Endogenous nitric oxide regulates the recovery of the radiation-resistant bacteriumDeinococcus radioduransfrom exposure to UV light

Authors:
Publisher website
Google Scholar
Abstract
Deinococcus radiodurans(Dr) withstands desiccation, reactive oxygen species, and doses of radiation that would be lethal to most organisms. Deletion of a gene encoding a homolog of mammalian nitric oxide synthase (NOS) severely compromises the recovery of Dr from ultraviolet (UV) radiation damage. The Δnosdefect can be complemented with recombinant NOS, rescued by exogenous nitric oxide (NO) and mimicked in the wild-type strain with an NO scavenging compound. UV radiation induces both upregulation of thenosgene and cellular NO production on similar time scales. Growth recovery does not depend on NO being present during UV irradiation, but rather can be manifested by NO addition hours after exposure. Surprisingly,nosdeletion does not increase sensitivity to oxidative damage, and hydrogen peroxide does not inducenosexpression. However, NOS-derived NO upregulates transcription ofobgE, a gene involved in bacterial growth proliferation and stress response. Overexpression of the ObgE GTPase in the Δnosbackground substantially alleviates the growth defect after radiation damage. Thus, NO acts as a signal for the transcriptional regulation of growth inD. radiodurans.

This publication has 52 references indexed in Scilit: