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Vaughan, S.

Publications and source records attributed to Vaughan, S..

At least 19 recordsLinked to original sources

Ultrastructural dynamics of basal bodies during microgamete formation and fertilisation in Plasmodium

Cilia and flagella are microtubule-based organelles found in a wide range of eukaryotic organisms that form cilia and flagella are assembled from basal bodies. In the malaria parasite, eight flagellated microgametes are assembled from 8 basal bodies that form de novo as a single group (not next to a parent basal body) in the cytoplasm of microgametocytes extremely rapidly, in as little 8 minutes but is not synchronised. The flagellated microgametes exit from a microgametocyte, each consisting of an axoneme and a haploid nucleus. Fertilisation occurs via a HAP2-mediated fusion with the macrogamete. Despite the essential role of microgametes in malaria transmission and being the only flagellated stage, little is known about the process of basal body formation, biogenesis at the ultrastructure level and their role in fertilisation. We used dual axis serial section electron tomography (ssET) to reveal the unusual single microtubule structure of the basal body and discovered an associated electron dense basal body granule. Using whole cell reconstructions of microgametocytes, free microgametes and macrogametes by serial block face scanning electron microscopy (SBF-SEM), we discovered a deuterosome-like structure only present during the initial formation of 8 basal bodies that could be a nucleating platform for de novo basal body formation. Finally, we reveal that entry of the microgamete into the macrogamete occurs via directed event at a single point of entry with the basal body and granule leading entry. These discoveries highlight the essential functions of basal bodies from initial microgamete assembly to male-female gamete fertilisation.

cell biology↗

Plasmodium Protein Kinase 2 is required for ookinete to oocyst transition, and parasite transmission by the mosquito.

Plasmodium spp., the parasites that are the causative agents of malaria, encode a repertoire of divergent protein kinases that coordinate essential processes including cell division and host cell invasion, yet the functions of many kinases are poorly defined. Plasmodium Protein Kinase 2 (PK2) is essential for asexual blood-stage proliferation and has been implicated in P. falciparum merozoite invasion of red blood cells. However, its role in the sexual stages of the Plasmodium life cycle responsible for transmission is unknown. Here, using live cell imaging, functional analyses, ultrastructure microscopy and phosphoproteomics, we demonstrate that PK2 has a significant role in the Plasmodium berghei life cycle in the mosquito. We show that PK2 is expressed in merozoites, ookinetes and sporozoites - the invasive stages of the parasite life cycle. A conditional knockdown approach revealed that PK2 is required for the ookinete to oocyst transition in the mosquito midgut, potentially associated with altered microneme positioning. Using haemocoel injection to bypass the midgut barrier revealed that PK2 is also required for sporozoite development after midgut invasion. Following PK2 knockdown, global proteome abundance was largely unaffected at 24 h post activation, whereas phosphoproteomics identified changes in phosphorylation of proteins linked to midgut traversal, parasite architecture, and gene regulation. These studies provide insight into the importance of PK2 function in Plasmodium sexual stages and parasite transmission through the mosquito, highlighting its essential function during the three invasive stages of the parasites life cycle.

microbiology↗

Hookworm genomic diversity and population structure from accessible sample types: A validated approach to generate genome-wide polymorphism datasets from individual third-stage larvae

