Kluyveromyces lactis: a suitable yeast model to study cellular defense mechanisms against hypoxia-induced oxidative stress

Abstract

Studies about hypoxia-induced oxidative stress in human health disorders take advantage from the use of unicellular eukaryote models. A widely extended model is the fermentative yeast Saccharomyces cerevisiae. In this paper, we describe an overview of the molecular mechanisms induced by a decrease in oxygen availability and their interrelationship with the oxidative stress response in yeast. We focus on the differential characteristics between S. cerevisiae and the respiratory yeast Kluyveromyces lactis, a complementary emerging model, in reference to multicellular eukaryotes.

Figure 1

A panorama of the multiple connections between hypoxia, metabolic rerouting, oxidative stress response, and cell defense mechanisms. Erg: ergosterol; PPP: pentoses phosphate pathway; TF: transcriptional factors.

Figure 2

Homologies (percentage of identity calculated according to BLASTp in Génolevures) between K. lactis and S. cerevisiae proteins related to the pathways summarized in Figure 1. Red, 100–70% identity; green 69–40% identity; blue, <40% identity. (A) heme biosynthesis; (B) ergosterol biosynthesis and supply; (C) NAD(P)H consuming oxidative defense reactions; (D) other oxidative defense reactions; E, NAD(P)-dehydrogenases from the inner membrane of mitochondria; (F) heme/respiration-related transcriptional factors; (G) sterol-related transcriptional factors; (H) peroxide-related transcriptional factors; (I) life span-related proteins; (J) mitophagy-related proteins.