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Cheeseman, I.

Publications and source records attributed to Cheeseman, I..

7 recordsLinked to original sources

Single-cell transcriptomics resolves the developmental transitions from schizont to invasive extracellular merozoite to ring-stage Plasmodium falciparum parasites

The progression from mature schizonts to newly formed ring-stage parasites represents one of the largest developmental transitions in the Plasmodium falciparum intraerythrocytic developmental cycle (IDC), encompassing parasite egress, erythrocyte invasion, and productive infection of the new host cell. While the transcriptional programs required for egress and invasion are well-documented, less is known about how the parasite prepares for intracellular survival inside the newly invaded erythrocyte. Here, we used single-cell RNA sequencing based on PIPseq chemistry to construct a transcriptional atlas spanning late schizogony, extracellular merozoites, and early ring-stage development. We show that schizogony is characterized by sequential waves of invasion gene expression that closely parallel secretory organelle biogenesis and are associated with cooperative regulation by ApiAP2 transcription factors. Immediately prior to egress, parasites shift from expression of invasion genes to genes required for establishing the intracellular host-parasite interface, including the parasitophorous vacuole and digestive vacuole. Extracellular merozoites separate into transcriptionally distinct invasive and non-invasive populations. Together, these findings provide high temporal resolution of late schizont development, reveal priming for intracellular survival prior to egress, and highlight the short lifespan of invasive merozoites and the resulting challenges of studying this elusive stage of the IDC.

microbiology↗

Efficient generation of marmoset primordial germ cell-like cells using induced pluripotent stem cells

Reconstitution of germ cell fate from pluripotent stem cells provides an opportunity to understand the molecular underpinnings of germ cell development. Here, we established robust methods for pluripotent stem cells (iPSCs) culture in the common marmoset (Callithrix jacchus, cj), which stably propagate in an undifferentiated state. Notably, iPSCs cultured on a feeder layer in the presence of a WNT signaling inhibitor upregulated genes related to ubiquitin-dependent protein catabolic processes and enter a permissive state that enables differentiation into primordial germ cell-like cells (PGCLCs) bearing immunophenotypic and transcriptomic similarities to pre-migratory cjPGCs in vivo. Induction of cjPGCLCs is accompanied by transient upregulation of mesodermal genes culminating in the establishment of a primate specific germline transcriptional network. Moreover, cjPGCLCs can be expanded in monolayer while retaining the germline state. Upon co-culture with mouse testicular somatic cells, these cells acquire an early prospermatogonia-like phenotype. Our findings provide a framework for understanding and reconstituting marmoset germ cell development in vitro, thus providing a comparative tool and foundation for a preclinical modeling of human in vitro gametogenesis.

developmental biology↗

Bulk Segregant Approaches to Nutritional Genomics in Plasmodium falciparum

What genes determine growth and nutrient utilization in asexual blood-stage malaria parasites? Competition experiments between a lab-adapted African parasite (NF54), and a recently isolated Asian parasite (NHP4026) reveal contrasting outcomes in different media: NF54 outcompetes NHP4026 in media containing human serum, while NHP4026 outcompetes NF54 in media containing AlbuMAX, a lipid-rich bovine serum formulation. We conducted parasite genetic crosses and compared genome-wide allele frequency changes in progeny populations cultured in media containing serum or AlbuMAX: this bulk segregant analysis (BSA) reveals three quantitative trait loci (QTL) underlying differential growth. The strongest QTL (chromosome 13) contains EBA-140: competition experiments between EBA-140-knockout and isogenic wildtype parasites showed fitness reversals in the two media types, validating this locus as the causative gene. These results (i) demonstrate the effectiveness of BSA for dissecting fitness traits in Plasmodium falciparum, and (ii) reveal an intimate link between red blood cell invasion and nutrient composition of growth media.

genetics↗

Cohesin removal reprograms gene expression upon mitotic entry

Entering mitosis, the genome is restructured to facilitate chromosome segregation, accompanied by dramatic changes in gene expression. However, the mechanisms that underlie mitotic transcriptional regulation are unclear. In contrast to transcribed genes, centromere regions retain transcriptionally active RNA Polymerase II (RNAPII) in mitosis. Here, we demonstrate that chromatin-bound cohesin is sufficient to retain RNAPII at centromeres while WAPL-mediated removal of cohesin during prophase is required for RNAPII dissociation from chromosome arms. Failure to remove cohesin from chromosome arms results in a failure to release elongating RNAPII and nascent transcripts from mitotic chromosomes and dramatically alters gene expression. We propose that prophase cohesin removal is the key step in reprogramming gene expression as cells transition from G2 to mitosis, and is temporally coupled with chromosome condensation to coordinate chromosome segregation with changes in gene expression.\n\nHighlightsO_LIMitotic centromere transcription requires cohesin\nC_LIO_LICohesin removal releases elongating RNA Pol II and nascent RNA from chromatin\nC_LIO_LIThe prophase pathway reprograms gene expression during mitosis\nC_LI

cell biology↗

Mode and tempo of microsatellite length change in a malaria parasite mutation accumulation experiment