Hookworm infection is a neglected tropical disease affecting hundreds of thousands of people annually in the tropics and sub-tropics. Population genomic approaches have the potential to improve our understanding of hookworm infection dynamics and control efficacy. Here, we validate an approach to generate genome-wide polymorphism datasets from accessible sample types in the zoonotic hookworm (Ancylostoma ceylanicum) then apply the validated approach in the human hookworm (Necator americanus) to compare laboratory- and field-derived samples. We first present an optimized method for purifying nucleic acid from individual third-stage hookworm larvae (L3s). We then measure the accuracy of variant call datasets generated through whole genome amplification (WGA) and next-generation sequencing (NGS). We demonstrate that WGA via multiple displacement amplification (MDA) introduces predictable biases that are exacerbated by low inputs and poor sample preservation but show that with sufficient input mass ([≥]0.1ng) we are still able to produce highly accurate variant call datasets from nucleic acid concentrations that reflect those of individual L3s. Using our validated approach, we infer laboratory- and field-collected samples of N. americanus as distinct populations, with higher levels of heterozygosity and nucleotide diversity identified in field-collected samples, suggesting signatures of inbreeding and/or drift are detectable in laboratory specimens within several years of initiation of infection. We also show that, despite expected reductions in heterozygosity, laboratory samples still possess numerous heterozygous sites, and we demonstrate that a reference genome generated from an adult worm from an early laboratory passage performs well for variant calling in both laboratory- and field-derived samples. Moving forward, our optimized method for nucleic acid purification can be broadly applied to generate input for any amplification-based approach where sequencing individual hookworm L3s, rather than a pool of specimens, is preferred. Our validated population genomics workflow can be used to characterize structure and connectivity of hookworm populations in endemic communities, with the goal of leveraging these insights to improve our approach to hookworm treatment and control. AUTHOR SUMMARYInfection with the human hookworm, Necator americanus, is a significant cause of morbidity in the global south. Population genomic techniques have the potential to improve our understanding of hookworm infection and control. However, third-stage larvae, or L3, which are the hookworm life-cycle stage we routinely have access to when screening infected people, are less than a millimeter long, and this small size makes generating genomic datasets from individual worms difficult. Here, we introduce an optimized approach for purifying DNA from individual L3s and validate its use with whole genome amplification (WGA) for population genomics. We found that WGA from L3s produces sequencing datasets that are biased in their breadth and depth of coverage across the hookworm genome. But by ensuring a minimum threshold for the mass of DNA input to WGA and setting strict criteria for variant filtration, these biases can be overcome to produce highly accurate variant calls genome-wide. We then use this approach to demonstrate reduced genetic diversity in a recently established laboratory hookworm strain as compared to field-collected samples. Our study outlines a specimen-through-analysis workflow that can be used with accessible sample types to measure population structure and diversity of hookworms in endemic communities.

genomics↗

A divergent Plasmodium NEK4 acts as a key regulator driving the early events of meiosis

Meiosis is a conserved yet evolutionarily varied process underpinning sexual reproduction in eukaryotes. In the malaria parasite Plasmodium, meiosis is unconventional: it occurs immediately after fertilisation (post-zygotic) and must be coordinated with the transformation of the zygote into a motile ookinete. The mechanisms synchronising these meiotic and morphogenetic programmes remain unknown. Here, we identify the Plasmodium berghei NIMA-related kinase NEK4 as a key regulator that couples meiotic initiation with zygote morphogenesis. Using ultrastructure expansion microscopy, we show that NEK4 accumulates at the microtubule-organising centre (MTOC) and the apical polar complex (APC) shortly after fertilisation, preceding the assembly of perinuclear and cortical microtubules. We reveal that Plasmodium zygotes undergo MTOC-associated nuclear migration, analogous to the meiotic nuclear movement in fission yeast. Deletion of the Pbnek4 gene results in complete developmental arrest: MTOC duplication and microtubule formation are blocked, chromatin remains uncondensed, and nuclear migration and cell polarity fail to establish. Transcriptomic and phosphoproteomic analyses reveal that absence of NEK4 causes a collapse in transcriptional and phosphoregulatory networks governing meiosis and cytoskeletal organisation, leading to reduced expression and phosphorylation of important players, including HOP1, REC8, and AP2-O. These findings establish NEK4 as a key regulator driving meiotic entry and zygote maturation.

microbiology↗

Plasmodium ARK1 regulates spindle formation during atypical mitosis and forms a divergent chromosomal passenger complex

Mitosis in Plasmodium spp., the causative agent of malaria, is fundamentally different from model eukaryotes, proceeding via a bipartite microtubule organising centre (MTOC) and lacking canonical regulators such as Polo kinases. During schizogony, asynchronous nuclear replication produces a multinucleate schizont, while rapid male gametogony generates an octaploid nucleus before gamete formation. Here, we identify Aurora-related kinase 1 (ARK1) as a key component of inner MTOC and spindle formation, controlling kinetochore dynamics and driving mitotic progression. Conditional ARK1 depletion disrupts spindle biogenesis, kinetochore segregation, karyokinesis and cytokinesis in both stages, and affects parasite transmission. Interactome analysis shows that ARK1 forms the catalytic core of a non-canonical chromosomal passenger complex (CPC) containing two highly divergent inner centromere proteins (INCENPs), which we term INCENP-A and INCENP-B, and lacking the canonical chromatin-targeting subunits Survivin and Borealin. Comparative genomics suggests that apicomplexan INCENPs arose through recurrent lineage-specific duplications, reflecting an evolutionary rewiring of CPC architecture in this eukaryotic lineage. Together, these findings reveal key adaptations in Plasmodium mitosis involving ARK1 and its INCENP scaffolds, and identify the ARK1-INCENP interface as a potential multistage target for antimalarial intervention.

microbiology↗

Discovery of a novel flagellar filament system underpinning Leishmania adhesion to surfaces

Adhesion to surfaces is a common strategy employed across biology, especially by pathogens. Within their sand fly vector, Leishmania parasites undergo multiple developmental stages, including the understudied haptomonad form, which adheres to the sand fly stomodeal valve via a highly modified flagellum. This adhesion, likely critical for efficient transmission, is mediated by a complex adhesion plaque from which filaments in the modified flagellum extend towards the cell body and likely connect to the flagellum attachment zone (FAZ), a cytoskeletal structure important for cell morphogenesis. However, the role of the FAZ in adhesion and its relationship with the Kinetoplastid-Insect Adhesion Proteins (KIAPs) and the filamentous structures of the plaque itself remains unclear. Here, to examine the role of the FAZ in adhesion, we generated FAZ2, FAZ5, and FAZ34 deletion mutants. Deletion of any of these FAZ proteins impaired parasite adhesion in vitro. Furthermore, we identified a novel and distinct set of extra-axonemal flagellar filaments important for adhesion and demonstrated that KIAP2 is an essential component of these filaments. Our findings underscore the importance of a robust connection from the cell body to the adhesion plaque for stable Leishmania adhesion via the highly modified flagellum.

cell biology↗

Malaria parasites undergo a rapid and extensive metamorphosis after invasion of the host erythrocyte

Within the human host, the symptoms of malaria are caused by the replication of malaria parasites within erythrocytes. Growth inside the erythrocyte exposes the parasites to the normal surveillance of erythrocytes by the host organism, in particular the clearance of erythrocytes in the spleen. Here we show that the malaria parasite Plasmodium falciparum undergoes a rapid, multi-step metamorphosis that transforms the invasive merozoite into an amoeboid-shaped cell within minutes after invading erythrocytes. This transformation involves an increase in the parasite surface area and is mediated by factors already present in the merozoite, including the parasite phospholipid transfer protein PV6. Parasites lacking PV6 do not assume an amoeboid form and instead are spherical and have a smaller surface area than amoeboid forms. Furthermore, erythrocytes infected with parasites lacking PV6 undergo a higher loss of surface area upon infection by P. falciparum, which affects the traversal of infected erythrocytes through the spleen. This is the first evidence that after invasion, the parasite undergoes a rapid, complex metamorphosis within the host erythrocyte that promotes survival in the host.

microbiology↗

The C-terminus of CFAP410 forms a tetrameric helical bundle that is essential for its localization to the basal body

Cilia are antenna-like organelles protruding from the surface of many cell types in the human body. Defects in ciliary structure or function often lead to diseases that are collectively called ciliopathies. Cilia and flagella associated protein 410 (CFAP410) localizes at the basal body of cilia/flagella and plays essential roles in ciliogenesis, neuronal development, and DNA damage repair. It remains unknown how its specific basal body location is achieved. Multiple single amino acid mutations in CFAP410 have been identified in patients with various ciliopathies. One of the mutations, L224P, is located in the C-terminal domain (CTD) of human CFAP410 and causes severe spondylometaphyseal dysplasia, axial (SMDAX). However, the molecular mechanism for how the mutation causes the disorder remains unclear. Here, we report our structural studies on the CTD of CFAP410 from three distantly related organisms, Homo sapiens, Trypanosoma brucei, and Chlamydomonas reinhardtii. The crystal structures reveal that the three proteins all adopt the same conformation as a tetrameric helical bundle. Our work further demonstrates that the tetrameric assembly of the CTD is essential for the correct localization of CFAP410 in T. brucei, as the L224P mutation that disassembles the tetramer disrupts its basal body localization. Taken together, our studies reveal that the basal body localization of CFAP410 is controlled by the CTD and provide a mechanistic explanation for how the mutation L224P in CFAP410 causes ciliopathies in humans.

biochemistry↗

3D electron microscopy of the Leishmania mexicana cell cycle: Patterns of organelle duplication and segregation and their implications for parasite biology

