TORC2 is required to maintain genome stability during S phase in fission yeast.

DNA damage can occur due to environmental insults or intrinsic metabolic processes and is a major threat to genome stability. The DNA damage response is composed of a series of well coordinated cellular processes that include activation of the DNA damage checkpoint, transient cell cycle arrest, DNA damage repair, and reentry into the cell cycle. Here we demonstrate that mutant cells defective for TOR complex 2 (TORC2) or the downstream AGC-like kinase, Gad8, are highly sensitive to chronic replication stress but are insensitive to ionizing radiation.

TOR complex 2 controls gene silencing, telomere length maintenance, and survival under DNA-damaging conditions.

The Target Of Rapamycin (TOR) kinase belongs to the highly conserved eukaryotic family of phosphatidylinositol-3-kinase-related kinases (PIKKs). TOR proteins are found at the core of two distinct evolutionarily conserved complexes, TORC1 and TORC2. Disruption of TORC1 or TORC2 results in characteristically dissimilar phenotypes.

YbeY, a heat shock protein involved in translation in Escherichia coli.

Here we provide evidence that YbeY, a conserved heat shock protein with unknown function, is involved in the translation process. ybeY deletion mutants are temperature sensitive and have a significantly reduced thermotolerance. Nonetheless, there appears to be no damage of the protein quality control of mature polypeptides, as the levels of chaperones and proteases are normal and there is no accumulation of aggregates.

Opposite effects of tor1 and tor2 on nitrogen starvation responses in fission yeast.

The TOR protein kinases exhibit a conserved role in regulating cellular growth and proliferation. In the fission yeast two TOR homologs are present. tor1(+) is required for starvation and stress responses, while tor2(+) is essential.