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PXD007042

PXD007042 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitleIdentification of Plasmodium yoelii CCR4/CAF1/CAF1d Binding partners and total proteomics of Py17XNL by Immunoprecipitation/nano LC-MS/MS
DescriptionThe transmission of the malaria parasite between mosquitoes and mammals requires translational repression to ensure that only the proper proteins are expressed at the right time, while still allowing the parasite to prepare the mRNAs it will need for the next developmental stage. With relatively few known specific transcription factors (ApiAP2 family) that may specifically initiate gene transcription, Plasmodium parasites also regulate the stability and turnover of transcripts to provide more comprehensive gene regulation. The CAF1/CCR4/NOT complex has been shown in model organisms to be important for not only mRNA degradation, but also translational control through its deadenylases CAF1 and CCR4. However, few proteins that impose translational repression in Plasmodium sexual stages are known, and those that are characterized primarily affect female gametocytes. Therefore, we have characterized two deadenylases and have uncovered their roles in transmission. We have identified and characterized CCR4-1, which we show plays a role in activating male gametocytes, stabilizing transcripts in gametocytes, and regulating host-to-vector transmission. We find that when ccr4-1 is genetically deleted, there is a loss in the coordination of male gametocyte activation and a reduction in the ability of the parasite to productively infect the mosquito, which is independent of its effect upon male activation. Comparative RNA-seq shows that the deletion of ccr4-1 affects many transcripts that are translationally repressed in females, are related to male gamete function, and/or are important for early mosquito stage development. In contrast, we found that genetic deletion of the major deadenylase Caf1 is lethal. However, we observed that expression of only the N-terminal Caf1 domain is permissive, yet prevents proper complex assembly and phenocopies the ccr4-1 deletion. We therefore conclude that the general and transmission-specialized deadenylases of the CAF1/CCR4/NOT complex play critical and intertwined roles in parasite growth and transmission.
HostingRepositoryPRIDE
AnnounceDate2024-10-22
AnnouncementXMLSubmission_2024-10-22_04:39:16.390.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterScott Lindner
SpeciesList scientific name: Plasmodium yoelii yoelii 17XNL; NCBI TaxID: 352914;
ModificationListNo PTMs are included in the dataset
InstrumentLTQ Orbitrap Elite
Dataset History
RevisionDatetimeStatusChangeLog Entry
02017-07-13 13:41:58ID requested
12019-01-07 08:01:20announced
22019-02-07 04:09:18announcedUpdated publication reference for PubMed record(s): 30703164.
32024-10-22 04:39:17announced2024-10-22: Updated project metadata.
Publication List
Hart KJ, Oberstaller J, Walker MP, Minns AM, Kennedy MF, Padykula I, Adams JH, Lindner SE, Plasmodium male gametocyte development and transmission are critically regulated by the two putative deadenylases of the CAF1/CCR4/NOT complex. PLoS Pathog, 15(1):e1007164(2019) [pubmed]
10.1371/journal.ppat.1007164;
Keyword List
curator keyword: Biological, Biomedical
submitter keyword: CCR4,Plasmodium, PY17XNL, CAF1
Contact List
Scott Lindner
contact affiliationCenter for Malaria Research, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802
contact emailScott.Lindner@psu.edu
lab head
Scott Lindner
contact affiliationPenn State University
contact emailScott.Lindner@psu.edu
dataset submitter
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Dataset FTP location
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PRIDE project URI
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