The unicellular parasite Leishmania has a precisely defined cell architecture that is inherited by each subsequent generation, requiring a highly coordinated pattern of duplication and segregation of organelles and cytoskeletal structures. A framework of nuclear division and morphological changes is known from light microscopy, yet this has limited resolution and the intrinsic organisation of organelles within the cell body and their manner of duplication and inheritance is unknown. Using volume electron microscopy approaches, we have produced three-dimensional reconstructions of different promastigote cell cycle stages to give a spatial and quantitative overview of organelle positioning, division and inheritance. The first morphological indications seen in our dataset that a new cell cycle had begun were the assembly of a new flagellum, the duplication of the contractile vacuole and the increase in volume of the nucleus and kinetoplast. We showed that the progression of the cytokinesis furrow created a specific pattern of membrane indentations and sub-pellicular microtubule organisation indicates that is likely a preferred site of new microtubule insertion. The daughter cells retained these indentations in their cell body for a period post-abscission. By comparing cultured and sand fly derived promastigotes, we found an increase in the number and overall volume of lipid droplets in the promastigotes from the sand fly, reflecting a change in their metabolism to ensure transmissibility to the mammalian host. Our insights into the cell cycle mechanics of Leishmania will be invaluable for future molecular cell biology analyses of these important parasites.

cell biology↗

Association of mitochondrial fucosyltransferase TbFUT1 with the assembly of the mitochondrial FoF1-ATP synthase in bloodstream form Trypanosoma brucei.

The gene TbFUT1 encodes an essential fucosyltransferase which, unexpectedly, localises to the mitochondrion of the protist parasite Trypanosoma brucei. The expression of TbFUT1 is required for the maintenance of mitochondrial membrane potential ({Psi}{Delta}m) in the bloodstream form (BSF) of the parasite, but the precise functions of TbFUT1 are unknown. Here, we demonstrate that depletion of TbFUT1 causes the accumulation of dyskinetoplastid cells; i.e., cells lacking concatenated complexes of mini- and maxicircle kinetoplast DNA (kDNA), the mitochondrial DNA of these organisms. Morphological analysis by serial face block-scanning electron microscopy showed that the dyskinetoplastid mitochondria were otherwise unperturbed with respect to structure and volume. Proteomics analyses showed that TbFUT1 depletion caused a decrease in the steady-state levels of several subunits of the Fo-subcomplex and peripheral stalk components of the mitochondrial FoF1-ATP synthase, as well as a pronounced reduction in mitochondrial ribosomal large subunit (LSU) proteins and more minor reduction in small subunit (SSU) proteins. TbFUT1 was rendered redundant with respect to cell survival and {Psi}{Delta}m generation upon F1-{gamma}WT/L262P mutation; a mutation that allows the generation of {Psi}{Delta}m in the absence of mitochondrial translation. Additionally, depletion of TbFUT1 no longer perturbs kDNA replication in these cells, indicating that dyskinetoplasty is a downstream consequence of impaired {Psi}{Delta}m. Depletion of TbFUT1 in wild type cells leads to the collapse of {Psi}{Delta}m via a functional FoF1-ATP synthase complex. We therefore conclude these mutants are inhibited in the synthesis of Fo-subcomplex components and, thus, impairing the assembly of functional FoF1-ATP synthase complexes. Curiously, mitochondrial transcript levels exhibit similar changes in abundance after FUT1 ablation in the parental and F1-{gamma}WT/L262P mutants. Further, the [~]5-fold overexpression of TbFUT1 in the TbFUT1 conditional knockout mutant under permissive conditions selectively inhibits the formation of the fully RNA-edited A6 transcript by an unknown mechanism, partially suppressing FoF1-ATP synthase assembly in these mutants. Together, these data suggest that mitochondrial fucosylation is essential for the assembly of protein complexes containing kDNA encoded subunits.

molecular biology↗

Identification of 30 transition fibre proteins reveals a complex and dynamic structure with essential roles in ciliogenesis

Transition fibres are appendages that surround the distal end of mature basal bodies (also called distal appendages) and are essential for ciliogenesis, but only a small number of proteins have been identified and functionally characterised. Here, through genome-wide analysis, we have identified 30 additional transition fibre proteins (TFPs) in the flagellated eukaryote Trypanosoma brucei and mapped the arrangement of the molecular components. We discovered TFPs recruited to the basal body pre- and post-initiation of ciliogenesis with differential expression of TFPs at the assembling new flagellum compared to the existing old flagellum. Knockdown by RNAi of 17 TFPs revealed 6 were necessary for ciliogenesis and a further 3 were necessary for normal flagellum length. We identified 9 TFPs that had a detectable orthologue in at least one basal body-forming eukaryotic organism outside of the kinetoplastid parasites. Our work demonstrates that transition fibres are complex and dynamic in their composition throughout the cell cycle which relates to their essential roles in ciliogenesis and length regulation.

