Transcriptional profiling of P. yoelii SAP1 knockout
Ontology highlight
ABSTRACT:
ORGANISM(S): Plasmodium yoelii
PROVIDER: GSE12397 | GEO | 2009/08/01
SECONDARY ACCESSION(S): PRJNA113155
REPOSITORIES: GEO
Similar Datasets
Project description:To study the function of gene SAP1. We knocked out SAP1 gene in P. yoelii, and compared the global gene expression profiles of the P. yoelii SAP1 knockout parasites isolated from mosquito salivary gland to that of wild type P. yoelii parasites. RNA samples from SAP1 knock out (SAP1ko) were directly hybridized to RNA samples obtained from mosquito salivary gland (sgSpz). Two independent biological replicates with dye swaps for each pairs of biological replicates were performed. Also we included in the analysis two direct hybridizations between sgSpz and ooSpz from our previous study.
2010-05-15 | E-GEOD-12397 | biostudies-arrayexpress
Project description:Proteomic analysis of Plasmodium yoelii salivary gland sprozoites
2019-10-02 | PXD009727 | Pride
Project description:Transcriptional profiling of P. yoelii SAP1 knockout
| PRJNA113155 | ENA
Project description:MalariaM-bM-^@M-^Ys cycle of infection requires parasite transmission between a mosquito vector and a vertebrate host. Plasmodium regulates transmission by translationally repressing specific mRNAs until their products are needed. We demonstrate that the Plasmodium yoelii Pumilio-FBF family member Puf2 allows the sporozoite to retain its infectivity in the mosquito salivary glands while awaiting transmission. Puf2 mediates this critical feature solely through its RNA-Binding Domain (RBD) likely by protecting and silencing specific mRNAs. Puf2 storage granules are distinct from stress granules and P-bodies and dissolve rapidly after infection of hepatocytes, likely releasing the protected and silenced transcripts for M-bM-^@M-^Xjust-in-timeM-bM-^@M-^Y translation by early exoerythrocytic forms (EEFs). Further corroborating this model, pypuf2- sporozoites have no apparent defect in host infection early after invading the salivary glands, but become progressively noninfectious and subsequently prematurely transform into EEFs during prolonged salivary gland residence. In contrast, the premature overexpression of Puf2 in oocysts causes striking deregulation of sporozoite maturation, resulting in fewer oocyst sporozoites that are non-infectious and unable to colonize the salivary glands. Maintenance of Puf2 expression in liver stage parasites produces no phenotype, suggesting that a window of permissive expression exists. Finally, by conducting the first comparative RNAseq analysis of Plasmodium sporozoites, we have uncovered that Puf2 may play a role in both the protection of specific transcripts as well as RNA turnover via the CCR4/Not complex. These findings uncover requirements for maintaining a window of opportunity for the malaria parasite to accommodate the unpredictable moment of transmission from mosquito to vertebrate host. Wild-type (Py17XNL) and pypuf2 -salivary gland sporozoites
2012-10-27 | E-GEOD-41873 | biostudies-arrayexpress
Project description:Many eukaryotic developmental and cell fate decisions are effected post-transcriptionally that mechanistically involve RNA binding proteins as regulators of translation of key mRNAs. In the unicellular eukaryote malaria parasite, Plasmodium, one of the most dramatic changes in cell morphology and function occurs during transmission between mosquito and human host. In the mosquito salivary glands, Plasmodium sporozoites are slender, motile and remain infectious for several weeks; only after transmission and liver cell invasion, does the parasite rapidly transform into a round, non-motile exo-erythrocytic form (EEF) that gives rise to thousands of infectious merozoites to be released into the blood stream. Here we demonstrate a Plasmodium homolog of the RNA binding protein, Pumilio, as a key regulator of the sporozoite to EEF transformation. In the absence of Pumilio-2 (Puf2) Plasmodium berghei sporozoites initiate early stage EEF development inside mosquito salivary glands with characteristic morphological changes; puf2- salivary gland sporozoites lose gliding motility, cell traversal ability and are less infective. Global expression profiling confirmed that transgenic parasites exhibit genome-wide transcriptional adaptations typical for Plasmodium intra-hepatic development. The data demonstrate that Puf2 is a key player in regulating developmental control, and imply that transformation of salivary gland-resident sporozoites into early liver stage parasites is regulated by a post-translational mechanism.
