Core Concepts
Nitrogen availability and the TOR signaling network play a critical role in ensuring successful progression through mitosis and maintaining mitotic fidelity in fission yeast.
Abstract
The study investigates the role of nitrogen availability and the TOR signaling network in regulating mitotic fidelity in the fission yeast Schizosaccharomyces pombe.
Key highlights:
- Supplementation of the growth medium with good nitrogen sources, such as ammonium or glutamate, can partially rescue the catastrophic mitotic phenotypes observed in various mutants, including those with perturbed lipid metabolism.
- The nitrogen-dependent rescue of mitotic defects is not achieved by restoring the aberrant lipid composition or nuclear envelope expansion in the mutants. Instead, it is mediated by the TOR signaling network, particularly the growth-promoting Tor2/TORC1 complex.
- Inhibition of the stress-responsive Tor1/TORC2 branch or activation of Tor2/TORC1 also improves mitotic fidelity, suggesting a novel role for the TOR network in regulating successful progression through mitosis.
- The nitrogen-dependent rescue effect is not limited to lipid metabolism mutants but can also be observed in a diverse panel of other "cut" mutants, indicating a more general role of nitrogen availability and TOR signaling in mitotic fidelity.
- The authors propose that the signaling of nitrogen availability, rather than the physical presence of nutrients, is the key factor in mediating the rescue, potentially by establishing conditions more favorable for smooth mitotic progression early in the cell cycle.
Stats
Δcbf11 cells have lower fatty acid content per unit of dry cell weight compared to WT.
The degree of fatty acid saturation is higher in Δcbf11 cells compared to WT.
The abundance of selected fatty acid species (C18:1, C18:0, C16:0) is altered in Δcbf11 cells compared to WT.
The content of squalene and sterol esters is markedly increased in Δcbf11 cells compared to WT.
Quotes
"Ammonium, a prototypical good nitrogen source, had the most profound effect, suppressing mitotic defects even at reduced concentrations."
"Glutamate, another good nitrogen source, could also improve mitotic fidelity, albeit only at higher concentration."
"The poor nitrogen sources proline and uracil did not suppress the mitotic defects of Δcbf11 cells at the concentrations tested."