cell biology↗

Atypical flagella assembly and haploid genome coiling during male gamete formation in Plasmodium

Plasmodium spp. sexual reproduction occurs within the Anopheles mosquito and is essential for gametogenesis and onwards transmission to mammalian hosts. Upon activation, the male P. berghei gametocyte undergoes three rounds of inter-nuclear mitosis and assembles eight basal bodies and axonemes around the nucleus prior to ex-flagellation, resulting in 8 flagellated male gametes in 12-15 minutes. However there is little understanding of the 3D organisation of this rapid process of male gametogenesis. In this study we used serial block face scanning electron microscopy (SBF-SEM) and cellular electron tomography (ssET) of P. berghei microgametocytes to examine the 3D architecture of key structures during male gamete formation. Our data has revealed an exquisite organisation of axonemes coiling around the nucleus in opposite directions forming a central axoneme band in microgametocytes. Furthermore, we discovered that the nucleus of microgametes is tightly coiled around the axoneme in an exquisitely complex structure whose formation starts before microgamete emergence during ex-flagellation. Our discoveries of the detailed 3D organisation of the flagellated microgamete and the haploid genome highlights some of the atypical mechanisms of axoneme assembly and haploid genome organisation during male gamete formation in the malaria parasite Plasmodium spp.

cell biology↗

Unlocking Trypanosome Biology: A Comprehensive Protein-Tagging Toolkit for Localization and Functional Analysis

African trypanosomes are medically important parasites that cause Sleeping sickness in humans and nagana in animals. In addition to their pathogenic role, they have emerged as valuable model organisms for studying fundamental biological processes. Protein tagging is a powerful tool for investigating protein localization and function. In a previous study, we developed two plasmids for rapid and reproducible protein tagging in trypanosomes, which enabled the localisation of all proteins in the trypanosome cell. However, the limited selection of fluorescent protein tags and selectable markers restricted the flexibility of this approach. Here, we present an expanded set of >100 vectors that utilizes universal primer annealing sequences, enabling protein tagging with a range of fluorescent and biochemical tags using five different selection markers. We evaluated the suitability of various fluorescent proteins for live cell imaging and determined their brightness and stability under different fixation conditions. Finally, we determined the optimal fluorescent protein for a set of specific experimental conditions demonstrating the utility of this toolkit.

cell biology↗

Structural studies of cilia and flagella associated protein 410 (CFAP410) reveal its bimodular organization with an N-terminal LRR motif and a C-terminal tetrameric helical bundle

Cilia and flagella associated protein 410 (CFAP410) is a protein localized at the basal body of cilia/flagella and plays essential roles in ciliogenesis. Multiple single amino acid mutations in CFAP410 have been identified in patients. However, the molecular mechanism for how the mutations cause these disorders remains poorly understood due to a lack of high-resolution structures of the protein. Our studies demonstrate that CFAP410 adopts a bimodular architecture. We have previously reported our structural studies on the C-terminal domain (CTD) of CFAP410 from various organisms. Here we report a 1.0-[A] resolution crystal structure of the N-terminal domain (NTD) of Trypanosoma brucei CFAP410. We further examined how the disease-causing mutations in this domain may affect the folding and structural stability of CFAP410. Our results suggest that the single-residue mutations in the CFAP410-NTD cause human diseases by destabilizing the structure that subsequently disrupts its interaction with other partners.

biochemistry↗

Genome-wide subcellular protein localisation in the flagellate parasite Trypanosoma brucei

Trypanosoma brucei is a prototypical trypanosomatid, an important group of human, animal and plant unicellular parasites. Understanding their complex cell architecture and life cycle is hindered since, as with most eukaryotic microbes, [~]50% of the proteins encoded in the genome have completely unknown function. Using fluorescence microscopy and cell lines expressing endogenously tagged proteins we mapped the subcellular localisation of 89% of the proteome, giving clues to function, defining the lineage-specific organelle adaptations for obligate parasitism and mapping the ultra-conserved cellular architecture of eukaryotes. This includes the single flagellum, vital for morphogenesis and pathology: the first comprehensive cartographic analysis of the flagellum in any organism. To demonstrate the power of this resource, we identify novel specialisation of organelle molecular composition through the cell cycle and in specialised subdomains. This is a transformative resource, important for hypothesis generation for both eukaryotic evolutionary molecular cell biology and fundamental parasite cell biology.