2010-11-01 | E-TABM-1067 | biostudies-arrayexpress
Project description:Microarray studies using synchronized Plasmodium falciparum parasites have revealed a ‘continuous cascade’ of gene expression. Reports vary regarding the stability in these transcriptional patterns in the presence of external stressors. Using Plasmodium yoelii 17X parasites replicating in vivo, we have examined differential gene expression in parasites isolated from individual mice, from independent infections, during ascending and peak parasitemia and in the presence and absence of host antibody responses. Across experimental conditions, transcription was surprisingly stable. Differential gene expression was greatest when comparing differences due to parasite load and/or host cell availability; however, even these changes were modest. Of genes that were differentially expressed, many are of unknown function. There was little to no differential expression of members of the yir and pyst-a multigene families, although a relatively large number of these were expressed during blood-stage infection regardless of experimental condition. Taken together, these results indicate that 1) P. yoelii gene expression remains stable in the presence of a changing host environment and 2) concurrent expression of a large number of the yir and pyst-a genes may function to divert host immune responses away from invariant protective antigens. 1. P. yoelii 17X gene expression profiles were determined in blood-stage parasites isolated from infected Balb/c mice (male, 8-12 weeks old) as follows: a. Mouse 1 (M1), Mouse 2 (M2), Mouse 3 (M3), Donor (D) mouse – three mice simultaneously infected with P. yoelii 17X iRBCs from a single donor mouse. Parasite RNA was isolated early during infection when parasitemia was ascending as follows: M1 - day 11 at 13.0% parasitemia; M2 - day 10 at 11.1% parasitemia; M3 - day 10 at 18.6% parasitemia; D – day 11 at 18.7% parasitemia. b. Infection #1 (I1), infection #2 (I2), infection #3 (I3), infection #4 (I4) – four groups of mice infected on four separate occasions using P. yoelii 17X iRBCs obtained from four separate donor mice. In each case, P. yoelii 17X RNA was isolated from iRBCs obtained on days 10-11 of infection when parasitemia was ascending and was ~15%. c. Day 10 (D10), Day 14 (D14) – P. yoelii 17X RNA isolated from iRBCs during infection #2 on day 10 (14% parasitemia, 14.4% reticulocytes) and on day 14 of infection #2 (43.5% parasitemia, 57.9% reticulocytes). d. WT and JHD - P. yoelii 17X RNA isolated from iRBCs during infection #4 from immunologically intact, wild-type Balb/c mice and B cell deficient, JHD mice on a Balb/c background (ascending infection, 15% parasitemia). e. QA and RMP - P. yoelii 17X RNA isolated from iRBCs during infection #1 from mice previously immunized with a preparation of membrane proteins isolated from P. yoelii 17X infected reticulocytes (PyRMP) (day 12, 13.3% parasitemia and Quil A immunized (QA) control mice (day 10, 15.6% parasitemia) 2. On each array, gene expression in P. yoelii 17X blood-stage parasites was evaluated relative to a standard comparator of purified P. yoelii 17XL total RNA (pooled RNA from 45 mice, mean parasitemia ~35%). Each sample was analyzed on three replicate arrays, one of which was a standard dye-flip. One exception was the infection #3 sample which was analyzed on only on two arrays. On each array, oligonucleotides were spotted in duplicate. 3. Through the use of the standard reference RNA, the following 15 pairwise comparisons across samples were made: (M1 vs M2); (M2 vs M3); (M1 vs M3); (D vs M1); (D vs M2); (D vs M3); (I1 vs I2); (I1 vs I3); (I1 vs I4); (I2 vs I3); (I2 vs I4); (I3 vs I4); (D10 vs D14); (WT vs JHD); (QA vs RMP)
2011-11-01 | E-GEOD-31274 | biostudies-arrayexpress
Project description:Plasmodium yoelii yoelii Transcriptome or Gene expression
| PRJNA657305 | ENA
Project description:Plasmodium yoelii YM asexual blood stage parasites express multiple members of the py235 gene family, part of the super-family of genes including those coding for Plasmodium vivax reticulocyte binding proteins and Plasmodium falciparum RH proteins. Dr Tony Holder's laboratory (NIMR, London) has been successful in deleting one of the RH family genes (Py01365) by transfection and insertion of the TgDHFR gene, and cloned the resulting parasite in YM background. The gene expression patterns of the mutant parasite line were compared to that of the wild type YM parasite.
2011-04-25 | E-MTAB-636 | biostudies-arrayexpress
Project description:These data were used to assess gene expression and dynamics between oocyst sporozoites and salivary gland sporozoites for both Plasmodium falciparum and Plasmodium yoelii.
2019-10-01 | GSE113582 | GEO
Project description:Simultaneous analysis of Plasmodium falciparum and Anopheles gambiae gene expression: an assessment of parasite maturation and of the mosquito response to infection. Malaria is probably the most lethal and most prevalent parasitic disease in the world, causing more than one million deaths per year. In spite of intensive research, no vaccine exists and good vaccine candidates are still a necessity. Plasmodium sporozoites from mosquito midguts are not as infective as those from salivary glands, presenting a different type of motility which is presumably associated with their invasive capacity. It is assumed that these differences are due to maturation of sporozoites, which happens either in the salivary glands or somewhere along the way from the midgut to the glands. Indeed, the invasion of the salivary gland is considered to be an essential step for malaria transmission to the host and it is known to causes expression of multiple genes in the parasite and activation of some immune-response genes in the insect. Here we compared the gene expression profile of P. falciparum parasites from midgut and salivary glands in order to search for genes involved in parasite maturation; on the assumption that any differentially expressed genes found under this condition could be potentially related to the higher infectivity of the salivary gland derived sporozoites and therefore would be potentially good vaccine candidates. Also, because very little is known about mosquito genes involved in the response to Plasmodium, we compared the gene expression profile of infected and uninfected midguts and salivary glands. Our results demonstrate that, upon infection, at least 13 genes are differentially expressed in the mosquito midgut and 43 in the salivary gland. Gene ontology enrichment analysis showed that among other things, in mosquito salivary glands, infection causes multiple genes related to chitin metabolism to be differentially expressed. Also and more importantly, at least 54 genes were differentially expressed in P. falciparum from salivary glands in comparison to midgut (19 down-regulated and 35 up-regulated). Last, we show for the first time that P. falciparum causes multiple genes in the salivary gland to be regulated and that some of those genes could be potentially beneficial to the parasite.
2014-10-01 | GSE18780 | GEO