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Biology subjects

Auchynnikava, T.

Publications and source records attributed to Auchynnikava, T..

14 recordsLinked to original sources

ESX-1 remodels the Mycobacterium tuberculosis antigen storage compartment in macrophages

Mycobacterium tuberculosis (Mtb) secretes antigenic proteins that drive protective T cell responses, yet how Mtb intracellular localization affects the trafficking and spatiotemporal distribution of mycobacterial antigens in macrophages remains elusive. Here, we developed a split fluorescent protein reporter to monitor the dynamics of the TB vaccine lead antigen Ag85B in infected human macrophages. We discovered that Mtb triggers the formation and remodeling of two distinct types of Mtb Antigen Storage Compartment (MASC) that retains Ag85 within macrophage membranes. Using subcellular spatial proteomics, we profiled the composition of the MASC, identifying both the Mtb and macrophage proteins that constitute these compartments. Unexpectedly, MASCs are defined by metabolic compartmentalization and rewiring to lipid metabolism in both the macrophage and Mtb. Thus, Mtb builds via the ESX-1 system a metabolically distinct antigen storage compartment in immune cells, with potential implications for antigen selection and delivery in TB vaccine development.

cell biology↗

Pervasive binding of the stem cell transcription factor SALL4 shapes the chromatin landscape

Mechanistic understanding of how gene activity is regulated has focussed on the roles of transcription factors at promoters and enhancers, whereas mechanisms capable of globally fine-tuning gene expression through dispersed binding across large genomic regions have received less attention. Here we provide evidence that the essential stem cell transcription factor SALL4 modulates gene expression according to DNA base composition by reading the frequency of its AT-rich target motifs. Using an acute depletion strategy, we establish that SALL4-repressed genes localise to AT-rich genomic domains with high levels of dispersed SALL4 occupancy. While SALL4 is localised within peaks and distributed broadly across the genome, explainable machine learning revealed that its occupancy across the gene body is a strong predictor of transcriptional output. We observed rapid increases in chromatin accessibility and histone acetylation independent of transcriptional activity, suggesting that SALL4 primarily acts upon chromatin, while transcriptional changes are secondary. Accordingly, preventing SALL4 from recruiting the histone deacetylase and nucleosome remodelling corepressor NuRD mimicked a Sall4-null phenotype in stem cells and animal models. Our findings reveal that SALL4s interpretation of DNA sequence optimises the global epigenome and transcriptome, a process integral to maintaining the stem cell gene expression programme.

genomics↗

A structural and regulatory framework for Atg9-containing vesicle formation and their Atg1-dependent remodelling during autophagy initiation

Autophagy is a complex intracellular degradation pathway that depends on the coordinated interplay between the core autophagy machinery and diverse membrane sources to drive the de novo formation of double-membrane vesicles, known as autophagosomes. Golgi-derived Atg9-containing vesicles are essential for this process, delivering membranes to the pre-autophagosomal structure (PAS). These vesicles contain the transmembrane proteins Atg9 and Atg27 and the peripheral membrane protein Atg23; however, the nature, function, and regulation of their interactions remain poorly understood. Here, we systematically dissect the molecular interactions between Atg9, Atg23 and Atg27, and uncover their regulation in space and time. The bipartite binding mode by which Atg23 engages Atg9 provides a structural model for how Atg23 promotes vesicle budding. Furthermore, Atg1-dependent phosphorylation of Atg9 remodels its interactions with Atg23 and Atg27 at the PAS to support autophagy initiation. Together, these findings establish a molecular and regulatory framework for the earliest steps of autophagy.

biochemistry↗

Biomolecular tracking by FIRESCAPE reveals distinct modes of clearance, damage induction and cellular uptake for extracellular histone H3

