecular changes occurring in plant diurnal rhythmicity upon aphid infestation. Under control conditions, 15,366 out of the 66,559 genes in the tetraploid wheat cultivar Svevo, representing approximately 25% of the transcriptome, exhibited diurnal rhythmicity. Upon aphid infestation, 5,682 genes lost their rhythmicity, while additional 5,203 genes began to exhibit diurnal rhythmicity. The aphid-induced rhythmic genes were enriched in GO terms associated with plant defense, such as protein phosphorylation and cellular response to ABA and were enriched with motifs of the WRKY transcription factor families. Conversely, the genes that lost rhythmicity due to aphid infestation were enriched with motifs of the TCP and ERF transcription factor families. While the core circadian clock genes maintain their rhythmicity during infestation, we observed that approximately 60% of rhythmic genes experience disruptions in their rhythms during aphid infestation. These changes can influence both the plant’s growth and development processes as well as defense responses. Furthermore, analysis of rhythmic metabolite composition revealed that several monoterpenoids gained rhythmic activity under infestation, while saccharides retained their rhythmic patterns. Our findings highlight the ability of insect infestation to disrupt the natural diurnal cycles in plants, expanding our knowledge of the complex interactions between plants and insects.

The release of antibiotic compounds into wastewater constitutes a significant and growing health and environmental hazard, particularly contributing to the spread of antibiotic resistant bacterial strains. Here, we demonstrate that amyloid fibrils, consisting of an alternating lysine/phenylalanine -sheet forming short peptide, catalyze hydrolysis of β-lactam antibiotics, the most prominent family of antibiotic compounds, which is further widespread in wastewater. Peptide variant analysis, molecular dynamics (MD) simulations, and cryogenic electron microscopy (cryo-EM) reveal that the β-lactam molecules dock onto the fibrils’ surface via electrostatic interactions with the lysine sidechains. Importantly, catalytic hydrolysis occurs via an allosteric mechanism mediated by a unique coiled double fibril structure in which the anchored β-lactam molecules are embedded within twisted fiber strands, facilitating nucleophilic attacks by the lysine sidechains. Utilization of the catalytic lysine-displaying amyloid fibrils for hydrolytic degradation and removal of β-lactam antibiotics from water was accomplished through display of the fibrils on silica beads placed in a conventional column filtration setup. Amyloid fibrils displaying lysine arrays may furnish a versatile platform for hydrolysis and removal of β-lactam antibiotics in water, underscoring new avenues for addressing the considerable threat of antibiotics water contamination.

Background: Phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase (PFK‐2) is a critical glycolytic regulator responsible for upregulation of glycolysis in response to insulin and adrenergic signaling. PFKFB2, the cardiac isoform of PFK‐2, is degraded in the heart in the absence of insulin signaling, contributing to diabetes‐induced cardiac metabolic inflexibility. However, previous studies have not examined how the loss of PFKFB2 affects global cardiac metabolism and function. Methods and Results: To address this, we have generated a mouse model with a cardiomyocyte‐specific knockout of PFKFB2 (cKO). Using 9‐month‐old cKO and control mice, we characterized the impacts of PFKFB2 on cardiac metabolism, function, and electrophysiology. cKO mice have a shortened life span of 9 months. Metabolically, cKO mice are characterized by increased glycolytic enzyme abundance and pyruvate dehydrogenase activity, as well as decreased mitochondrial abundance and beta oxidation, suggesting a shift toward glucose metabolism. This was supported by a decrease in the ratio of palmitoyl carnitine to pyruvate‐dependent mitochondrial respiration in cKO relative to control animals. Metabolomic, proteomic, and Western blot data support the activation of ancillary glucose metabolism, including pentose phosphate and hexosamine biosynthesis pathways. Physiologically, cKO animals exhibited impaired systolic function and left ventricular dilation, represented by reduced fractional shortening and increased left ventricular internal diameter, respectively. This was accompanied by electrophysiological alterations including increased QT interval and other metrics of delayed ventricular conduction. Conclusions: Loss of PFKFB2 results in metabolic remodeling marked by cardiac ancillary pathway activation. This could delineate an underpinning of pathologic changes to mechanical and electrical function in the heart.