Microsatellite sequences are widely assumed to evolve neutrally, but also play an important role in bacterial pathogenesis, human disease and transcript abundance. The malaria parasite Plasmodium falciparum genome is extraordinarily AT-rich, containing 132,449 microsatellites-stretches of perfect 1-9 bp repeats between 10-1000bp, which comprise 10.74% of the 23 Mb genome. This project was designed to determine the mode and tempo of microsatellite mutations in malaria parasites. We maintained 31 parasite lines derived from a single 3D7 parasite cell for 114-267 days, with frequent bottlenecking to a single cell to minimize effective population size, allowing us to measure mutations accumulated over ~13,207 mitotic divisions. We Illumina sequenced the genomes of both progenitor and end-point mutation accumulation (MA) parasite lines in duplicate to validate stringent calling parameters. Calls were 99.89% (GATK), 99.99% (freeBayes) and 99.96% (HipSTR) concordant in duplicate sequence runs from independent sequence libraries. We observed 98 microsatellite mutations, giving rates of 2.11 x 10-7 - 1.46 x 10-8 /cell division that were strongly influenced by repeat motif and array length. Mutation rate was low relative to other organisms. However, despite this, in a single infection (1011 parasites) there will be 1.46 x 103 - 2.11 x 104 independent mutations at any single microsatellite locus. Given that many microsatellites are found in promotors, introns, within or close to coding sequences, we suggest that they may be important regulators of transcriptional and phenotypic variation in this pathogen. Author summaryMutation is central to evolution: in pathogens, the rate of mutation may determine how rapidly drug resistance evolves or how effectively pathogens can escape immune attack. Malaria parasites have small extremely AT-rich genomes, and genetic variation in natural populations is dominated by repeat number changes in short tandem repeats (microsatellites) rather than point mutations. We therefore focused on quantifying microsatellite mutation. We established 31 parasite cultures in the laboratory all derived from a single parasite cell. These were maintained for 114-267 days with frequent reductions to a single cell, so parasites accumulated mutations during ~13,207 cell divisions. We sequenced the parasite genomes at the end of the experiment to count the mutations. We highlight several conclusions: like other organisms studied, microsatellite mutation rates are associated with both repeat number and repeat motif. However, 41% of changes resulted from loss or gain of more than one repeat: this was particularly true for long repeat arrays. Unlike other eukaryotes, we found no insertions or deletions that were not associated with repeats or homology regions. Overall, we found that microsatellite mutation rates in malaria were amongst the lowest recorded and comparable to those in another AT-rich protozoan (the slime mold Dictyostelium).

evolutionary biology↗

Quiescent cells actively replenish CENP-A nucleosomes to maintain centromere identity and proliferative potential

Centromeres provide a robust model for epigenetic inheritance as they are specified by sequence-independent mechanisms involving the histone H3-variant CENP-A. Prevailing models indicate that the high intrinsic stability of CENP-A nucleosomes maintains centromere identity indefinitely. Here, we demonstrate that CENP-A is not stable at centromeres, but is instead gradually and continuously incorporated in quiescent cells including G0-arrested tissue culture cells and prophase I-arrested oocytes. Quiescent CENP-A incorporation involves the canonical CENP-A deposition machinery, but displays distinct requirements from cell cycle-dependent deposition. We demonstrate that Plk1 is required specifically for G1 CENP-A deposition, whereas transcription promotes CENP-A incorporation in quiescent oocytes. Preventing CENP-A deposition during quiescence results in significantly reduced CENP-A levels and perturbs chromosome segregation following the resumption of cell division. In contrast to quiescent cells, terminally differentiated cells fail to maintain CENP-A levels. Our work reveals that quiescent cells actively maintain centromere identity providing an indicator of proliferative potential.

cell biology↗

Astrin-SKAP complex reconstitution reveals its kinetochore interaction with microtubule-bound Ndc80

Chromosome segregation requires robust interactions between the macromolecular kinetochore structure and dynamic microtubule polymers. A key outstanding question is how kinetochore-microtubule attachments are modulated to ensure that bi-oriented attachments are selectively stabilized and maintained. The Astrin-SKAP complex localizes preferentially to properly bi-oriented sister kinetochores, representing the final outer kinetochore component recruited prior to anaphase onset. Here, we reconstitute the 4-subunit Astrin-SKAP complex, including a novel MYCBP subunit. Our work demonstrates that the Astrin-SKAP complex contains separable kinetochore localization and microtubule binding domains. In addition, through cross-linking analysis in human cells and biochemical reconstitution, we show that the Astrin-SKAP complex binds synergistically to microtubules with the Ndc80 complex, the core component of the kinetochore-microtubule interface, to form an integrated interface. We propose a model in which the Astrin-SKAP complex acts together with the Ndc80 complex to stabilize correctly formed kinetochore-microtubule interactions.

cell biology↗