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The first characterization of W08E12.2 , W08E12.3 , W08E12.4 and W08E12.5 , four putative metalloproteins in C. elegans . (A) phase contrast microscopy, (B) fluorescence microscopy of PW08E12.3 ; W08E12.4 ::GFP.
The solar water-splitting protein complex, photosystem II (PSII), catalyzes one of the most energetically demanding reactions in nature by using light energy to drive a catalyst capable of oxidizing water. The water oxidation reaction is catalyzed at the Mn 4 Ca-oxo cluster in the oxygen-evolving complex (OEC), which cycles through five light-driven S-state intermediates (S 0 –S 4 ). A detailed mechanism of the reaction remains elusive as it requires knowledge of the delivery and binding of substrate water in the higher S-state intermediates. In this paper, we use two-dimensional (2D) hyperfine sublevel correlation spectroscopy, in conjunction with quantum mechanics/molecular mechanics (QM/MM) and density functional theory (DFT), to probe the binding of the substrate analog, methanol, in the S 2 state of the D1-N87A variant of PSII from Synechocystis sp. PCC 6803. The results indicate that the size and specificity of the “narrow” channel is altered in D1-N87A PSII, allowing for the binding of deprotonated 13 C-labeled methanol at the Mn4(IV) ion of the catalytic cluster in the S 2 state. This has important implications on the mechanistic models for water oxidation in PSII.
Comparison of microbial strains for tolerance to and catabolism of lignin stream constituents toward evaluating microbial hosts for lignin bioconversion.
Nature routinely exploits liquid–liquid phase separation (LLPS) of proteins to control the assembly and mineralization of hybrid materials. Here, we show that fusion of the Car9 silica-binding peptide to an elastin-like polypeptide (ELP) yields temperature- and sequence-programmable soft matter templates for the synthesis of silicified architectures ranging in size from nanometers to micrometers. Specifically, we demonstrate unprecedented control over the diameter of silica nanoparticles (SiNP) in the 30–60 nm range with 4 nm precision, show that a single arginine residue (R4) in the Car9 sequence underpins the transition from micelles to proteinosomes, and find that substitutions in other basic residues modulate electrostatic repulsion and solvation to enable access to kinetically trapped species. These structures, which include interconnected micelles, small (∼200 nm) and large (>5 µm) vesicles, are readily visualized by SEM imaging following silicification. Molecular dynamics (MD) simulations and AlphaFold predictions reveal that mutations in positively charged residues alter interfacial packing, hydration, and conformational freedom of the silica-binding segments. Overall, our results establish sequence and thermal energy as synergistic levers for morphological control across length scales using solid-binding ELPs and establish mineralization as a powerful tool to visualize the structure of dynamic soft matter assemblies.
We present a density functional theory study of the oxidation of 1D periodic rods supported along the [001] direction on the rutile TiO{sub 2}(110) surface. The study shows evidence for an oxidation of the interface between the supported Au and the TiO{sub 2} crystal. The added O atoms adsorb at the 5f-Ti atoms in the through under the Au rod and are stabilized by charge transfer from the nearest Au atoms. Despite an extensive search, we find no low energy barrier pathways for CO oxidation involving CO adsorbed on Au and O at the perimeter of the Au/TiO{sub 2} interface. This is in part attributed the weak adsorption of CO on cationic Au at the perimeter.
The Fluctuation-Dissipation theorem (FDT) connects the “memory” in the fluctuation in equilibrium to the response of a system after a perturbation, which has been a fundamental ground in many branches of physics. When viewing a cell as a stochastic biochemical system, the cell's response under a perturbation is related to its intrinsic steady-state correlation functions via the FDT, a theorem we derived and present in this work. FDT allows us to use the noise to derive dynamic response and infer dynamic properties in the system. We tested FDT's validity with gene regulation models and found that it is limited to the linear response. For an indirect regulation pathway where unknown components may exist, FDT still works within the linear response region. Thus, FDT may be used for systems with partial knowledge, and it is potentially possible to identify the existence of unobserved components. With FDT, the dynamic response can be composed of steady-state measurements without the complete detailed knowledge for the regulation or kinetics. The response function derived can give important insights into the dynamics and time scales of the system.
We describe a set of basic stochastic biocircuits for which the Master Equation is completely solvable. Beside linear circuits, which are known to be solvable, we show that tree-like circuits with polynomial transition functions are also completely solvable. We associate a simple but unambiguous graphical representation to such circuits. The graphical representation shows the signal propagation through these simple circuits.
The purpose of this article is to optimize the tube in tube structural systems for tall buildings under the horizontal wind loads. It is well-known that the horizontal wind loads is the main criteria when choosing the structural system, the types and the dimensions of structural elements in the majority of tall buildings. Thus, the structural response of tall buildings under the horizontal wind loads will be analyzed for 40 story buildings and a total height of 120 meters; the horizontal dimensions will be 30m × 30m for the first two optimization problems and 15m × 15m for the third. The optimization problems will have the following as objective function the cross section area, as restrictions the displacement of the building< the admissible displacement (H/500), and as variables the cross section dimensions of the structural elements.
