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SRX3097554: GSM2743712: F12/gdv1-asKO 40-48 hpi; Plasmodium falciparum; RNA-Seq
1 ILLUMINA (NextSeq 500) run: 9.6M spots, 720.2M bases, 264.3Mb downloads

Submitted by: NCBI (GEO)
Study: GDV1 triggers sexual conversion and differentiation in malaria parasites by antagonizing HP1-dependent gene silencing
show Abstracthide Abstract
Malaria is caused by Plasmodium parasites that proliferate through iterative cycles of intra-erythrocytic replication. During each cycle a small number of parasites differentiate into gametocytes, the only forms able to infect the mosquito vector and transmit malaria. Sexual commitment is triggered by activation of AP2-G, the master transcriptional regulator of gametocytogenesis. Heterochromatin protein 1 (HP1)-dependent silencing of ap2-g prevents sexual conversion and secures proliferation. Here, we identify gametocyte development 1 (GDV1) as the first upstream activator of the sexual differentiation pathway in P. falciparum. Induction of GDV1 expression is sufficient to activate AP2-G expression and sexual differentiation. We found that GDV1 targets heterochromatin and triggers HP1 eviction preferentially at ap2-g and other gametocyte-specific genes. We further demonstrate that GDV1-dependent activation of ap2-g is controlled via a gdv1 antisense RNA. In summary, we identify GDV1 as an unprecedented cell fate decision factor that induces sexual differentiation by antagonizing HP1-dependent gene silencing. Overall design: ChIP-seq experiments were performed for the gametocyte development protein 1 (PfGDV1, PF3D7_0935400) in the malaria parasite Plasmodium falciparum strain 3D7. An inducible ectopic overexpression 3D7/PfGDV1-GFP-DD transgenic parasite line was created using the FKBP-destabilization domain Shield-1 system on an episomal expression plasmid. The resulting PfGDV1-GFP-DD transgenic parasite line was used in a comparative ChIP-sequencing time-course experiment. 3D7/GDV1-GFP-DDOFF parasites were split at 28-34 hours post-invasion (hpi), cultured in parallel in absence or presence of Shield-1 and paired chromatin samples were harvested two (TP1), six (TP2) and ten (TP3) hours after Shield-1 addition. Chromatin immunoprecipitations were performed using mouse anti-GFP (Roche Diagnostics, #11814460001). In parallel the effect of PfGDV1 overexpression on global PfHP1 occupancy was investigated ten hours (TP3) after Shield-1 addition using anti-rabbit PfHP1 (Brancucci et al. 2014). Additionally, directional RNA-seq was performed for Plasmodium falciparum F12 wildtype parasites and a gdv1-antisense RNA loss-of-function mutant parasite line (F12/gdv1-asKO) generated using CRISPR/Cas9-based genome editing. F12 and F12/gdv1-asKO parasites were synchronized to obtain an eight hour growth window and were harvested at 32-40hpi and 40-48hpi.
Sample: F12/gdv1-asKO 40-48 hpi
SAMN07511313 • SRS2434071 • All experiments • All runs
Library:
Instrument: NextSeq 500
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: SINGLE
Construction protocol: Total RNA was isolated using Ribozol (Amresco) according to the manufacturer’s manual and further purified using the RNeasy Plus Mini Kit (Qiagen) for removal of gDNA. Residual gDNA was digested with TURBO DNA-freeTM DNaseI (Ambion) and the RNA was quantified by NanoDrop. Isolated total RNA was PolyA-selected using the Oligotex mRNA Mini Kit (Qiagen, #70022) according to manufacturer’s instructions. Subsequently, 2µ of PolyA-selected total RNA equivalent were fragmented by alkaline hydrolysis (5x fragmentation buffer: 200mM Tris acetate pH 8.2, 500mM potassium acetate, 150mM magnesium acetate) for 1min 45sec at 85°C in a 150µl volume and precipitated as previously described in (Hoeijmakers, Bártfai and Stunnenberg 2013), followed by two TURBO DNase treatments (Ambion, #AM2238) to remove remnants of genomic DNA . Further library preparation for strand-specific RNA-seq was carried out as in (Kensche et al. 2015). In short, first strand cDNA synthesis was performed with AT-corrected Random N9 primers (76% AT) and in presence of 0.2µg Actinomycin D (Thermo 446 Fisher Scientific) to prevent unwanted DNA-dependent second strand cDNA synthesis. To maintain the strand-specific information during second strand synthesis dTTPs were replaced with dUTPs. Resulting double stranded cDNAs (1.9-3.2ng) were end repaired and extended with 3’ A-overhangs. After ligation of NextFlex adapters (Bio Scientific, #514122), libraries were treated with USER enzyme (NEB, #M5505L) to specifically degrade the dUTP-containing second strand and subsequently amplified by PCR (98°C for 2min; 4 cycles of 98°C for 20sec, 62°C for 3min; 62°C for 5 min) using KAPA HiFi HotStart ready mix (KAPA Biosystems, #KM2602) and NEXTflex primer mix (Bio Scientific, #514122). Next, libraries were size-selected for 300-400 bp fragments using 2% E-Gel Size Select agarose gels (Invitrogen, #G6610-02) and amplified for another 12 cycles using the same PCR protocol as above. Subsequent depletion of adapter dimers and library purification was performed using Agencourt AMPure XP beads (Beckman Coulter, #A63880) in a 1:1 library beads ratio.
Experiment attributes:
GEO Accession: GSM2743712
Links:
Runs: 1 run, 9.6M spots, 720.2M bases, 264.3Mb
Run# of Spots# of BasesSizePublished
SRR59376039,602,092720.2M264.3Mb2018-05-07

ID:
4387385

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