FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2599977247> ?p ?o ?g. }

• W2599977247 abstract "ABSTRACT The target of rapamycin complex 1 ( TORC1 ) pathway is a highly conserved signaling pathway across eukaryotes that integrates nutrient and stress signals to regulate the cellular growth rate and the transition into and maintenance of dormancy. The majority of the pathway’s components, including the central TOR kinase, have been lost in the apicomplexan lineage, and it is unknown how these organisms detect and respond to nutrient starvation in its absence. Plasmodium falciparum encodes a putative ortholog of the RNA polymerase (Pol) III repressor Maf1 , which has been demonstrated to modulate Pol III transcription in a TOR-dependent manner in a number of organisms. Here, we investigate the role of P. falciparum Maf1 ( PfMaf1 ) in regulating RNA Pol III expression under conditions of nutrient starvation and other stresses. Using a transposon insertion mutant with an altered Maf1 expression profile, we demonstrated that proper Maf1 expression is necessary for survival of the dormancy-like state induced by prolonged amino acid starvation and is needed for full recovery from other stresses that slow or stall the parasite cell cycle. This Maf1 mutant is defective in the downregulation of pre-tRNA synthesis under nutrient-limiting conditions, indicating that the function of Maf1 as a stress-responsive regulator of structural RNA transcription is conserved in P. falciparum . Recent work has demonstrated that parasites carrying artemisinin-resistant K13 alleles display an enhanced ability to recover from drug-induced growth retardation. We show that one such artemisinin-resistant line displays greater regulation of pre-tRNA expression and higher survival upon prolonged amino acid starvation, suggesting that overlapping, Pf Maf1-associated pathways may regulate growth recovery from both artemisinin treatment and amino acid starvation. IMPORTANCE Eukaryote organisms sense changes in their environment and integrate this information through signaling pathways to activate response programs to ensure survival. The TOR pathway is a well-studied signaling pathway found throughout eukaryotes that is known to integrate a variety of signals to regulate organismal growth in response to starvation and other stresses. The human malaria parasite Plasmodium falciparum appears to have lost the TOR pathway over the course of evolution, and it is unclear how the parasite modulates its growth in response to starvation and drug treatment. Here, we show that Maf1, a protein regulated by TOR in other eukaryotes, plays an important role in maintaining the parasite’s viability in the face of starvation and other forms of stress. This suggests that PfMaf1 is a component of a yet-to-be-described nutrient and stress response pathway." @default.
• W2599977247 created "2017-04-07" @default.
• W2599977247 creator A5001978382 @default.
• W2599977247 creator A5050825635 @default.
• W2599977247 date "2017-05-03" @default.
• W2599977247 modified "2023-10-18" @default.
• W2599977247 title "<i>Plasmodium falciparum Maf1</i> Confers Survival upon Amino Acid Starvation" @default.
• W2599977247 cites W1483456869 @default.
• W2599977247 cites W1519084876 @default.
• W2599977247 cites W1847517966 @default.
• W2599977247 cites W1945957817 @default.
• W2599977247 cites W1966612206 @default.
• W2599977247 cites W1972073123 @default.
• W2599977247 cites W1983696650 @default.
• W2599977247 cites W1986934465 @default.
• W2599977247 cites W1993347313 @default.
• W2599977247 cites W2016266809 @default.
• W2599977247 cites W2016747889 @default.
• W2599977247 cites W2018425570 @default.
• W2599977247 cites W2021341670 @default.
• W2599977247 cites W2022819817 @default.
• W2599977247 cites W2023633070 @default.
• W2599977247 cites W2026681127 @default.
• W2599977247 cites W2034308627 @default.
• W2599977247 cites W2035826427 @default.
• W2599977247 cites W2036748062 @default.
• W2599977247 cites W2038634768 @default.
• W2599977247 cites W2068413127 @default.
• W2599977247 cites W2068879129 @default.
• W2599977247 cites W2079838847 @default.
• W2599977247 cites W2084459589 @default.
• W2599977247 cites W2086438483 @default.
• W2599977247 cites W2086937968 @default.
• W2599977247 cites W2090453051 @default.
• W2599977247 cites W2099767800 @default.
• W2599977247 cites W2101792514 @default.
• W2599977247 cites W2102343384 @default.
• W2599977247 cites W2103441770 @default.
• W2599977247 cites W2106578986 @default.
• W2599977247 cites W2109937180 @default.
• W2599977247 cites W2113312959 @default.
• W2599977247 cites W2117528871 @default.
• W2599977247 cites W2119180969 @default.
• W2599977247 cites W2122534122 @default.
• W2599977247 cites W2126493366 @default.
• W2599977247 cites W2129282380 @default.
• W2599977247 cites W2129316442 @default.
• W2599977247 cites W2129428401 @default.
• W2599977247 cites W2133040714 @default.
• W2599977247 cites W2133913001 @default.
• W2599977247 cites W2135500790 @default.
• W2599977247 cites W2135970036 @default.
• W2599977247 cites W2137529385 @default.
• W2599977247 cites W2138138136 @default.
• W2599977247 cites W2138743983 @default.
• W2599977247 cites W2142248826 @default.
• W2599977247 cites W2144250394 @default.
• W2599977247 cites W2149992227 @default.
• W2599977247 cites W2152344953 @default.
• W2599977247 cites W2154628764 @default.
• W2599977247 cites W2154898068 @default.
• W2599977247 cites W2154947561 @default.
• W2599977247 cites W2155471120 @default.
• W2599977247 cites W2155937527 @default.
• W2599977247 cites W2158297569 @default.
• W2599977247 cites W2158377245 @default.
• W2599977247 cites W2161222316 @default.
• W2599977247 cites W2161311583 @default.
• W2599977247 cites W2161340657 @default.
• W2599977247 cites W2163736445 @default.
• W2599977247 cites W2169230642 @default.
• W2599977247 cites W2171102256 @default.
• W2599977247 cites W2394668152 @default.
• W2599977247 cites W4230096730 @default.
• W2599977247 cites W4321429217 @default.
• W2599977247 doi "https://doi.org/10.1128/mbio.02317-16" @default.
• W2599977247 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5371417" @default.
• W2599977247 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28351924" @default.
• W2599977247 hasPublicationYear "2017" @default.
• W2599977247 type Work @default.
• W2599977247 sameAs 2599977247 @default.
• W2599977247 citedByCount "26" @default.
• W2599977247 countsByYear W25999772472018 @default.
• W2599977247 countsByYear W25999772472019 @default.
• W2599977247 countsByYear W25999772472020 @default.
• W2599977247 countsByYear W25999772472021 @default.
• W2599977247 countsByYear W25999772472022 @default.
• W2599977247 countsByYear W25999772472023 @default.
• W2599977247 crossrefType "journal-article" @default.
• W2599977247 hasAuthorship W2599977247A5001978382 @default.
• W2599977247 hasAuthorship W2599977247A5050825635 @default.
• W2599977247 hasBestOaLocation W25999772471 @default.
• W2599977247 hasConcept C104317684 @default.
• W2599977247 hasConcept C138885662 @default.
• W2599977247 hasConcept C158448853 @default.
• W2599977247 hasConcept C166703698 @default.
• W2599977247 hasConcept C179926584 @default.
• W2599977247 hasConcept C203014093 @default.
• W2599977247 hasConcept C2776449523 @default.
• W2599977247 hasConcept C2778048844 @default.

• next