The TOR Signaling Network in the Model Unicellular Green Alga Chlamydomonas reinhardtii

Abstract

Cell growth is tightly coupled to nutrient availability. The target of rapamycin (TOR) kinase transmits nutritional and environmental cues to the cellular growth machinery. TOR functions in two distinct multiprotein complexes, termed TOR complex 1 (TORC1) and TOR complex 2 (TORC2). While the structure and functions of TORC1 are highly conserved in all eukaryotes, including algae and plants, TORC2 core proteins seem to be missing in photosynthetic organisms. TORC1 controls cell growth by promoting anabolic processes, including protein synthesis and ribosome biogenesis, and inhibiting catabolic processes such as autophagy. Recent studies identified rapamycin-sensitive TORC1 signaling regulating cell growth, autophagy, lipid metabolism, and central metabolic pathways in the model unicellular green alga Chlamydomonas reinhardtii. The central role that microalgae play in global biomass production, together with the high biotechnological potential of these organisms in biofuel production, has drawn attention to the study of proteins that regulate cell growth such as the TOR kinase. In this review we discuss the recent progress on TOR signaling in algae.

Keywords: Chlamydomonas; FKBP12; algae; autophagy; lipid metabolism; rapamycin; target of rapamycin (TOR).

Figure 1

Sensitivity of Chlamydomonas cells to rapamycin. Nomarski images of wild-type and rap2 mutant cells treated with 500 nM rapamycin for 24 h. Bleaching and pronounced vacuolization is observed in wild-type treated cells but not in the rapamycin-resistant mutant rap2, which lacks the FKBP12 (FK506-binding protein of 12 kDa) protein. Scale bar, 10 μm. Adapted from [13].

Figure 2

Proposed model of target of rapamycin (TOR) signaling in Chlamydomonas. A rapamycin-sensitive TORC1 complex composed by TOR, LST8, and Raptor/KOG1 is conserved in Chlamydomonas, whereas TORC2 core components are missing in this model alga. Inhibition of Chlamydomonas TORC1 signaling by rapamycin-FKBP12 activates autophagy, promotes the accumulation of TAGs and the formation of lipid bodies, inhibits protein synthesis, and blocks central metabolic pathways such as the TCA cycle. TORC1 may control these processes by perceiving nutrient (carbon, nitrogen) availability and the intracellular level of inositol polyphosphates. Solid lines indicate interactions that have been experimentally demonstrated (red, inhibition), while links represented by dashed arrows need to be tested. Rap, rapamycin; InsPs, inositol polyphosphates; TAGs, triacylglycerols; TCA, tricarboxylic acid.