In attempting to observe the behaviour of a protein of interest in vivo, akin to other observer effects, current techniques require modifications or interventions that inherently alter the protein or its host, leaving one uncertain as to whether natural behaviour remains unperturbed. The study of chromatin has mostly been restricted to defining its function in the nucleus, where histone proteins fulfil vital roles in packaging genomic DNA and regulating transcription. However, chromatin components can be released into the extracellular space, either intentionally via cellular secretion or during disease-induced cell death. These extracellular chromatin components, depending on the context, can consist of: free histones, free DNA, intact nucleosomes (histone octamers wrapped by DNA), or heterogeneous, higher order structures such as neutrophil extracellular traps (NETs). They have been associated with diverse pathologies such as inflammation, cancer, and sepsis, and distinct toxic effects. However, there is a widely acknowledged lack of methods that distinguish between them and between their unique functions. Here, we now address protein observer effects to explore the fate and function of extracellular free histones by utilizing FIRESCAPE ([18F]-Fluorine Isotopic Radiolabeling Enabling Scanning of Clearance After Proteolytic Events), a novel radiolabeling concept that leverages the unique, high-sensitivity properties of the radioisotope fluorine-18, 18F, and residue-specific protein editing chemistry. By installing close and then true 18F-containing protein sidechain mimics site-specifically, FIRESCAPE enables the hierarchical in vivo scanning of the half-lives, proteolytic susceptibility and clearance of single residues in a protein of interest, and at microdoses far below toxic levels (low nanomole). These radioequivalent proteins bearing near-zero-size, zero-background labels now precisely reveal the strikingly distinct distribution, half-lives, damage-inducing abilities and accumulation of free extracellular histones in cellulo and in vivo compared to intact nucleosomes. Free extracellular histone H3 is rapidly cleared from circulation, mediated first by proteolysis of the histone tail. By contrast, direct injection of free histones vs nucleosomes into tissue that is unprotected by such proteolysis (brain), provokes a starkly different response; free histones exhibited limited diffusion and swiftly promoted damage both in cell culture and in vivo, whilst intact nucleosomes were essentially passive and benign. Remarkably, synthetic extracellular histone H3 was observed to enter cells and integrate into chromatin, indistinguishable from native H3 in both localization and post-translational modification (PTM) accumulation, yet paired with cellular and tissue damage. The exploratory studies described here now provide much needed clarity to the distinct fates and effects of extracellular histones vs nucleosomes, in particular the strongly damaging effects of free histones, their rapid uptake into cells, and an associated histone-specific proteolysis pathway via the removal of the histone tail.

biochemistry↗

Control of CDK activity and the cell cycle by CKS proteins

The eukaryotic cell cycle is orchestrated by the activity of Cyclin-Dependent Kinases (CDKs)1. Although most mechanisms controlling CDK activity are well understood, one class of proteins - the CDK regulatory subunit (CKS) proteins - remain highly enigmatic. There is no generally accepted consistent molecular or functional characterisation of CKS in vivo, despite being essential across eukaryotes and implicated in a range of cell cycle processes and cancer2,3. Here, we provide a unifying framework for CKS function. We show in a single, genetically tractable system, the fission yeast, that CKS regulates the onset and progression of both S-phase and mitosis. We find that CKS modulates the phosphorylation of more than 200 CDK phosphosites in vivo, located on 133 substrate proteins. These are involved in diverse processes across the entire cell cycle, including DNA replication, chromosome condensation, the spindle assembly checkpoint, and the metaphase-anaphase transition. We demonstrate that CKS enhances CDK activity to drive phosphorylation of sites with low affinity for CDK. This acts both on specific substrates, likely by stabilizing CDK-substrate interactions, and through control of overall CDK activity, by regulating its interaction with Wee1 and Cdc25. Our findings establish CKS proteins as major multifaceted regulators of the cell cycle, operating through the global and local control of CDK activity.

cell biology↗

Defining the chromatin-associated protein landscapes on Trypanosoma brucei repetitive elements using synthetic TALE proteins

