This defect in long-term viability of Δphx1 mutant

was re

This defect in long-term viability of Δphx1 mutant

was rescued by ectopic expression of phx1 + (Figure 4B). In addition, overproduction of Phx1 in the wild-type strain greatly enhanced long-term viability (Figure 4B). Therefore, it is clear that Phx1 confers cells with fitness during long-term cultures, enhancing their survival rates. When the long-term survival experiments of Figure 4A were repeated with the strains (wild type 972 and Δphx1 JY01) without auxotrophic markers, similar pattern was observed (data not shown). Ibrutinib supplier Figure 4 Viability of  Δphx1  mutant cells in long-term culture. Wild type and Δphx1 mutant cells were grown in liquid EMM until they reached the stationary phase at OD600 of 8–9 (day 0). From this time point, aliquots were plated out on

solid complex medium daily, and the surviving colonies were counted after 3 ~ 4 days of incubation at 30°C. At least three independent experiments were carried out to obtain survival curves for each strain. (A) The viability of wild type (JH43) and Δphx1 mutant (ESX5) in EMM. (B) The viability in EMM of wild type (JH43) and Δphx1 mutant cells containing pWH5 vector or pWH5-phx1 + plasmid. (C, D) The viability of prototrophic wild type (972) and Δphx1(JY01) in modified EMM without N-source (C) or with 0.5% glucose (D). We then examined the viability of Δphx1 under nutrient-starved conditions. The wild type (strain 972) maintained its viability for a longer period of time in N-starved medium. In comparison, Δphx1 (strain JY01) lost its viability at earlier time (Figure 4C). In C-starved condition as well, www.selleckchem.com/products/BKM-120.html Δphx1 lost its viability much quicker than the wild type (Figure 4D). Therefore, it appears clear that Phx1 serves a critical role in conferring fitness to the stationary-phase cells or cells under nutrient starvation, and thus enables them to maintain viability for longer period of time. Genetic studies have identified some genes that function in extending lifespan. In S. pombe, as in S.cerevisiae, cAMP/Pka1 and Sck2 signaling pathways Org 27569 have been shown to regulate chronological

aging [21–23]. It has also been reported that respiration-defective mitochondrial dysfunction shortens chronological life span through elevating oxidative stresses [24, 25]. Whether Phx1 is related with these signaling pathways and/or mitochondrial functions, and how, if it is, will be an interesting question to solve in the near future. Phx1 provides stress tolerance to oxidation and heat It is widely accepted that cells in the stationary phase experience not only nutrient starvation, but also other stresses such as oxidation of cell components that include proteins and nucleic acids [26, 27]. Therefore, stationary-phase cells activate various stress defense systems, and this defense is critical for long-term survival.

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