Abstract
Membrane-less biomolecular compartmentalization is a core phenomenon involved in many physiological activities that occur ubiquitously in cells. Condensates, such as promyelocytic leukemia (PML) bodies, stress granules, and P-bodies (PBs), have been investigated to understand the process of membrane-less cellular compartmentalization. In budding yeast, PBs dispersed in the cytoplasm of exponentially growing cells rapidly accumulate in response to various stresses such as osmotic stress, glucose deficiency, and heat stress. In addition, cells start to accumulate PBs chronically in post-exponential phases. Specific protein–protein interactions are involved in accelerating PB accumulation in each circumstance, and discovering the regulatory mechanism for each is the key to understanding cellular condensation. Here, we demonstrate that Nst1 of budding yeast Saccharomyces cerevisiae is far more densely associated with PBs in post-exponentially growing phases from the diauxic shift to the stationary phase than during glucose deprivation of exponentially growing cells, while the PB marker Dcp2 exhibits a similar degree of condensation under these conditions. Similar to Edc3, ectopic Nst1 overexpression induces self-condensation and the condensation of other PB components, such as Dcp2 and Dhh1, which exhibit liquid-like properties. Altogether, these results suggest that Nst1 has the intrinsic potential for self-condensation and the condensation of other PB components, specifically in post-exponential phases.
Highlights
Published: 24 February 2022Understanding the mechanism of intracellular molecular compartmentalization is essential to understanding the mechanics of life
Since we discovered that the Nst1-overexpressed cells show growth retardation compared to the vector control, we screened the deletion mutants of the genes related to the function of PBs or stress granules (SGs), which suppressed the growth retardation phenotype of the Nst1-overexpressed cells (Supplementary Figure S1A)
PSP2, LSM12, DCS1, TIF4631, and POP2 were identified as suppressor genes whose deletion suppressed the growth retardation phenotype induced by Nst1 overexpression
Summary
Published: 24 February 2022Understanding the mechanism of intracellular molecular compartmentalization is essential to understanding the mechanics of life. The membrane-less compartmentalization of biomolecules by liquid–liquid phase separation (LLPS) has been reported ubiquitously in cells [1,2]: Cajal bodies, nuclear speckles, paraspeckles, histone-locus bodies, nuclear gems, promyelocytic leukemia (PML) nuclear bodies (NBs) in the nucleus and processing(P)-bodies (PBs), stress granules (SGs), and germ granules in the cytoplasm. But a few molecular factors, are reported to be required to form condensates. Specific proteins such as PML (TRIM19) of PML NB, SFPQ of paraspeckles, COILIN of Cajal bodies, G3BP of SGs, and DDX6/LSM14A of PBs in mammalian cells are known representatives of the essential proteins for condensation to form membrane-less organelles [8]. Banani et al, designated these essential molecular components with the potential to induce condensation as ‘scaffolds’
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