Publications by authors named "Svetlana E Moskalenko"
Rational Design of Far-Red Archaerhodopsin-3-Based Fluorescent Genetically Encoded Voltage Indicators: from Elucidation of the Fluorescence Mechanism in Archers to Novel Red-Shifted Variants.
ACS Phys Chem Au
July 2024
Article Synopsis
- Genetically encoded voltage indicators (GEVIs), especially those based on archaerhodopsin-3, are useful for visualizing changes in cell membrane potential.
- To improve these tools, researchers aimed to create new GEVIs with better fluorescence and absorption properties.
- The study successfully enhanced the fluorescence of archaerhodopsin-3 by stabilizing specific protein conformations through targeted mutations, leading to the design of new variants with a broader absorption range and significantly brighter emissions.
Article Synopsis
- Yeast have two critical translation termination factors, eRF1 and eRF3, whose mutations lead to the amplification of their mutant alleles, which is vital for cell survival.
- The study used RNA-Seq and proteome analysis to explore how yeast cells adapt to nonsense mutations and found significant gene expression changes affecting the cell cycle.
- The researchers suggest that the adaptation involves a delay in cell cycle progression, particularly at the G2-M transition, resulting in extended S and G2 phases that promote the replication of the mutant alleles.
The gene encodes a cytosolic protein that binds to the signaling cascade component neuronal nitric oxide synthase (nNOS). It is associated with many different disorders, such as schizophrenia, post-traumatic stress disorder, autism, cardiovascular disorders, and breast cancer. The NOS1AP (also known as CAPON) protein mediates signaling within a complex which includes the NMDA receptor, PSD-95, and nNOS.
View Article and Find Full Text PDFArticle Synopsis
- Protein synthesis (translation) is essential for living cells and consists of three main steps: initiation, elongation, and termination, with specific factors like eRF1 and eRF3 involved in yeast termination.
- Deletion of the genes encoding these factors is lethal for yeast, but some strains with nonsense mutations can survive through a feedback mechanism related to readthrough of stop codons, though the details of this mechanism are still unclear.
- Whole-genome sequencing revealed no common genetic changes, but increased copy numbers of mutant alleles were observed, with qPCR confirming that gene amplification is a key adaptation strategy for yeast with nonsense mutations in release factor genes.
Amyloids are fibrillar protein aggregates with a cross-β structure and unusual features, including high resistance to detergent or protease treatment. More than two hundred different proteins with amyloid or amyloid-like properties are already known. Several examples of nucleoporins (e.
View Article and Find Full Text PDFThousands of yeast genomes have been sequenced with both traditional and long-read technologies, and multiple observations about modes of genome evolution for both wild and laboratory strains have been drawn from these sequences. In our study, we applied Oxford Nanopore and Illumina technologies to assemble complete genomes of two widely used members of a distinct laboratory yeast lineage, the Peterhof Genetic Collection (PGC), and investigate the structural features of these genomes including transposable element content, copy number alterations, and structural rearrangements. We identified numerous notable structural differences between genomes of PGC strains and the reference S288C strain.
View Article and Find Full Text PDFTermination of translation in eukaryotes is governed by two release factors encoded by the and genes in . Previously, a set of mutations in these genes had been obtained. However, the exact sequence change associated with one mutation, , was not identified by Sanger sequencing of the region.
View Article and Find Full Text PDFYeast self-perpetuating protein aggregates (prions) provide a convenient model for studying various components of the cellular protein quality control system. Molecular chaperones and chaperone-sorting factors, such as yeast Cur1 protein, play key role in proteostasis via tight control of partitioning and recycling of misfolded proteins. In this study, we show that, despite the previously described ability of Cur1 to antagonize the yeast prion [URE3], it enhances propagation and phenotypic manifestation of another prion, [PSI ].
View Article and Find Full Text PDF[PSI ] is the prion form of the translation termination factor Sup35 (eRF3); [PSI ] strains display nonsense suppression. Another prion-like element, [ISP ], is linked to antisuppression in a specific background. Transcriptional regulator Sfp1 was shown to be responsible for [ISP ] propagation.
View Article and Find Full Text PDFBackground: Termination of protein synthesis in eukaryotes involves at least two polypeptide release factors (eRFs) - eRF1 and eRF3. The highly conserved translation termination factor eRF1 in Saccharomyces cerevisiae is encoded by the essential gene SUP45.
Results: We have isolated five sup45-n (n from nonsense) mutations that cause nonsense substitutions in the following amino acid positions of eRF1: Y53 --> UAA, E266 --> UAA, L283 --> UAA, L317 --> UGA, E385 --> UAA.