Year-end Sale % OFF 
Abstract
In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Delta phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the pentose phosphate pathway. The apparent connection between Sod1 and the pentose phosphate pathway prompted an investigation of mutants defective in glucose-6-phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this pathway. We confirmed that zwf1Delta mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Delta, leading us to propose that increased flux through the oxidative reactions of the pentose phosphate pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Delta and zwf1Delta mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the pentose phosphate pathway as being critical for maintenance of the cellular redox state.
Highlights
In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity
It is well documented that this pathway and, glucose-6-phosphate dehydrogenase play a protective role during oxidative stress [39, 40]
We discovered that elevated expression of the S. cerevisiae transketolase gene of the pentose phosphate pathway had the ability to suppress specific oxidative stress phenotypes caused by Sod1 deficiency
Summary
Leu112, ura, trp, his, canlr Mata, leu112, ura, trp, his, canlr, sod1⌬::TRP Mata, leu112, ura, trp, his, canlr, sod1⌬::TRP1, pmr1⌬::LEU2 Mata, leu112, ura, trp, his, canlr, zwf1⌬::URA3 Mata, leu112, ura, trp, his, canlr, tal1⌬::LEU2 Mata, leu112, ura, trp, his, canlr, tkl1⌬::LEU2 Mata, leu112, ura, trp, his, canlr, tkl2⌬::LEU2 Mata, leu112, ura, trp, his, canlr, sod1⌬::TRP1, zwf1⌬::URA3 Mata, leu112, ura, trp, his, canlr, zwf1⌬::URA3, pmr1⌬::LEU2 Mata, leu112, ura, trp, his, canlr, sod1⌬::TRP1, zwf1⌬::URA3, pmr1⌬::LEU2 Mat␣, leu112, his3⌬1, GALϩ, trp1-289a, ura, sod1⌬::TRP1 Mat␣, ade2-1oc, ade3⌬-100, trp, leu112, lys2⌬::HIS3, ura, his, can100, trx1⌬::LYS2, trx2⌬::LEU2. Copy suppressors that would rescue specific sod1⌬-related phenotypes. The work reported here describes the isolation of such a suppressor, the TKL1 gene, encoding the transketolase enzyme of the pentose phosphate pathway. The identification of TKL1 as a sod suppressor provided an opportunity to explore the role of the pentose phosphate pathway in protection against oxidative stress in yeast. This work has improved our understanding of the sod methionine auxotrophy and has provided insight into the relationships between the Cu,Zn-SOD, the pentose phosphate pathway, and the critical maintenance of the cellular redox state
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