Kinetoplastids, such as Trypansoma brucei, are eukaryotes that likely separated from the main lineage at an exceptionally early point in evolution. Consequently, many aspects of kinetoplastid biology differ significantly from other eukaryotic model systems, including yeasts, plants, worms, flies and mammals. As in many eukaryotes the T. brucei genome contains repetitive elements at various chromosomal locations including centromere- and telomere-associated repeats and interspersed retrotransposon elements. T. brucei also contains intermediate-sized and mini-chromosomes that harbor abundant 177 bp repeat arrays, and 70 bp repeat elements implicated in Variable Surface Glycoprotein (VSG) gene switching. In many eukaryotes repetitive elements are assembled in specialised chromatin such as heterochromatin, however, apart from centromere- and telomere-associated repeats, little is known about chromatin-associated proteins that decorate these and other repetitive elements in kinetoplastids. Here we utilize affinity selection of synthetic TALE DNA binding proteins designed to target specific repeat elements to identify enriched proteins by proteomics. Validating the approach, a telomere repeat binding TelR-TALE identifies many proteins previously implicated in telomere function. Furthermore, the 70R-TALE designed to bind 70 bp repeats indicates that proteins involved in DNA repair are enriched on these elements that reside adjacent to VSG genes. Interestingly, the 177 bp repeat binding 177R-TALE enriches for many kinetochore proteins suggesting that intermediate-sized and mini-chromosomes assemble kinetochores related in composition to those located on the main megabase chromosomes. This provides a first insight into the chromatin landscape of repetitive regions of the trypanosome genome with relevance for their mechanisms of chromosome integrity, immune evasion and cell replication.

cell biology↗

Phosphatase specificity influences phosphorylation timing of CDK substrates during the cell cycle

Cell cycle events are ordered by cyclin-dependent kinases (CDKs), which phosphorylate hundreds of substrates. Multiple phosphatases oppose CDK substrate phosphorylation, yet a systematic understanding of how these phosphatases collectively influence phosphorylation timing is lacking. Here, we show that phosphatases influence the timing of CDK substrate phosphorylation during G2 and mitosis in fission yeast. We identify substrates of four phosphatases (PP2A-B55, PP2A-B56, CDC14, and PP1), showing that each phosphatase targets a distinct subset of CDK substrate sites. On average, sites dephosphorylated by CDC14 and PP2A-B56 are phosphorylated earlier during G2, followed by sites dephosphorylated by PP1 and then PP2A-B55. This suggests that the identity of the phosphatase impacts the timing of CDK substrate phosphorylation, establishing different phosphorylation thresholds at the G2/M transition. Consistent with this, depletion of PP2A-B55 and CDC14 advances mitotic onset independently of CDK activity regulation, likely due to the earlier phosphorylation of their respective CDK substrates.

cell biology↗

Dissecting PADI6 function defines oocyte cytoplasmic lattices as regulatory hubs for fundamental cellular processes

Oocyte cytoplasmic lattices are critical for early embryo development but their composition and function are not fully understood. Mutations in PADI6, an essential component of cytoplasmic lattices, lead to early embryonic developmental arrest and female infertility. To investigate PADI6 function in mRNA storage, global protein levels, and lattice composition during early mammalian development we used single cell transcriptomics and proteomics methods to study two mouse models. Padi6 null mutation resulted in inhibition of embryonic genome activation, defective maternal mRNA degradation, and disruption to protein storage on the cytoplasmic lattices. Distinct developmental phenotypes were observed with a hypomorphic Padi6 mutation. By developing a powerful single cell proteomic fractionation method, we define the cytoplasmic lattice enriched proteome in which we find essential components of another major oocyte-specific compartment, the endolysosomal vesicular assembly (ELVA), suggesting previously unknown interconnections between them. Our findings highlight a critical scaffolding function of PADI6 and implicate cytoplasmic lattices as regulatory hubs for key processes in the oocyte and early embryo, including translation, respiration and protein degradation.

developmental biology↗

Isostere 18F-protein post-translational editing enables dynamic tracking of neurodegeneration biomarkers

The neurofilament light chain protein (NfL) is a suggested general marker for neuronal loss. Its release from brain parenchyma into cerebral spinal fluid, and presumed detection in blood has seen it established as a first blood-based marker of disease activity and drug efficacy in multiple sclerosis (MS) and in the presymptomatic diagnosis and assessment of disease course for other neurodegenerative disorders.1 However, the lack of characterisation of its behaviour in circulation, largely due to its antibody-dependent measurement, have hampered the biological interpretation of these measurements, especially after acute injury such as in MS relapse or head trauma.2 Here, we describe a strategy for exploiting positron emission tomography (PET) imaging using isosteric protein mimics following the installation of a fluorine-18 label that is benign enough to provide sensitive, real-time information on the dynamics and trafficking of NfL protein. This circumvents the limits of current methods that integrate 18F into proteins through the bio-conjugation of bulky, unnatural groups, which we show perturb NfLs assembly and functional properties from those in the natural state. We use a visible-light-driven reaction to access radioactive isostere proteins that are unperturbed and so closely resemble their native form. In this way, generation of [18F]fluoroalkyl radicals that can be rapidly reacted at pre-defined sites on proteins creates mimics of proteinogenic side chains bearing near-zero-size labels to probe proteins in functionally true form. These prosthetic-free, protein radiotracers can be generated in excellent radiochemical yield (up to 67%) via a semi-automated protocol in just 15 mins. High associated molar activities (precursor up to 102 GBq mol-1) allowed high sensitivity dynamic observations in blood, brain and cerebrospinal fluid, enabling even the first unambiguous observations of spinal flow kinetics using proteins. These dynamics, including the high rate of spinal flow (on the order of mm per min) and drainage of NfL from CSF into sacral lymph nodes, now provides evidence that the slow fall rate of antibody-detected markers that is observed after acute neural insults is not due to a long half-life, but rather reflects sustained neuronal loss. This discovery will now help to better correlate clinical and radiological features of disease with NfL blood levels. Our methodology now demonstrates the broad potential of a near-zero-size labelling method for the functional study of proteins in whole organisms without interfering with their biological activity and native assembly.

synthetic biology↗

Identification of RING E3 pseudoligases in the TRIM protein family

TRIpartite Motif (TRIM) family proteins have diverse roles across a broad variety of cellular functions, which are largely presumed to depend on their ubiquitin E3 ligase activity, conferred by a RING domain. However, recent reports have shown that some TRIMs lack detectable ubiquitination activity in isolation, despite containing a RING domain. Here, we present parallel in cellulo, in vitro, and in silico structure-function analyses of the ubiquitin E3 ligase activity and RING domain structural characteristics of whole TRIM protein family. In-depth follow-up studies of this comprehensive dataset reveals a number of pseudoligases, whose RING domains have structurally diverged at either the homodimerisation or E2[~]ubiquitin interfaces, thereby disrupting their ability to catalyse ubiquitin transfer. Together, these data raise intriguing open questions regarding the unknown TRIM functions in physiology and disease. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=83 SRC="FIGDIR/small/614675v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@7c851org.highwire.dtl.DTLVardef@f06afdorg.highwire.dtl.DTLVardef@3cd7org.highwire.dtl.DTLVardef@19a60e6_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

CDK activity at the centrosome regulates the cell cycle

Cyclin-dependent kinases (CDKs) complexed with cyclins drive progression through the eukaryotic cell cycle. From yeast to human cells, cyclin-CDK localises to the centrosome, but the importance of this localisation is unclear. The conserved hydrophobic patch substrate docking site on human Cyclin B1 and on the equivalent fission yeast Cdc13 mediates their localisation to the centrosome and the spindle-pole body (SPB, yeast centrosome equivalent). A hydrophobic patch mutant (HPM) of Cdc13 cannot enter mitosis, but whether this mitotic defect is due to defective SPB localisation or defective cyclin-substrate docking is unknown. Here we show that artificially restoring Cdc13HPM SPB localisation in fission yeast partially rescues both mitosis and defective CDK substrate phosphorylation at both the SPB and within the cytoplasm. In addition, we found that an HPM of the S-phase cyclin Cig2 has defective SPB localisation but is still able to perform bulk DNA synthesis. Our results demonstrate that the hydrophobic patch mediates the SPB localisation of both S- and M-phase cyclins, and that Cdc13 SPB localisation is essential for mitotic entry and for full phosphorylation of CDK substrates, supporting the view that the centrosome plays a role as a signalling hub regulating CDK cell cycle control.

