ArticleMolecular microbiology2013
A nucleolar AAA-NTPase is required for parasite division.
Article in Molecular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Mutations in the acetylation hotspots of Rbl2 are associated with increased risk of breast cancer.PloS one · 2022Article
- Transcriptional changes in Toxoplasma gondii in response to treatment with monensin.Parasites & vectors · 2020Article
- Shaping the Nascent Ribosome: AAA-ATPases in Eukaryotic Ribosome Biogenesis.Biomolecules · 2019Review
- Apicomplexa Cell Cycles: Something Old, Borrowed, Lost, and New.Trends in parasitology · 2018Review
- Checks and balances? DNA replication and the cell cycle in Plasmodium.Parasites & vectors · 2018Review
- ThemBio · 2017Article
- Checkpoints of apicomplexan cell division identified in Toxoplasma gondii.PLoS pathogens · 2017Article
- The Ubiquitin Proteome of Toxoplasma gondii Reveals Roles for Protein Ubiquitination in Cell-Cycle Transitions.Cell host & microbe · 2015Article
- A novel bipartite centrosome coordinates the apicomplexan cell cycle.PLoS biology · 2015Article
- Article
- Toxoplasma gondii Hsp90: potential roles in essential cellular processes of the parasite.Parasitology · 2014Review
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Apicomplexa division involves several distinct phases shared with other eukaryote cell cycles including a gap period (G1) prior to chromosome synthesis, although how progression through the parasite cell cycle is controlled is not understood. Here we describe a cell cycle mutant that reversibly arrests in the G1 phase. The defect in this mutant was mapped by genetic complementation to a gene encoding a novel AAA-ATPase/CDC48 family member called TgNoAP1. TgNoAP1 is tightly regulated and expressed in the nucleolus during the G1/S phases. A tyrosine to a cysteine change upstream of the second AAA+ domain in the temperature sensitive TgNoAP1 allele leads to conditional protein instability, which is responsible for rapid cell cycle arrest and a primary defect in 28S rRNA processing as confirmed by knock-in of the mutation back into the parent genome. The interaction of TgNoAP1 with factors of the snoRNP and R2TP complexes indicates this protein has a role in pre-rRNA processing. This is a novel role for a cdc48-related chaperone protein and indicates that TgNoAP1 may be part of a dynamic mechanism that senses the health of the parasite protein machinery at the initial steps of ribosome biogenesis and conveys that information to the parasite cell cycle checkpoint controls.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.