Abstract
Target of rapamycin complex 1 (TORC1) is a central regulator of cell growth. It balances anabolic and catabolic processes in response to nutrients, growth factors, and energy availability. Nitrogen- and carbon-containing metabolites have been shown to activate TORC1 in yeast, animals, and plants. Here, we show that phosphorus (P) regulates TORC1 signaling in the model green alga Chlamydomonas (Chlamydomonas reinhardtii) via LST8, a conserved TORC1 subunit that interacts with the kinase domain of TOR. P starvation results in a sharp decrease in LST8 abundance and downregulation of TORC1 activity. A hypomorphic lst8 mutation resulted in decreased LST8 abundance, and it both reduced TORC1 signaling and altered the cellular response to P starvation. Additionally, we found that LST8 levels and TORC1 activity were not properly regulated in a mutant defective in the transcription factor PSR1, which is the major mediator of P deprivation responses in Chlamydomonas. Unlike wild-type cells, the psr1 mutant failed to downregulate LST8 abundance and TORC1 activity when under P limitation. These results identify PSR1 as an upstream regulator of TORC1 and demonstrate that TORC1 is a key component in P signaling in Chlamydomonas.
Highlights
Target of rapamycin (TOR) is a kinase that is an evolutionarily conserved protein and is an essential regulator of cell growth
These results indicated that P starvation inhibits TOR complex 1 (TORC1) signaling in Chlamydomonas in concert with reduced LST8 levels
We found that the psr1 mutant is partially resistant to the TOR inhibitors rapamycin, AZD8055, and Torin1 (Figure 3A), suggesting a link between PSR1 and TORC1 signaling in Chlamydomonas
Summary
Target of rapamycin (TOR) is a kinase that is an evolutionarily conserved protein and is an essential regulator of cell growth. It perceives the cell’s nutritional status and transmits appropriate signals to the cell growth machinery. TOR exists in two structurally and functionally distinct multiprotein complexes termed TOR complex 1 (TORC1) and TOR complex 2 (TORC2) These complexes were originally described in Saccharomyces cerevisiae (Loewith et al, 2002) but are conserved in many other eukaryotes (Soulard et al, 2009; Eltschinger and Loewith, 2016; González and Hall, 2017; Saxton and Sabatini, 2017). Growth factors, and energy status send signals to mTORC1 via different pathways: Leu and Glu induce mTORC1 via RAG GTPases (Jewell et al, 2013; Bar-Peled and Sabatini, 2014) and glutaminolysis (Durán et al, 2012); growth factors activate mTORC1 via the small GTPase RHEB (González and Hall, 2017; Saxton and Sabatini, 2017); and Glc availability regulates mTORC1 through AMPK (Yuan et al, 2013)
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