microbiology↗

Plasmodium SAS4/CPAP is a flagellum basal body component during male gametogenesis but is not essential for parasite transmission

The centriole/basal body (CBB) is an evolutionarily conserved organelle acting as a microtubule organising centre (MTOC) to nucleate cilia, flagella and the centrosome. SAS4/CPAP is a conserved component associated with BB biogenesis in many model flagellated cells. Plasmodium, a divergent unicellular eukaryote and causative agent of malaria, displays an atypical closed mitosis with an MTOC, reminiscent of the acentriolar MTOC, embedded in the nuclear membrane at most proliferative stages. Mitosis during male gamete formation is accompanied by flagellum formation: within 15 minutes, genome replication (from 1N to 8N) and three successive rounds of mitosis without nuclear division occur, with coordinated axoneme biogenesis in the cytoplasm resulting in eight flagellated gametes. There are two MTOCs in male gametocytes. An acentriolar MTOC located with the nuclear envelope and a centriolar MTOC (basal body) located within the cytoplasm that are required for flagellum assembly. To study the location and function of SAS4 during this rapid process, we examined the spatial profile of SAS4 in real time by live cell imaging and its function by gene deletion. We show its absence during asexual proliferation but its presence and coordinated association and assembly of SAS4 with another basal body component, kinesin8B, which is involved in axoneme biogenesis. In contrast its separation from the nuclear kinetochore marker NDC80 suggests that SAS4 is part of the basal body and outer centriolar MTOC residing in the cytoplasm. However, deletion of the SAS4 gene produced no phenotype, indicating that it is not essential for male gamete formation or parasite transmission through the mosquito.

cell biology↗

Cellular electron tomography of the apical complex in the apicomplexan parasite Eimeria tenella shows a highly organised gateway for regulated secretion.

The apical complex of apicomplexan parasites is essential for host cell invasion and intracellular survival and as the site of regulated exocytosis from specialised secretory organelles called rhoptries and micronemes. Despite its importance, there is little data on the three-dimensional organisation and quantification of these organelles within the apical complex or how they are trafficked to this specialised region of plasma membrane for exocytosis. In coccidian apicomplexans there is an additional tubulin-containing hollow barrel structure, the conoid, which provides a structural gateway for this specialised secretion. Using a combination of cellular electron tomography and serial block face-scanning electron microscopy (SBF-SEM) we have reconstructed the entire apical end of Eimeria tenella sporozoites. We discovered that conoid fibre number varied, but there was a fixed spacing between fibres, leading to conoids of different sizes. Associated apical structures varied in size to accommodate a larger or smaller conoid diameter. However, the number of subpellicular microtubules on the apical polar ring surrounding the conoid did not vary, suggesting a control of apical complex size. We quantified the number and location of rhoptries and micronemes within cells and show a highly organised gateway for trafficking and docking of rhoptries, micronemes and vesicles within the conoid around a set of intra-conoidal microtubules. Finally, we provide ultrastructural evidence for fusion of rhoptries directly through the parasite plasma membrane early in infection and the presence of a pore in the parasitophorous vacuole membrane, providing a structural explanation for how rhoptry proteins (ROPs) may be trafficked between the parasite and the host cytoplasm. SignificanceApicomplexan parasites cause a wide range of human and animal diseases. The apical complex is essential for motility, host cell invasion and intracellular survival within a specialised vacuole called the parasitophorous vacuole. We know that molecules important for all of these processes are secreted from the apical complex via a set of secretory organelles and there is even evidence that some parasite molecules can enter the host cell from the parasitohorous vacuole, but there is little understanding of exactly how this occurs. Here we have used three dimensional electron microscopy to reconstruct the entire apical end of the parasite and whole individual parasites. Our results provide important insights into the structural organisation and mechanisms for delivery of parasite molecules via this important area of the cell.

microbiology↗

Identification of a molecular fingerprint for synaptic glia

The inability to specifically identify and manipulate synaptic glial cells remains a major obstacle to understanding fundamental aspects of synapse formation, stability and repair. Using a combinatorial gene expression approach, we discovered molecular markers that allow us to specifically label perisynaptic Schwann cells (PSCs), glial cells at neuromuscular synapses. Using these markers, we demonstrate that PSCs fully-differentiate postnatally and have a unique molecular signature that includes genes predicted and known to play critical roles at synapses. These findings will serve as a springboard for unprecedented approaches for studying molecular determinants of PSC differentiation and function at neuromuscular synapses and possibly synapse-associated glia throughout the CNS.

neuroscience↗