Nitric oxide signaling in yeast

Abstract

As a cellular signaling molecule, nitric oxide (NO) is widely conserved from microorganisms, such as bacteria, yeasts, and fungi, to higher eukaryotes including plants and mammals. NO is mainly produced by NO synthase (NOS) or nitrite reductase (NIR) activity. There are several NO detoxification systems, including NO dioxygenase (NOD) and S-nitrosoglutathione reductase (GSNOR). NO homeostasis based on the balance between NO synthesis and degradation is important for the regulation of its physiological functions because an excess level of NO causes nitrosative stress due to the high reactivity of NO and NO-derived compounds. In yeast, NO may be involved in stress responses, but NO and its signaling have been poorly understood due to the lack of mammalian NOS orthologs in the genome. Even though the activities of NOS and NIR have been observed in yeast cells, the gene encoding NOS and the NO production mechanism catalyzed by NIR remain unclear. On the other hand, yeast cells employ NOD and GSNOR to maintain an intracellular redox balance following endogenous NO production, exogenous NO treatment, or environmental stresses. This article reviews NO metabolism (synthesis, degradation) and its regulation in yeast. The physiological roles of NO in yeast, including the oxidative stress response, are also discussed here. Such investigations into NO signaling are essential for understanding the NO-dependent genetic and physiological modulations. In addition to being responsible for the pathology and pharmacology of various degenerative diseases, NO signaling may be a potential target for the construction and engineering of industrial yeast strains.

Nitric Oxide Modulates Lead Content during Lead-Induced Cell Killing in Yeast Cells

“…In that study and in ours, an increase in the NO level is closely correlated with the toxic effect of Pb on cells. In yeast, NO is generated mainly via NO synthase-like activity [48]. An increased level of NO in response to Pb exposure is mainly due to an increase in the expression of NO synthase-like genes [49][50].…”

Lactoferricin B like peptide triggers mitochondrial disruption‐mediated apoptosis by inhibiting respiration under nitric oxide accumulation inCandida albicans

“…Nitric oxide (NO) is a diffusible free radical with a strong antimicrobial effect. NO is produced by nitric oxide synthase (NOS), which catalyzes the conversion of l ‐arginine into NO and l ‐citrulline 13 . In yeast, NOS‐like enzyme has been identified and its activity is regulated in a manner similar to NOS in mammalian cells 14 .…”

“…However, excessive endogenous NO level can cause damage to the cell system as a result of the nitrosative stress development 15 . In particular, posttranslational modification of biomolecules induced by nitrosylation leads to specific pathways that inhibit cell growth or induce cell death 13 . Previous reports have shown that yeast cells treated with H 2 O 2 or menadione cause increased intracellular NO, thereby reducing cell viability 16 .…”

Horizontal gene transfer in the human and skin commensalMalassezia: a bacterially-derived flavohemoglobin is required for NO resistance and host interaction

“…While little is known about NO synthesis in fungi, in mammals NO is synthesized by NO synthases (NOS isoforms), and NO functions as a signaling molecule and biomolecule modifier affecting various cellular processes. Imbalance in cellular NO levels leads to altered redox homeostasis, resulting in the production of reactive nitrogen species (RNS) responsible for nitrosative stress 8,9 . Type I flavohemoglobin constitutes the main enzyme deployed by microbes to counteract NO toxicity by converting it to inert nitrate, a source of nitrogen, via the NO-dioxygenation reaction 8,9 .…”

“…Imbalance in cellular NO levels leads to altered redox homeostasis, resulting in the production of reactive nitrogen species (RNS) responsible for nitrosative stress 8,9 . Type I flavohemoglobin constitutes the main enzyme deployed by microbes to counteract NO toxicity by converting it to inert nitrate, a source of nitrogen, via the NO-dioxygenation reaction 8,9 . A type II flavohemoglobin has also been identified in Mycobacterium tuberculosis and other actinobacteria, but it lacks NO consuming activity and it utilizes D-lactate as an electron donor to mediate electron transfer 10,11 .…”