Light-Stress Response Mediated by the Transcription Factor KlMga2 in the Yeast Kluyveromyces lactis

Abstract

In unicellular organisms like yeasts, which do not have specialized tissues for protection against environmental challenges, the presence of cellular mechanisms to respond and adapt to stress conditions is fundamental. In this work, we aimed to investigate the response to environmental light in Kluyveromyces lactis. Yeast lacks specialized light-sensing proteins; however, Saccharomyces cerevisiae has been reported to respond to light by increasing hydrogen peroxide level and triggering nuclear translocation of Msn2. This is a stress-sensitive transcription factor also present in K. lactis. To investigate light response in this yeast, we analyzed the different phenotypes generated by the deletion of the hypoxia responsive and lipid biosynthesis transcription factor KlMga2. Alterations in growth rate, mitochondrial functioning, ROS metabolism, and fatty acid biosynthesis provide evidence that light was a source of stress in K. lactis and that KlMga2 had a role in the light-stress response. The involvement of KlMsn2 and KlCrz1 in light stress was also explored, but the latter showed no function in this response.

Light Stress in Yeasts: Signaling and Responses in Creatures of the Night

“…Similarly, Kl Mga2 was a hypoxic regulator of lipid biosynthesis in K. lactis [ 42 , 43 ]; however, as compared to S. cerevisiae , it was also involved in respiration and an oxidative stress response [ 44 , 45 ]. The lipid content and composition were modified in K. lactis that had been exposed to white light: Defects in growth, mitochondrial structure, respiration rate, and hydrogen-peroxide metabolism (catalase and superoxide dismutase genes) caused by KlMGA2 deletion were exacerbated in the mutant strain by light, suggesting an antagonistic and/or protective role for Kl Mga2 against light stress [ 46 ]. Interestingly, the deletion of KlMSN2 ( KLLA0F26961g ) did not generate the same light-dependent defects/phenotypes as the deletion of KlMGA2 .…”