In stem cell differentiation, a pluripotent stem cell becomes progressively specialized and generates specific cell types through a series of epigenetic processes. How cells can precisely determine their fate in a fluctuating environment is a currently unsolved problem. In this paper, we suggest an abstract gene regulatory network to describe mathematically the differentiation phenomenon featuring stochasticity, divergent cell fates, and robustness. The network consists of three functional motifs: an upstream chaotic motif, a buffering motif of incoherent feed forward loop capable of generating a pulse, and a downstream motif which is bistable. The dynamic behavior is typically a transient chaos with fractal basin boundaries. The trajectories take transiently chaotic journeys before divergently settling down to the bistable states. The ratio of the probability that the high state is achieved to the probability that the low state is reached can maintain a constant in a population of cells with varied molecular fluctuations. The ratio can be turned up or down when proper parameters are adjusted. The model suggests a possible mechanism for the robustness against fluctuations that is prominently featured in pluripotent cell differentiations and developmental phenomena.
We recently proposed a Quantum Optimal Control (QOC) method constrained to build pulses from analytical pulse shapes [R. D. Guerrero et al., J. Chem. Phys. 143(12), 124108 (2015)]. This approach was applied to control the dissociation channel yields of the diatomic molecule KH, considering three potential energy curves and one degree of freedom. In this work, we utilized this methodology to study the strong field control of the cis-trans photoisomerization of 11-cis retinal. This more complex system was modeled with a Hamiltonian comprising two potential energy surfaces and two degrees of freedom. The resulting optimal pulse, made of 6 linearly chirped pulses, was capable of controlling the population of the trans isomer on the ground electronic surface for nearly 200 fs. The simplicity of the pulse generated with our QOC approach offers two clear advantages: a direct analysis of the sequence of events occurring during the driven dynamics, and its reproducibility in the laboratory with current laser technologies.
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Gene expression is highly regulated at the step of transcription initiation, and transcription activators play a critical role in this process. RbpA, an actinobacterial transcription activator that is essential in Mycobacterium tuberculosis (Mtb), binds selectively to group 1 and certain group 2 σ-factors. To delineate the molecular mechanism of RbpA, we show that the Mtb RbpA σ-interacting domain (SID) and basic linker are sufficient for transcription activation. We also present the crystal structure of the Mtb RbpA-SID in complex with domain 2 of the housekeeping σ-factor, σ A . The structure explains the basis of σ-selectivity by RbpA, showing that RbpA interacts with conserved regions of σ A as well as the nonconserved region (NCR), which is present only in housekeeping σ-factors. Thus, the structure is the first, to our knowledge, to show a protein interacting with the NCR of a σ-factor. We confirm the basis of selectivity and the observed interactions using mutagenesis and functional studies. In addition, the structure allows for a model of the RbpA-SID in the context of a transcription initiation complex. Unexpectedly, the structural modeling suggests that RbpA contacts the promoter DNA, and we present in vivo and in vitro studies supporting this finding. As a result, our combined data lead to a better understanding of the mechanism of RbpA function as a transcription activator.
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Dilated cardiomyopathy (DCM) is a devastating heart disease that affects about 1 million people in the United States, but the underlying mechanisms remain poorly understood. In this study, we aimed to determine the biomechanical and structural causes of DCM in transgenic mice carrying a novel mutation in the MYL2 gene, encoding the cardiac myosin regulatory light chain. Transgenic D94A (aspartic acid-to-alanine) mice were created and investigated by echocardiography and invasive hemodynamic and molecular structural and functional assessments. Consistent with the DCM phenotype, a significant reduction of the ejection fraction (EF) was observed in ~5- and ~12-mo-old male and female D94A lines compared with respective WT controls. Younger male D94A mice showed a more pronounced left ventricular (LV) chamber dilation compared with female counterparts, but both sexes of D94A lines developed DCM by 12 mo of age. The hypocontractile activity of D94A myosin motors resulted in the rightward shift of the force–pCa dependence and decreased actin-activated myosin ATPase activity. Consistent with a decreased Ca 2+ sensitivity of contractile force, a small-angle X-ray diffraction study, performed in D94A fibers at submaximal Ca 2+ concentrations, revealed repositioning of the D94A cross-bridge mass toward the thick-filament backbone supporting the hypocontractile state of D94A myosin motors. Our data suggest that structural perturbations at the level of sarcomeres result in aberrant cardiomyocyte cytoarchitecture and lead to LV chamber dilation and decreased EF, manifesting in systolic dysfunction of D94A hearts. The D94A-induced development of DCM in mice closely follows the clinical phenotype and suggests that MYL2 may serve as a new therapeutic target for dilated cardiomyopathy.
The small GTPase RABL3 is an oncogene of unknown physiological function. Homozygous knockout alleles of mouse Rabl3 were embryonic lethal, but a viable hypomorphic allele (xiamen [xm]) causing in-frame deletion of four amino acids from the interswitch region resulted in profound defects in lymphopoiesis. Impaired lymphoid progenitor development led to deficiencies of B cells, T cells, and natural killer (NK) cells in Rabl3 xm/xm mice. T cells and NK cells exhibited impaired cytolytic activity, and mice infected with mouse cytomegalovirus (MCMV) displayed elevated titers in the spleen. Myeloid cells were normal in number and function. Further, biophysical and crystallographic studies demonstrated that RABL3 formed a homodimer in solution via interactions between the effector binding surfaces on each subunit; monomers adopted a typical small G protein fold. RABL3 xm displayed a large compensatory alteration in switch I, which adopted a β-strand configuration normally provided by the deleted interswitch residues, thereby permitting homodimer formation. Dysregulated effector binding due to conformational changes in the switch I–interswitch–switch II module likely underlies the xm phenotype. One such effector may be GPR89, putatively an ion channel or G protein-coupled receptor (GPCR). RABL3, but not RABL3 xm , strongly associated with and stabilized GPR89, and an N-ethyl-N-nitrosourea (ENU)-induced mutation (explorer) in Gpr89 phenocopied Rabl3 xm .