cell biology↗

The SPARC complex defines RNAPII promoters in Trypanosoma brucei

Kinetoplastids are a highly divergent lineage of eukaryotes with unusual mechanisms for regulating gene expression. We previously surveyed 65 putative chromatin factors in the kinetoplastid Trypanosoma brucei. Our analyses revealed that the predicted histone methyltransferase SET27 and the Chromodomain protein CRD1 are tightly concentrated at RNAPII transcription start regions (TSRs). Here we report that SET27 and CRD1, together with four previously uncharacterized constituents, form the SET27 promoter-associated regulatory complex (SPARC), which is specifically enriched at TSRs. SET27 loss leads to aberrant RNAPII recruitment to promoter sites, accumulation of polyadenylated transcripts upstream of normal transcription start sites, and conversion of some normally unidirectional promoters to bidirectional promoters. Transcriptome analysis in the absence of SET27 revealed upregulated mRNA expression in the vicinity of SPARC peaks within the main body of chromosomes in addition to derepression of genes encoding variant surface glycoproteins (VSGs) located in subtelomeric regions. These analyses uncover a novel chromatin-associated complex required to establish accurate promoter position and directionality.

molecular biology↗

A systematic analysis of Trypanosoma brucei chromatin factors identifies novel protein interaction networks associated with sites of transcription initiation and termination

Nucleosomes composed of histones are the fundamental units around which DNA is wrapped to form chromatin. Transcriptionally active euchromatin or repressive heterochromatin is regulated in part by the addition or removal of histone post-translational modifications (PTMs) by writer and eraser enzymes, respectively. Nucleosomal PTMs are recognised by a variety of reader proteins which alter gene expression accordingly. The histone tails of the evolutionarily divergent eukaryotic parasite Trypanosoma brucei have atypical sequences and PTMs distinct from those often considered universally conserved. Here we identify 68 predicted readers, writers and erasers of histone acetylation and methylation encoded in the T. brucei genome and, by epitope tagging, systemically localize 63 of them in the parasites bloodstream form. ChIP-seq demonstrated that fifteen candidate proteins associate with regions of RNAPII transcription initiation. Eight other proteins exhibit a distinct distribution with specific peaks at a subset of RNAPII transcription termination regions marked by RNAPIII-transcribed tRNA and snRNA genes. Proteomic analyses identified distinct protein interaction networks comprising known chromatin regulators and novel trypanosome-specific components. Notably, several SET-domain and Bromo-domain protein networks suggest parallels to RNAPII promoter-associated complexes in conventional eukaryotes. Further, we identify likely components of TbSWR1 and TbNuA4 complexes whose enrichment coincides with the SWR1-C exchange substrate H2A.Z at RNAPII transcriptional start regions. The systematic approach employed provides detail of the composition and organization of the chromatin regulatory machinery in Trypanosoma brucei and establishes a route to explore divergence from eukaryotic norms in an evolutionarily ancient but experimentally accessible eukaryote.

molecular biology↗

Hap2-Ino80 facilitated transcription promotes de novo establishment of CENP-A chromatin

Centromeres are maintained epigenetically by the presence of CENP-A, an evolutionarily-conserved histone H3 variant, which directs kinetochore assembly and hence, centromere function. To identify factors that promote assembly of CENP-A chromatin, we affinity selected solubilised fission yeast CENP-ACnp1 chromatin. All subunits of the Ino80 complex were enriched, including the auxiliary subunit Hap2. In addition to a role in maintenance of CENP-ACnp1 chromatin integrity at endogenous centromeres, Hap2 is required for de novo assembly of CENP-ACnp1 chromatin on naive centromere DNA and promotes H3 turnover on centromere regions and other loci prone to CENP-ACnp1 deposition. Prior to CENP-ACnp1 chromatin assembly, Hap2 facilitates transcription from centromere DNA. These analyses suggest that Hap2-Ino80 destabilises H3 nucleosomes on centromere DNA through transcription-coupled histone H3 turnover, driving the replacement of resident H3 nucleosomes with CENP-ACnp1 nucleosomes. These inherent properties define centromere DNA by directing a program that mediates CENP-ACnp1 assembly on appropriate sequences.

molecular biology↗