[Objective] To explore the role of SRO9 in the endoplasmic reticulum stress (ERS) in saccharomyces cerevisiae. [Methods] The SRO9-deletion yeast strain was made by PCR-mediated homologous recombination in wild-type yeast. Colony-forming ability of SRO9-deletion and wild-type strains was analyzed under the tunicamycin-treated ERS condition. The cell proliferation assay was performed using the Microbial viability assay kit. The intracellular H2O2 levels and total SOD activity were detected using the colorimetric method according to the assay kit. The expression levels of endoplasmic reticulum stress target genes, SOD1 and SOD2 were determined by quantitative RT-PCR (qRT-PCR). [Results] We observed significantly higher resistance to ER stress in the SRO9-deletion cells than in wild-type cells. The mRNA expression levels of endoplasmic reticulum stress target genes were up-regulated in the SRO9-deletion strain. The intracellular H2O2 levels, total SOD activity, SOD1 and SOD2 mRNA expression levels were down-regulated in the SRO9-deletion strain. Further more, the SRO9-deletion cells show increased sensitivity to oxidant CHP and VK3, the replicative lifespan also reduced in SRO9-deletion cells. [Conclusion] SRO9 deficiency enhances the resistance ability of the strain to ERS, and these might due to the ER stress responses that triggered by SRO9-deficiency.