Although oxygen is essential for the majority of organisms, some reactive forms of oxygen, so called reactive oxygen species (ROS) such as single oxygen (1O2), hydrogen peroxide (H2O2) and superoxide (O2-•) or organic peroxide (tBOOH) are able to damage essential biomolecules within the cell and lead to different diseases or even to death. Exogenous as well as endogenous processes can be sources of these damaging oxygen species. Therefore evolution has developed mechanisms to defend against these damaging ROS in organisms. Although many studies were performed to reveal mechanisms involved in defence to ROS such as H2O2, O2-• and organic peroxides only little is known about the defence of the cell against 1O2. The goal of this diploma thesis was to identify new aspects of the defence against 1O2 by analysing the response to 1O2 in Saccharomyces cerevisiae on a global level. We used yeast gene arrays to investigate the gene expression in response to 1O2 of the whole genome. Real time polymerase chain reaction (RT-PCR) was then applied to confirm the inductions of some genes by 1O2 and to analyse the specificity of the response to 1O2. To reveal possible functions of the proteins which are encoded by these genes in the defence against 1O2, the phenotype of mutant strains lacking the genes was investigated. For this purpose the growth of the strains when exposed to 1O2 or other ROS was analysed using spot experiments. We found 14 genes whose expression was up-regulated in response to 1O2. As they were also induced by the other investigated ROS (H2O2, O2-• and tBOOH) we assume that there exist no specific response to 1O2. The response to 1O2 is probably rather a part of the general defence against oxidative stress in general. When the corresponding mutant strains were analysed most strains showed no specific phenotype toward 1O2 or other ROS. Because of poor quality of the spot experiments we might have missed some phenotypes. However, two strains, sod1 lacking the Cu, Zn superoxide dismutase and trx2, a thioredoxin synthease mutant showed a clear sensitivity to 1O2 while ylr108c, missing a protein of unknown function showed even an enhanced resistance against 1O2. The exact role of these proteins and of the induction of the 14 genes in the defence against 1O2 however needs further investigation.